What Disease Was Plague?

What Disease was Plague?
Ole Benedictow - 978-90-04-19391-8

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Brill’s Series in the History
of the Environment
General Editor
Aleks Pluskowski, University of Reading
VOLUME 2
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What Disease was Plague?
On the Controversy over the Microbiological

Identity of Plague Epidemics of the Past
By
Ole J. Benedictow
LEIDEN • BOSTON
2010
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On the cover: “La peste.” From “Annales de Gilles le Muisit,” Tournai, 1353. Ms. 13076/77 f. 24v
Katalog Parler 3, S. 73. Bibliotheque Royale Albert I., Brussels, Belgium.
This book is printed on acid-free paper.
Library of Congress Cataloging-in-Publication Data
Benedictow, Ole Jørgen.

What disease was plague? : on the controversy over the microbiological identity of plague
epidemics of the past / by Ole J. Benedictow.
p. ; cm. -- (Brill’s series in the history of the environment, ISSN 1876-6595 ; v. 2)
Includes bibliographical references and index.
ISBN 978-90-04-18002-4 (hardback : alk. paper) 1. Plague--Microbiology. 2. Plague--
Epidemiology. 3. Plague--History. 4. Communicable diseases--History. I. Title. II. Series:
Brill’s series in the history of the environment ; v. 2. 1876-6595
[DNLM: 1. Plague--microbiology. 2. Plague--epidemiology. 3. Plague--history. WC 355]
R172.B47 2010
614.5’732--dc22
2010030516
ISSN 1876-6595
ISBN 978 90 04 18002 4
Copyright 2010 by Koninklijke Brill NV, Leiden, The Netherlands.

Koninklijke Brill NV incorporates the imprints BRILL, Hotei Publishing,
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For my sons
Andreas and Tancred
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CONTENTS
List of Figures and Tables ........................................................................xiii

Preface ......................................................................................................... xv
PART ONE
THE ISSUE
1. The Issue and the Problems .................................................................. 3
Introduction............................................................................................ 3
The Human-Flea Theory of Plague Epidemiology ............................ 9
The Revisionists ....................................................................................16
PART TWO
HOW S.K. COHN MAKES PHYSICIANS AND HISTORIANS
“SQUARE THE CIRCLE”
2. The Ethics of Scholarly Work .............................................................25
Introduction..........................................................................................25
How Cohn Makes Medical Scientists “Square the Circle” ..............26
Hankin 1: Cohn’s Attack on Hankin’s Observation of Inverse
Correlation between Mortality and Population Density ............34
Hankin 2: A Brief Study of Cohn’s Technique of Argument ..........38
“The Ugly Americans” .........................................................................44
Cohn’s Accusations of Racism against J. Ashburton
Thompson and L.F. Hirst ................................................................46
How Cohn Makes “Historians Square the Circle” ...........................54
The Attack on Schofield (and Benedictow and L. Bradley) ............62
PART THREE
BASIC CONDITIONS FOR BUBONIC PLAGUE IN
MEDIEVAL EUROPE
3. Rats.........................................................................................................73
Introduction: How to Study Rats in History ....................................73
The Nature of Rats and the Frame of Reference of the
Medieval Mind .................................................................................78
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viii contents
The Question of the Presence of Rats and the

Methodological Fallacy of Inference ex silentio ......................... 85
Ars Moriendi Rattorum: Where Have all the Dead
Rats Gone? ........................................................................................91
Zoobiological and Zoogeographical Arguments on the
Question of Significant Presence of Black Rats in
Medieval Europe ..............................................................................98
The Significance of Evolutionary Theory and Adaptation
by Selection.....................................................................................116
Rat Bones: Material Evidence of the Presence of Rats in
the Middle Ages .............................................................................122
Sociology of Rat-Based Plague .........................................................142
4. The Spread of Bubonic Plague over Distances ...............................151
Contiguous Spread and Metastatic Spread .....................................151
5. Mortality in India ...............................................................................194
Effects of the Anti-epidemic Efforts by British
Colonial Authorities ......................................................................194
6. Was Historical Plague a Viral or Bacterial Disease? The
Question of Immunity .......................................................................205
Introduction........................................................................................205
Re-infection or Immunity? ...............................................................212
Did Plague Become a Child Disease after the Black Death? ........218
Plague according to Social Class, Age and Gender .......................235
A Demographic Case Study: The Necrology of the
Monastery of San Domenico in Camporegio ............................245
The Real Problem and its Solution: Marriage Rates
and Fertility Rates after the Black Death ....................................268
PART FOUR
DEFINING FEATURES
Introduction: Concept of Defining Feature ....................................277
7. Defining Feature 1: Latency Periods ................................................279
8. Defining Feature 2: Inverse Correlation between Mortality
Rate and Population Density ........................................................289
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contents ix
Introduction ......................................................................................289
More Data on the Inverse Correlation in India and
Historical Europe..........................................................................291
Scott and Duncan and the Correlation between Population
Density and Mortality ..................................................................301
Epilogue: Sweating Sickness and the Inverse Correlation ..........311
9. Defining Feature 3: Buboes as a Normal Clinical
Feature in Epidemics ...................................................................312
General Introduction.......................................................................312
Contemporary Notions and Observations of Buboes
(and Associated Secondary Clinical Manifestations) .............322
Scott and Duncan: The Problem of Buboes ..................................334
Cohn: The Problem of Buboes .......................................................340
Cohn and Boccaccio: Buboes, Pustules and Spots ......................359
10. Defining Feature 4: DNA of Yersinia pestis from
Plague Graves ...............................................................................381
11. Defining Feature 5: Seasonality of Bubonic Plague .....................396
Introduction: Bubonic Plague’s Association with
Moderately Warm Temperatures and Seasons .........................396
Seasonality of Historical Bubonic-Plague Epidemics
with Emphasis on the Transseasonal Form ..............................398
The Seasonality of Plague and Mortality
in England 1340–1666.................................................................420
Duration of Vacancies in Parish Benefices during the
Black Death ...................................................................................436
Temporal Relationship between the Territorial Spread
of the Black Death and Increase in Institutions .......................463
Summary and Conclusion ..............................................................482
PART FIVE
THE ALTERNATIVE THEORIES
Introduction: The History and Essence of the
Alternative Theories ....................................................................487
12. The Beginning: The Alternative Theories of Shrewsbury
and Morris ....................................................................................489
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x contents
Shrewsbury: the Composite, Low-Intensity Theory ....................489

Morris: The Primary Pneumonic Theory......................................491
13. Gunnar Karlsson’s Alternative Theory: That Historical Plague
was Pure Epidemics of Primary Pneumonic Plague ...............493
Introduction ......................................................................................493
Karlsson and Benedictow ................................................................495
Could Plague Have Come to Iceland from Anywhere? ..............502
Pure Epidemics of Primary Pneumonic Plague: Fact
or Fiction? .....................................................................................511
Primary Pneumonic Plague in Manchuria: A Model
for Iceland? ...................................................................................514
The Spontaneous Decline of Epidemics of Primary
Pneumonic Plague .......................................................................518
The Icelandic Climatic Theory of Primary
Pneumonic Plague .......................................................................528
Mortality Rate of the Purported Plague Epidemics
in Iceland.......................................................................................530
Summary: Why There Never Was a Plague Epidemic
in Iceland.......................................................................................533
Was the Black Death in Bergen (Norway) 1349 Primary
Pneumonic Plague? .....................................................................536
14. Twigg’s Alternative Theory .............................................................553
Introduction ......................................................................................553
The Alternative Theory of Anthrax................................................555
The Historical Basis: The Use of Obsolete
and Peripheral Studies .................................................................560
The Telluric-Miasmatic Theory of Anthrax ..................................562
The Pace of Spread of Plague ..........................................................566
Anthrax and the Name Black Death ..............................................571
Anthrax’s Historical Association with Other Epizootics
among Domestic Animals and Plague ......................................574
The Black Death’s Origin and Spread and the
Anthrax Theory ................................................................................580
Twigg’s Demographic Argument ...................................................595
Concluding Remarks .......................................................................608
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contents xi
15. The Alternative Theory of Scott and Duncan...............................610

Introduction ......................................................................................610
Disparaging Views of Historians and Physicians: Motive
and Objective................................................................................611
The Material Scholarly Basis of Scott and Duncan’s
Alternative Theory .......................................................................615
The Demography of Historical Plague ..........................................628
The Reed-Frost Theory of Epidemiology ......................................633
The Filoviridal Theory of Historical Plague: A Study in
Academic Fiction .........................................................................636
The Significance of Autopsies .........................................................653
The African Confinement ...............................................................661
16. Cohn’s Alternative Theory ..............................................................664
Epilogue ....................................................................................................673
Appendix 1 Black Death Mortality in Siena: The Material Provided
by the Necrology of the Monastery
of San Domenico in Camporegio and
Summarized in Table 5 .....................................................675
Appendix 2 The Accounts of the Icelandic Epidemics of
1402–4 and 1494–5 Given in Icelandic Annals ............680
Appendix 3 The Extrinsic Incubation Period and the Structure
and Composition of the Latency Period ........................682
Glossary ....................................................................................................688
Bibliography .............................................................................................693
Index of Subjects......................................................................................717
Index of Geographical Names and People ...........................................730
Index of Names ........................................................................................740
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LIST OF FIGURES AND TABLES
Map
1. Spread of the Black Death in the Old World, 1346–53 ..................... 2
Figures
1. Population density and morbidity (epidemics of plague).............297
2. Plague in Bergen 1565–6. Mortality in the Cathedral’s
parish ...............................................................................................408
Tables
1. Life table, model south, level 3: life expectancy and
mortality at various ages in a population of females
with life expectancy at birth (eo) of 25 years ..............................230
2. Interments by month and week in the Dominican
cemetery in Siena in 1348 .............................................................249
3. Interments by month and week in the Dominican
cemetery in Siena in 1363 .............................................................250
4. Proportion of child burials in the cemetery of Camporegio
in Siena, 1337–78 ...........................................................................254
5. Proportion of child and female burials registered in the
necrology of the Dominican cemetery in Siena, 1337–78........258
6. Microbiological identifications of Yersinia pestis: year of
publication, time of epidemic(s), and localities .........................390
7. Plague in Bergen 1565–6. Mortality in the Cathedral’s
parish ...............................................................................................406
8. Percentage of mortality July–October 1340–500 among
English tenants-in-chiefs ..............................................................423
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PREFACE
Den som vill mitt fotspor fylgje

Lær’kje a blidom hjarta.
Olav Åsteson
This monograph is not a work of intellectual love and joy, but of schol-
arly duty. I consider it a duty to examine and repudiate some alterna-
tive theories of the microbiological and epidemiological nature of
historical plague epidemics. I do so not only because I consider that
they are methodologically and factually grossly flawed, but also because
they misrepresent the life work of a large number of fine and dedicated
medical and historical scholars, many of whom cannot rise from their
graves to defend themselves. Against this backdrop, it cannot come as
a surprise that I believe that this monograph will provide substantial
material for discussion of the ethics of scholarly investigation. I also
believe that parts will be useful for the teaching of the basic tenets of
the methodology of social science and history. Thus, only very reluc-
tantly have I embarked on writing this monograph, and only because I
consider it absolutely necessary and an ethical duty.
In the great medieval Norwegian visionary poem the Dream Lay the
narrator Olav Åsteson, after having visited hell and a part of paradise in
his great dream, warns his audience that “those who follow in my foot-
steps will not laugh from joy in their hearts.” Long ago, in the autumn
term of 1967, I studied late medieval Russian history at the University
of Moscow after having received a scholarship from the Norwegian
Ministry of Foreign Affairs. The opportunity of meeting Russian schol-
ars and students made a lasting impression on me, not least their icy
black humour conveyed in anecdotes that reflected the life of scholars
who had endured the not-so-distant years of Stalinist terror. T.D.
Lysenko, the fraudulent biologist of Stalinist theory, was not dismissed
from his post until 1965. During my work on this monograph, one of
these anecdotes repeatedly came to mind: Professor Tarakanov [i.e.,
“Cockroachson”] carried out a research project on cockroaches. He
took a cockroach from his box of healthy and agile specimens, tore off
a pair of legs, put it down on the table and screamed at it at the top of
his voice: “Run! Run!” And the cockroach crawled across the table as
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xvi preface
best it could. When it reached the end of the table, the researcher
grabbed it, tore off another pair of legs, put it down and screamed at it
again: “Run! Run!” And the desperate cockroach actually managed to
move across the table. However, at the end of the table the researcher
grabbed it again, tore off its last pair of legs, put it down on the table
and screamed: “Run! Run!” But this time the cockroach did not move.
The researcher noted his conclusion in the project’s notebook: “With
this experiment, I have proved that cockroaches are animals with their
hearing organs on their legs.”
However, in upbeat moments I entertain the hope that the medical
and historical plague research brought together in this monograph will
make it more difficult to launch misguided alternative theories in the
future. I also hope that any new alternative theories will take into
account the actual tenets of earlier scholars and the latest data of plague
research.
OJB
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PART ONE
THE ISSUE
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Map 1. Spread of the Black Death in the Old World, 1346–53
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CHAPTER ONE
THE ISSUE AND THE PROBLEMS
Introduction
Most of our knowledge of bubonic plague was established by medical

scholars and entomologists, often organized in research teams who
studied the great wave of plague epidemics in China, India, Indonesia,
Madagascar, and elsewhere in the period c. 1894–1940, the so-called
third pandemic (the early medieval or Justinianic pandemic of 541–766
being the first, and the late medieval and early modern pandemic of
1346–1722 being the second). Much valuable research has also been
performed in Russia/Soviet Union and the U.S.A, both with respect to
laboratory work and field studies and on endemic cases of plague.
Recently, during the Vietnam War, American military physicians found
themselves in the midst of the last large epidemics of bubonic plague
and produced a number of valuable studies on epidemic plague. Prior
to this, at the end of the nineteenth century and in the early decades of
the twentieth century, medical scholars from various countries had the
opportunity to study epidemics of bubonic plague under various cul-
tural and climatic circumstances. They all reached the conclusion that
bubonic plague among human beings was caused by an epizootic
among black rats and was spread from these rodents to human beings
by their fleas. This is still the prevailing opinion: the World Health
Organization (WHO) and Centers for Disease Control (CDC), the
leading international organizations in the combat against communica-
ble diseases, are entirely clear on their internet home pages that bubonic
plague (for all practical purposes) is rat(-flea)-borne plague.1
Many of the scholars who studied modern plague epidemics in India,
China, Madagascar and elsewhere also took a keen interest in the his-
tory of plague, especially W.J. Simpson, G. Sticker, M. Greenwood and
W.G. Liston of the Indian Plague Research Commission, and W.P.
McArthur, L.F. Hirst, R. Pollitzer, J.J. van Loghem, and Wu Lien-Teh.
1
www.who.int/inf, under Global Alert and Response (GAR); www.cdc.gov.
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4 chapter one
They produced a number of very fine works which are indispensable for
all serious scholars of plague-related research.2 They all concluded that
the disease they studied had such close medical, clinical and epidemio-
logical resemblances to the historical plague epidemics that these epi-
demics must at least mainly have been the same disease.3 The fact that
they reached much the same conclusion corroborated their findings.
These outstanding scholars who served so valiantly in front-line com-
bat against bubonic plague reached and maintained this conclusion,
although they noted that historical sources rarely mention significant
mortality among rats.4 As will be shown below, contrary to the impres-
sion provided by modern critics, they argued their case with empirical
evidence, explaining why this should be the case. In recent decades,
this view on the (predominant) identity of modern bubonic plague and
historical plague has been challenged by several scholars who have pre-
sented alternative theories of the microbiological nature of historical
plague and the mechanisms and dynamics of epidemic spread.
According to the standard works on bubonic plague, this disease is
characterized by a complex clinical and epidemiological panorama.
A simplified presentation sufficient for understanding the characteris-
tic manifestations and functions of plague disease and the comparative
aspects of the alternative theories of historical plague is given here,
beginning with a brief outline of the central epidemiological aspects,
which is followed by a similarly brief outline of the main clinical
features.
Plague is caused by a bacterium called Yersinia pestis. Basically,
plague is a disease among rodents, a zootic disease, transmitted by
fleas. This means that the terms “enzootic,” meaning sporadic incidence
of disease among animals, and “epizootic,” meaning significant inci-
dence of spread of a disease among animals, are usual and useful con-
cepts for many parts of the discussion. These terms correspond to
endemic and epidemic incidence of disease among human beings.
Bubonic plague. Plague contagion is mainly transmitted to human
beings by the normal fleas of the house or black rat Rattus rattus,
2
See especially Hirst 1953, Pollitzer 1954, Wu Lien-Teh 1926, Wu, Chun, Pollitzer
et al. 1936.
3
Simpson 1905: 1–39; Hankin 1905: 56–8; Sticker 1908; Greenwood, IPRC 1911b,
Appendix: 93–6; Liston 1924: 900–3. McArthur 1925–6: 355–72; Wu Lien-Teh 1926:
1–9; Wu Lien-Teh 1936a: 1–55; Hirst 1953: 1–100, 121–6; Pollitzer 1954: 13, 37, 102–3,
427; Van Loghem 1918.
4
See the standard works on plague of Hirst 1953: 121–35; Pollitzer 1954: 297; Wu
Lien-Teh 1936a: 8–9.
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the issue and the problems 5
specifically the species Xenopsylla cheopis. Central to the process of

transmission and dissemination of plague is the phenomenon of block-
age in fleas. When fleas ingest blood with sufficient numbers of bacte-
ria, i.e. a sufficient level of septicaemia, the bacteria will proliferate
faster in the stomach system than they are passed through the digestive
canal and will eventually form (more or less) a blockage consisting of
bacteria and blood mass. This means that when a blocked flea attempts
to feed, the ingested blood will hit the blockage and be forced back or
regurgitated into the bite wound, taking with it small bits of the block-
age containing thousands of plague bacteria. This is the only way that
fleas can transmit infectious doses of plague contagion to human
beings. Blocked fleas will discharge this contagion at a subcutaneous
level suitable for being handled by the body’s first-line defence, the
lymphatic system, and the contagion is drained through a lymphatic
vein to a lymph node which as a result of the infection swells, produc-
ing the characteristic bubo which is the reason the disease is designated
bubonic plague. This form is called primary bubonic plague.
Because human fleas are bloodsucking insects, they can become
contaminated with plague bacteria ingested with septicaemic blood,
i.e., blood from patients with plague bacteria in their blood, and could
hypothetically become infective and transmit plague bacteria to other
persons when they feed again. However, it has been clearly shown that
in about half of plague cases human beings develop either insignificant
or only slight and transient septicaemia, and that in the other half of
cases they do not develop sufficient levels of septicaemia, except per-
haps in exceptional cases, to produce (sufficient) blockage of the fleas’
ventricular system which alone makes fleas infective. The incidence of
septicaemia is much higher in rats and the level of septicaemia is gen-
erally 500–1000 times higher than in humans. This is the reason that
rat fleas so often become grossly infected, and since Xenopsylla cheopis
also has a particular natural biological propensity for it, develops block-
age far more easily and often than any other species of flea. These are
two of the main conditions which make these fleas the preeminent vec-
tor of plague to human beings and why interhuman cross-infection by
human fleas between cases of bubonic plague has not been observed
and must be an improbable occurrence.5
5
Wu Lien-Teh 1926: 184–7; Bibikova and Klassovskiy 1974: 110–2. See also Girard
1943: 4–41; Pollitzer 1954: 482–4; Benedictow 1993/1996: 228–64. A brief summary
can be found in Benedictow 2004: 11–7.
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6 chapter one
All of the above-mentioned leading scholars and researchers of

bubonic plague agree on the epidemiological mechanisms and struc-
tures governing the spread of bubonic plague. The two main forms are
contiguous spread by contact between rat colonies and metastatic
spread by the movement mainly of rat fleas, but also of infected rats, by
human agency in clothing, luggage or merchandise, which is by far the
most important form. The last method of spread is denied by all advo-
cates of alternative theories despite massive empirical documentation
in primary studies as well as broad presentation in all standard works,
and this denial therefore constitutes a denial of fact. This point will be
presented in great detail in chapter 4.6
The fact that bubonic plague has its basis in black rats and their rat
fleas gives the disease a characteristic pattern of development. When
an infective rat flea of the usual species Xenopsylla cheopis has been
introduced into a rat colony, it takes ten to fourteen days before the rat
colony has become so decimated that it becomes difficult for the great
numbers of fleas which have gathered on the remaining but soon-to-
die rats to find new hosts. After about three days of fasting, hungry rat
fleas will also feed on nearby human beings. When human beings have
been infected with bubonic plague, the infection takes on average three
to five days to incubate before the disease breaks out: the course of the
illness takes on average three to five days. This means that from the
introduction of plague contagion among rats in a human habitation it
normally takes nineteen to twenty-seven days on average, and usually
around twenty-three days, before the first person dies from plague.
This time lag or latent period between importation of contagion and
the first human case(s) is one of the defining features of bubonic plague.
This process is repeated by the spread of infective rat fleas (by contigu-
ous spread or metastatic spread) to other rat colonies where the disease
will develop in a similar way. The development of a plague epidemic is
characterized by a slow initial phase, an endemic phase, with only a
sprinkling of human cases while the underlying epizootic processes
acquire increasing momentum, and an epidemic phase in which the
disease manifests itself in several concomitant deaths and cases of
severe illness. The transition into an epidemic phase takes around forty
days after the introduction of plague contagion into a rat colony in a
human community. The developmental phases of plague epidemics
6
See below: 151–93.
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from the introduction of an infective rat flea into a colony of black

rats to the full-scale epidemic developments are given in more detail
below.7
This background reveals a number of basic requirements if an epi-
demic of bubonic plague is to occur, such as broad distribution of black
rats in human habitats and housing and efficient mechanisms of terri-
torial spread in order to occasion high morbidity and mortality rates at
various levels of territorial organization: local societies, regions, coun-
tries, and so on. This background also produces a number of character-
istic clinical and epidemiological features or manifestations of bubonic
plague which represent singly or in combination the defining features
of the disease and, taken together, constitute a model of the disease.
This corresponds to the methodological distinction between necessary
conditions and sufficient conditions for the rise and spread of epidem-
ics of bubonic plague. This distinction is the central topics of Parts 3
and 4 of this monograph. Taken together, these conditions for bubonic
plague constitute a model which can serve as the basis for comparison
with historical plague epidemics and with other diseases, specifically
the alternative microbiological theories, in order to examine compati-
bility or correspondence and by this process determine which of them,
if any, could have functioned as the microbiological basis for historical
plague epidemics.
Septicaemic and pneumonic plague. In around half of the cases of
bubonic plague, contagion breaks out of the buboes and enters the
bloodstream producing septicaemia, in this case secondary septicae-
mic plague, because this condition is secondary to the primary bubonic
infection.8 This term serves also to distinguish this form from the form
of bubonic plague called primary septicaemic plague, which occurs
when the flea bites directly into a blood vessel and regurgitates plague
contagion directly into the blood stream. Since the contagion is depos-
ited directly into the blood stream, this mechanism of infection avoids
the lymphatic first-line defence system and therefore does normally
not produce buboes. This condition is so dramatic that the average
duration of the illness is about fifteen hours, and normally less than one
7
8
Pollitzer 1954: 205–6: “Of special importance is the fact that the high concentra-
tion of toxin within, and in the vicinity of, the primary buboes leads to haemorrhagic
infiltration of the walls of the neighbouring veins (first noted by Childe) and conse-
quently to the passage of the bacilli into the blood-stream.”
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8 chapter one
day.9 This form constitutes normally only a few per cent of cases in a
bubonic plague epidemic.
Secondary septicaemic plague means that plague bacteria are trans-
ported also to the lungs where they may consolidate and cause pneu-
monia, a condition called secondary pneumonic plague, because the
pneumonic condition is derived from and therefore secondary to the
primary bubonic infection and subsequent septicaemic developments.
This occurs in about 10 to 25 per cent of bubonic cases.10 Such patients
tend to develop a cough with bloody expectoration (sputum) contain-
ing plague bacteria which occasionally may infect others by droplet
infection, a condition called primary pneumonic plague since the dis-
ease originates in the diseased person’s lungs.
Since a person who has inhaled plague-infected droplets from a case
of secondary pneumonic plague may develop a lung infection that
reproduces the cough with bloody expectoration, and this person who
suffers from primary pneumonic plague may spread the disease to
other person(s), primary pneumonic plague can take on an independ-
ent epidemic form. Outbreaks of largish epidemics of primary pneu-
monic plague in Manchuria in 1910–1 and 1921–2 provided ample
opportunity to study this form of plague in which Yersinia pestis is
spread by interhuman cross-infection by droplets. These are the only
known instances of largish epidemics for the reasons explained below.
A considerable number of small and even tiny epidemics of primary
pneumonic plague have been medically and epidemiologically stud-
ied.11 It is also generally agreed among researchers of primary pneu-
monic plague that epidemics of this type always start from human cases
with bubonic plague who develop secondary pneumonia, and thus that
this form of plague always originates in a plague epizootic among
rodents; as a result, there is no such phenomenon as pure epidemics of
primary pneumonic plague.12 Primary pneumonic plague will be dis-
cussed in detail below, since it is represented by one of the alternative
theories.13
Taken together, cases of primary septicaemic plague which do not
exhibit buboes as a clinical feature constitute only a few per cent of the
9
Philip and Hirst 1914–6: 529–30, 534–5; Benedictow 1993/1996a: 23–4.
10
See, Benedictow 1993/1996: 25 and fn. 34.
11
Benedictow 1993/1996: 220–3; and see below: 518–27.
12
See below: 511–4.
13
Below: chapter 13: 493–552. Also see the thorough discussion of primary pneu-
monic plague in Benedictow 1993/1996: 23–32, 214–27.
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victims of a bubonic plague epidemic. Pneumonic plague introduces a

tiny element of cross-infection which does not affect the main thrust or
character of the epidemiological process of spread.
Lethality. The lethality rate, also called case mortality rate or fatality
rate, of bubonic plague epidemics is, on average, 80 per cent, meaning
that about 80 per cent of those who contract the disease die from it.14
A normal lethality rate of this order of magnitude is highly unusual for
epidemic diseases and signals therefore that the disease is bubonic
plague.
The Human-Flea Theory of Plague Epidemiology
The history of alternative theories of the transmission of bubonic

plague may be said to have begun with the theory which attributes
importance to the role of the human flea (and even lice), usually as a
contributory vector. This theory was launched early in the twentieth
century and attracted a few loyal supporters. It was revived by the
French scholars G. Blanc and M. Baltazard who published studies based
on a small outbreak in Morocco in 1941. Their work was carried out
mostly in the laboratory, although they also conducted some field work.
They argue enthusiastically that the human flea could take on an impor-
tant role in the spread of plague epidemics in Morocco and perhaps
elsewhere in Northern Africa where the density of human fleas is
exceptionally high due to particularly favourable climatic conditions
and the cultural habits of housing, clothing and (un)cleanliness, and
that the density of human fleas could compensate for its poor vector
capacity.15 It is important to note that Blanc and Baltazard did not argue
for the wide-reaching importance of their findings maintained by some
of their self-proclaimed supporters (below).
Blanc’s and Baltazard’s studies and conclusions were immediately
met with devastating criticism, first, in 1943 by G. Girard, then Director
of the Pasteur Institute of Paris.16 Next, L.F. Hirst took a close, compre-
hensive and very critical view of their studies in his standard work on
plague of 1953, closely followed by R. Pollitzer who in his standard
14
Benedictow 1993/1996: 146–9, summarizes all data on lethality in historical
plague epidemics.
15
Blanc and Baltazard 1941: 813–6; 1942: 446–8; 1943: 208–16; 1945: 173–354.
16
Girard 1943: 4–43. See also Girard 1955: 253–76.
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10 chapter one
work of 1954 thought it was “conceivable” that the human flea “might
play” an “important role in the transmission of plague” in Morocco, the
exceptional infestation of human fleas “compensating for what it lacks
in vector capacity,” but not elsewhere.17 These two scholars had vast
experience in the combat of plague in the field and in the laboratory.
Finally, in the last standard work, which however is a more general
work on Yersinia infections, T. Butler states bluntly: “The human flea
Pulex irritans is not an efficient plague vector and rarely, if ever, has
transmitted plague from man to man.”18
In my doctoral thesis of 1993, I carefully presented and discussed
Blanc’s and Baltazard’s studies and also had to conclude that they were
deeply flawed. Thus, the conclusions in my thesis in this respect were in
accordance with the highly competent criticism by Girard, Hirst and
Pollitzer. However, unlike Hirst and Pollitzer, I believe that “the possi-
bility of occasional or episodic incidence of interhuman transmission”
“should be seen as a possible slight undercurrent running concomi-
tantly and as an integral part of bubonic plague epidemics” also in the
Nordic countries.19 The internationally acclaimed plague specialist
T. Butler was attached to the doctoral committee appointed by the
Department of History, University of Oslo, to evaluate my thesis. While
his comments were generally very positive, he rejected my acceptance
of a small but arguably significant or noticeable role for the human flea.
I have since had occasion to reconsider my arguments and acknowl-
edge that Butler was right in his criticism. Decisive significance should
have been given to neglected Soviet research I presented which showed
that the minimum number of ingested bacteria which induced devel-
opment of blockage in the superior plague vector X. cheopis was in the
order of 50,000–100,000 bacteria, blockage occurring in three of
twenty-eight fleas.20 Since only three (20 per cent) of them were blocked,
it may appear reasonable to assume that the minimum number of
ingested bacteria conducive to the development of blockage under
these laboratory conditions would have to be in the upper reaches
of this range, in the order of magnitude of 75,000–100,000 bacteria.
In order to infect a feeding flea at this level, the host must have a level
of septicaemia on the order of 150–200 million bacteria per cc of
17
Hirst 1953: 239–46; Pollitzer 1954: 380–1. Cf. Pollitzer and Meyer 1961: 474–5.
18
Butler 1983: 51. Butler has not changed his mind on this point, see Butler 1993.
19
Benedictow 1993/1996: 263; Pollitzer 1954: 392.
20
Bibikova and Alekseyev 1969: 196–202; Bibikova and Klassovskiy 1974: 111–2.
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blood.21 This level of septicaemia and much higher levels occur quite
often in rats, but have never been found in human beings, where the
level only in exceptional cases reaches or surpasses one million bacte-
ria per cc, and normally is only a tiny fraction of this level.22 This
explains perfectly well why cross-infection of bubonic plague between
human beings has never been observed, and will not occur whatever
species of flea are present, and why the density of human ectoparasit-
ism does not matter.
Butler’s strong negative characterization of the human flea’s vector
capacity was repeated by Perry and Fetherston in a long review paper
on central points of plague epidemiology published in 1997, where
they state that “the so-called human flea (Pulex irritans)” was found to
be a “very poor vector.”23 Since then, no new significant research or
divergent opinions on this matter have been presented.
After the publication of my thesis in 1993, the studies by Blanc and
Baltazard have twice been thoroughly re-examined. B.E.B. Persson, the
Swedish physician and historian of epidemic diseases, made an inde-
pendent study of Blanc’s and Baltazard’s works shortly afterwards,
motivated perhaps by disbelief of my conclusions, and yet she reached
the same conclusions.24 In his monograph of 2003, F. Audoin-Rouzeau
takes Blanc’s and Baltazard’s studies to task, especially in a long appen-
dix, revealing unconditionally that they are profoundly flawed,25 appar-
ently independently of my similarly thorough discussion. Neither of
the two leading international organizations for the combat of epidemic
diseases, the World Health Organization (WHO) and the Centers for
Disease Control and Protection (CDC), mentions the human-flea the-
ory on their home pages, instead discussing only rat-borne plague in
relation both to modern and historical plague.26 In the WHO’s latest
Plague Manual, it is stated that plague “is only occasionally transmitted
between humans, either through the bites of human fleas (Pulex irri-
tans) infected after biting patients in the septicaemic stage, or through
direct contact between a healthy person with an infected person.” The
reference is indirectly to the works of Blanc and Baltazard.27 Thus cases
21
Bibikova and Klassovskiy 1974: 111–2; Benedictow 1993/1996: 257–8.
22
IPRC 1906c: 519–23; IPRC 1906d: 524–9; Benedictow 1993/1996: 242–63.
23
Perry and Fetherston 1997: 53.
24
Persson 1994: 98–102.
25
Audoin-Rouzeau 2003: 68–73, 297–343.
26
www.who.int/inf, under Global Alert and Response (GAR); www.cdc.gov.
27
Tikhomirov 1999: 12, 39.
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12 chapter one
of interhuman transmission by the human flea leading to bubonic

plague or by droplets leading to primary pneumonic plague occur only
“occasionally,” which implies that cases of interhuman transmission by
the human flea could have a sporadic incidence.
After all this thorough and devastating criticism of the human-flea
theory and the formation of a broad consensus, the notion of a signifi-
cant or important role for the human flea could be expected to have
been definitely laid to rest.28 However, it was recently revived by a
Professor of Medicine, L. Walløe. He first argued this view in a paper of
1982 which I felt obliged to counter with serious criticism focusing on
problematic correspondence between supporting references and their
factual contents, and subsequently in my doctoral thesis where diverse
points in his paper were discussed and found to be highly problemati-
cal.29 In his second paper on plague published in 2008, he provides no
new research in support of his stance. In the last footnote, he states that
Audoin-Rouzeau is “arguing for the importance of [the flea species]
Nosopsyllus fasciatus in northern Europe as a more likely vector than
Xenopsylla cheopis.”30 This proves that Walløe also knows Audoin-
Rouzeau’s devastating criticism of Blanc’s and Baltazard’s studies and
the foundation of the human-flea theory, yet he is silent on this crucial
point. I have already stated that the WHO and CDC do not mention
the human-flea theory on their home pages in order to underline the
broad consensus on the question of the rat(-flea)-borne foundation of
28
In 2006, prominent French (paleo)microbiologists who had been misled into
accepting the notion that plague spreads only between conterminous rat colonies and
therefore much more slowly than historical plague epidemics presented a research
project with an alternative explanatory model or hypothesis based on G. Blanc’s and
M. Baltazard’s theories which include human ectoparasites: see Drancourt, Houhamdi,
Raoult 2006: 234–41. However, in a personal communication by e-mail 30 April 2009
Professor M. Drancourt made it clear that this view of bubonic plague’s spread is unten-
able. Importantly, he also commented that it was a misunderstanding to consider their
project as support of the human-flea theory and that they had now abandoned this
hypothesis completely but were making studies of a possible role for the human louse.
As proof, the central parts of the e-mail of 30 April are cited: “[…] I am not sure that
our laboratory in Marseilles supported in particular the human flea theory. We indeed
suggested that plague could be transmited by human ectoparasite in special circon-
stances. We indeed already published experimental work on the potential role of
another human ectoparasite, the body louse which is a likely candidate for interhuman
transmission of Yersinia pestis […] I can tell you we are going-on this question.
Sincerely, Prof. Michel DRANCOURT.” [michel.drancourt@univmed.fr]
29
Walløe 1982: 1–45; in 1995 appeared a translation into English which I have not
examined. Benedictow 1985: 84–93; Benedictow 1993/1996a: 126–264.
30
Walløe 2008: 73.
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bubonic plague.31 It is therefore surprising that Walløe is silent on this

and asserts in an editorial or leading article in Journal of the Norwegian
Medical Association32 in a general fashion that the human-flea theory
has been “accepted by plague specialists in WHO, but has not found
great influence among Anglophone historians.”33 This is completely
untrue. The reference to WHO relates to a misquotation of Pollitzer
1960. In his second plague paper of 2008, which was probably at the
publisher when the first statement was made, Walløe maintains that “in
an official WHO publication on plague in 1960, Robert Pollitzer con-
cluded ‘Pulex irritans plays the main role in the spread of human
plague.’ ”34 What Pollitzer really states, referring explicitly to Blanc and
Balthazar, is that:
in areas like Morocco where […] thick layers of clothing and lack of
cleanliness tend to increase human infestation with ectoparasites, Pulex
irritans is apt to take an important part in the transmission of plague, the
high incidence of this species compensating for what it lacks in vector
capacity. At the same time, however, it is certain that in other plague
areas, for example, China, India and also Madagascar, the role of this flea
is negligible, the transmission of the infection depending upon the rat
fleas, particularly X. cheopis.35
This is a very different assertion. Another issue is that since then, almost
fifty years later, this partial and highly restricted admission by one
plague specialist has lost influence among historians of plague and
physicians alike. This shows that it is impossible for Walløe to defend
his position within the perimeters of ordinary scholarly work or
methodology.
In his pursuit of support for his human-flea theory, Walløe finally
states his conclusion couched in terms requiring an ethically impossi-
ble experiment for the falsification of his theory: “My point is that we
at the present know too little about the vector capability of Pulex
irritans, in particular its vector capacity between humans and in the
31
Benedictow 2006: 84, fn. 3.
32
Tidsskrift for Den norske legeforening.
33
Walløe 2007: 3193. My translation from Norwegian.
34
Walløe 2008: 71.
35
Pollitzer 1960: 360–1. Pollitzer should have added here that climate and tempera-
ture are exceptionally favorable to the procreation of fleas. Since Pulex irritans does not
ride with its host except incidentally, the amount of clothing worn by people is not
important nor is lack of personal cleanliness, it is the level of cleanliness within hous-
ing or habitation that matters for the level of infestation of human fleas.
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14 chapter one
environmental conditions found in a bed.”36 Fortunately, however,

more is known about the human flea’s vector capacity in relation to
human environments and sleeping arrangements than about any other
technical aspect of bubonic-plague epidemiology. Despite millions of
bubonic plague cases in India, China, Madagascar and elsewhere—
over thirteen million in India alone—and despite the extensive field
studies of the disease by highly competent teams of specialists, not a
single case of interhuman transmission of bubonic plague by cross-
infection by the human flea has ever been recorded. This is the biggest
conceivable empirical disproof of the potential role of the human flea
in the epidemiology of plague. This finding corresponds closely to the
study of the required levels of infection of fleas for the production of
blockage and the difference in levels of septicaemia between human
beings and rats and guinea pigs. On this crucial topic, there is full cor-
relation between the outcome of experiments in laboratories and
observations in the field. This demonstrates the problems Walløe must
confront as the last protagonist of the human-flea theory and the means
he is obliged to employ in order to try to support his argument.
It must be emphasized that Blanc’s and Baltazard’s opinions on the
significance of human ectoparasitism in historical plague epidemics
were very restricted and cannot satisfy the ambitions of Walløe. Blanc
and Baltazard maintain that, according to their studies, human fleas,
could have played an important part in plague epidemics only in the
great cities of the Middle Ages. Human fleas could not have played any
significant role in rural plague which exhibited only or mainly an
endemic type of spread. Around 1300, some 90 per cent of the popula-
tion of Medieval Europe lived in the countryside. At most, a couple of
per cent lived in urban centres that by any stretch of sociological imagi-
nation or even by relative historical standards for the classification of
urban centres according to size, could be designated large cities. Thus
it is difficult to discern not only the significance but even the relevance
of Blanc’s and Baltazard’s views to historical demography and plague
studies.37 In view of the fact that Norway, for instance, did not contain
any urban centre which can be designated a city (over 10,000 inhabit-
ants), Blanc’s and Baltazard’s studies and views are obviously glaringly
incompatible with the Norwegian social realities at the time of the
36
Walløe 2008: 73.
37
Benedictow 1993/1996: 230–7, 247–50.
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Black Death. If it were true that the Black Death was mainly spread by
human fleas, the effects would hardly have been noticeable, according
to the inferences of these scholars from their studies. The mind-
boggling demographic effects of the Black Death38 presuppose a
disease that spreads with enormous efficiency in sparsely populated
rural areas.
It must also be emphasized that Blanc and Baltazard maintain that
plague epidemics are always initiated by a murine epizootic, and that
there can be no large-scale epidemic of plague spread by human
ectoparasites unless supported by a concomitant epizootic among com-
mensal black rats. Baltazard concludes thus:
The duration of the epidemics [in the past: my insertion] must have been
dependent on the existence of a large murine background. Indeed, if any
proof of the presence of R. rattus in the ancient world is required, it is
furnished by the very existence of plague.39
Ignoring briefly for the sake of argument the serious weaknesses of
their research, Blanc’s and Baltazard’s studies and opinions are of little
consequence for historical plague research and do not provide support
for a notion of a significant role of human ectoparasitism in the spread
and mortality of historical plague epidemics. They also argue for the
pivotal importance of a large presence of black rats and their accompa-
nying of rat fleas. This proves that Blanc and Baltazard have not main-
tained, in fact that no other scholar than Walløe has ever maintained,
that human fleas could play a significant part or main part in the
transmission of plague independent of a large presence of black rats.
The theory that human fleas could spread plague devastatingly in the
countryside in the Late Middle Ages is without basis in any research,
and Blanc and Baltazard are certainly not to be blamed for this mis-
taken theory.
Walløe passes in silence by all crucial basic facts that independently
invalidate the human-flea theory. It has been shown above that human
beings are for all practical purposes excluded as sources of blockage-
producing levels of plague infection of fleas and explained that only
rats and some other rodents develop required levels of septicaemic
blood. He passes also over crucial defining epidemiological features,
38
Benedictow 2004: 273–384.
39
Blanc 1956: 546–8; Baltazard 1960: 261, 251. See also Baltazard, Bahmanyar,
Mostachfi et al. 1960: 153–4.
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16 chapter one
for instance the inverse correlation of morbidity and mortality rates

and population density which excludes that bubonic plague is spread
by cross-infection, and the latency period of c. 19–27 days which
reflects that outbreaks of a plague among human beings are preceded
by a plague epizootic in rat colonies, although they are all presented in
my doctoral thesis, my Norwegian plague history, and my 2004 history
of the Black Death with scholarly references40 (see thorough presenta-
tions below in chapters 7–8).
The Revisionists
The recent history of alternative theories began in 1971, when J.F.D.

Shrewsbury published his monograph on bubonic plague in England
in which he allotted only a marginal role to bubonic plague as a demo-
graphic factor. His work was followed by a number of even more scep-
tical accounts of the bubonic-plague theory which took on the character
of rejection, including C. Morris 1971, G. Twigg 1984, G. Karlsson
1996, S. Scott and C. Duncan 2001 (2004), and S.K. Cohn Jr. 2002, who
all insist that historical plague epidemics were not bubonic plague.
Instead, they argue that historical plague epidemics were pure epidem-
ics of primary pneumonic plague (Morris) or of a mutated version of
that disease (Karlsson) or that they were diseases caused by other
microbiological agents disseminated by other means or mechanisms.
In the first sentence of his monograph, Cohn states with absolute cer-
tainty that the Black Death and subsequent plague epidemics were not
bubonic plague caused by Yersinia pestis, but “was any disease other
than the rat-based bubonic plague.” However, at the end of the mono-
graph he is completely unable to identify any known disease that could
have been the cause of the plague epidemics: “In place of Yersinia pestis
I offer no alternatives.”41 The reality of this conclusion is that his par-
ticular approach to the subject has led him to a panorama of clinical
and epidemiological indications that are incompatible with any known
disease—for very good reasons. However, Cohn clearly has in mind a
viral disease, since he maintains, for instance, that after the Black Death
and increasingly with subsequent plague epidemics plague acquired
40
Benedictow 1993/ 1996: 177–81, 257–8, see also 238–9 for evidence excluding
the possibility of mechanical transmission; Benedictow 2002: 35–7, Benedictow 2004:
16–9, 31–3.
41
Cohn 2002: 1, 247.
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the character of a children’s disease, implying that adults were to a large

extent survivors who had acquired good and persistent immunity,
the hallmark of viral diseases.42 He has also in mind a disease spread
by cross-infection with high spread rates as emphasized on the first
page and repeatedly later; in a later work he asserts that the speed of
spread is similar to influenza.43 These six alternative theories are the
subject of this monograph. One should note that Shrewsbury is a
bacteriologist, Twigg a zoologist, Duncan a biologist, and the other
scholars are historians.
In my opinion, as a point of departure it is unlikely that the scholars
who worked in the midst of great mass bubonic plague tragedies, each
of them having the opportunity to study the spread of plague in the
field and the clinical manifestations of thousands of plague cases,
should individually and collectively have massively misconceived the
comparative clinical manifestations and epidemiological characteris-
tics of historical and modern plague epidemics. It is equally unlikely
that modern scholars without medical training or without ever having
seen a plague patient should discover the truth in their academic ivory
towers: my ivory tower has not bestowed any special insights on me.
All theories of the microbiological and epidemiological nature of
the Black Death have in common the assumption that it was a new
disease in Europe. In order to explain the sudden great mortality, Twigg
is obliged to argue that his alternative “Black Death” disease, anthrax,
was a new disease to Europe (see below). The alternative theories of
Shrewsbury, Morris and Twigg have in common the fact that they are
based on known and existing diseases, which ensures their testability
and comparability and permit discussion using standard scientific
premises. The alternative theories of Karlsson, Cohn and Scott and
Duncan have in common that they have “invented” a new contagion/
pathogen (Cohn) or a mutated variant of known pathogens (Scott and
Duncan, Karlsson).44 These hypothetical new or mutated pathogens are
also all held no longer to exist. This means that the various epidemio-
logical, clinical and demographic features which are attributed to them
were until recently materially untestable, and as such unfalsifiable
and ipso facto invalid and potentially methodologically fallacious.
However, recent developments of genetic science, specifically in
42
See below: chapter 6.
43
Cohn 2002: 1–3, 138–9, 209; Cohn 2005: 1354–5; Cohn and Alfani 2005: 203.
44
Below: 16–18, 487, 494–6, 636, 662.
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18 chapter one
paleomicrobiology, may provide the opportunity of testing genetic

material from skeletal remains in historical plague graves for microbio-
logical identification of the pathogen (see below).
First (in 2001) Scott and Duncan claimed that they had identified
the disease of historical plague to have been a disease caused by a type
of filoviridal contagion, a mutated variant of the Ebola or Marburg
virus. In their second monograph (2004), mostly a popular version of
the first, they wisely chose to be more vague about the type of disease:
We can be sure that the virus responsible for the Black Death is not one
that is known today, indeed, it is possible that it does not even belong to
any of the known families of viruses. However, the symptoms most nearly
resemble those of Ebola, Marburg and the viral haemorrhagic fevers and,
although it was certainly not identical to any of these, of all the diseases
known today they seem to be the most similar to it.45
Scott and Duncan have in reality invented an unknown disease: either
a completely unknown type of virus or an unknown variant of Ebola or
Marburg haemorrhagic disease. By establishing the term “haemor-
rhagic plague” at the beginning of their first monograph,46 they errone-
ously imply that bubonic plague is not characterized by frequent and
comprehensive haemorrhaging.47 Later they find it opportune to
emphasize the feature of necrosis, pretending (also erroneously) that
this is not a usual feature of bubonic plague, and without providing
supporting reference(s) to modern research on filoviridal diseases.48
The keen interest that Karlsson, Scott and Duncan and Cohn take in
genetics is highly selective, confined to a speculative mutational theory
that can be arbitrarily shaped to suit the defence of their alternative
theories, or indeed to any alternative microbiological theory they might
fancy. Mutations are a fact of (micro)biological life. However, to intro-
duce the theory of evolution without the concept of selection and with-
out any demonstration of how the selection mechanisms produced the
specified effects in the case in question, that is, to present in an arbi-
trary way hypothetical mutations that happen to suits a theory, is obvi-
ously unscientific. As it has been aptly put: “mutation absolutely can
not explain anything. It is simply an ad hoc call for a miracle.”49
45
Scott and Duncan 2004: 225.
46
47
48
Scott and Duncan 2001: 71, 381; Scott and Duncan 2004: 224. See below, 423–6.
49
Personal communication from Howard Reisner, Professor of Pathology, University
of North Carolina at Chapel Hill.
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There is a curious and conspicuous fragmentation of the alternative

theories which, except in the case of Morris and Karlsson, have nothing
in common with respect to the microbiological identity of the agent
and the modes of transmission and pattern of spread. The alternative
theories of Shrewsbury (1971), Morris (1971), Twigg (1984), Karlsson
(1996), Scott and Duncan (2001, 2004), and Cohn (2002) are all stri-
dently argued, but obviously incompatible, which is a major source of
scepticism. The two last alternative theories, for example, are based on
paradoxical or contradictory notions of the slowness of spread of
plague and the rapidity of spread respectively. Cohn asserts, as men-
tioned, that plague in the past was a disease spread by cross-infection
with high spread rates similar to influenza, Scott and Duncan argue for
an extraordinary and uniquely long incubation time and for mysteri-
ous infective agents which travel around and spread the disease far and
wide, while Twigg argues for anthrax, which has a short incubation
time, and claims that its dissemination among human beings is depend-
ent on the spread of the disease among domestic animals and is usually
contracted by ingestion of un(der)cooked infected meat. Morris and
Karlsson claim that historical plague was caused by some sort of plague
bacterium spread by cross-infection and transmitted by droplets.
All advocates of alternative theories of the nature of historical plague
have in common that they reject all other alternative theories, but only
the latest contender entering the fray had the opportunity of rejecting
all the other alternatives. It is worth noting that none of them has later
retracted their own theory and accepted any of the other theories.
Obviously, at least five of them must be wrong, and why not all six? In
my opinion, they are all untenable, and for several crucial reasons that
ought to be thoroughly analysed and discussed. Thus, for the time
being there are seven theories of the nature of historical plague epi-
demics: the theory that it was the bubonic plague, and six alternative
theories. We all reject six of the seven theories; the advocates of alterna-
tive theories reject all alternative theories except their own and also the
bubonic-plague theory, whilst I reject all six alternative theories for the
reasons presented in this monograph.
All advocates of alternative plague theories have in common several
basic assumptions that they consider sufficient conditions for rejecting
the idea that historical plague epidemics were bubonic plague. On this
basis, they have developed alternative theories of the microbiological
nature and epidemiology of the historical plague epidemics, emphasiz-
ing some epidemiological and clinical features which they claim
exclude bubonic plague and support their own alternative theories.
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20 chapter one
They take, for instance, the slight reflections of rat plague in the sources
as strong evidence that the European plague epidemics of the past were
not rat-borne bubonic plague transmitted by rat fleas, but some other
disease. This situation calls therefore, they assert, for alternative theo-
ries of the microbiological and epidemiological nature of historical
plague epidemics and forms the background or reason for their endeav-
ours. According to the standards of scholarly discussion, the central
views, assertions, and objections of the protagonists or advocates of
alternative theories will be addressed here in a serious and focused way.
The arguments emphasized by the advocates of alternative theories
against the bubonic-plague theory, and which clear the way for their
own alternative theories, indicate that the following topics are central
to the discussion:
(1) They reject the idea that the black rat was a common or widespread
animal in Europe in the fourteenth century, and they consequently
also deny that rats played a central part in the Black Death and
subsequent plague epidemics, concluding that this is a sufficient
argument for rejecting the bubonic-plague theory.
(2) They assert that bubonic plague spreads only by contiguous dis-
semination between rat colonies, emphasize the very slow pace of
this process of spread and the sharp contrast with the quite consid-
erable spread rates of historical plague epidemics, and maintain
that this constitutes a sufficient argument for rejecting the bubonic-
plague theory.
(3) They point out that the human mortality caused by bubonic plague
in India was only a few per cent, in sharp contrast to the dramatic
mortality rates cause by the Black Death and later plague epidem-
ics, and argue that this in itself constitutes sufficient proof that
bubonic plague and historical plague were two different diseases.
(4) They point out that epidemics of bubonic plague in India produced
higher levels of mortality in villages than in urban centres, and
thus exhibited an inverse correlation between population density
and mortality, but deny that was the case with historical plague
epidemics, which, consequently, would have to have been a differ-
ent disease.
In methodological terminology, each of these four arguments, if
valid, represents a sufficient condition for rejecting the notion that his-
torical plague epidemics were bubonic plague. This also means that
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each of them represents a necessary condition for the spread of bubonic

plague and that they must be collectively confirmed in order to uphold
the tenability of the bubonic plague theory.
Discussion of the tenability of the alternative theories must begin by
clarifying these basic factual issues, which is carried out in Part 3.
If one of these arguments proves to be tenable, historical plague cannot
have been bubonic plague, and the quest for a well-reasoned alternative
microbiological theory is justified. If none of these arguments is
sustainable, all alternative theories will be seriously undermined or
falsified, and the bubonic plague theory will be alive and well.
The fact that bubonic plague originates in rats and fleas produces a
number of characteristic clinical and epidemiological features or mani-
festations which singly or in combination constitute defining features
of the disease. While epidemics of bubonic plague cannot arise if one
of the necessary conditions is not met, the identification of one defin-
ing feature in modern and historical epidemics of plague suffices
to determine the disease with certainty. Defining features are discussed
in Part 4.
The next task must be to examine the tenability of the various alter-
natives through systematic comparison between the central clinical
and epidemiological features that characterize the alternative theories,
bubonic plague and historical plague epidemics, as these features deter-
mine compatibility and, thus, identification. This task is performed
in Part 5.
In principle, and as a point of departure, historical plague epidemics
may not have been bubonic plague, but this does not mean that any of
the six alternatives is tenable, and it is possible that all currently pub-
lished theories of the nature of historical plague epidemics are wrong.
However, if one of the alternatives can be shown to be tenable, it will
represent a very valuable advance in the study of historical plague.
It would mean the disclosure of serious misconceptions and the
identification of the responsible microbiological agent and its medical
and epidemiological characteristics, and would give historical plague
research crucial new tools of analysis and important explanatory
powers.
As the reader will have noted, so far Part 2 has not been mentioned.
In the course of denying the conclusions of outstanding scholars
and pioneers of plague research, some advocates of new theories
about plague have made disparaging remarks which are are utterly
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22 chapter one
misleading and in fact destructive of reality-based discussion of the

central topics at issue. Cohn’s case is so serious that it is the subject of
Part 2: “How S.K. Cohn Makes Physicians and Historians ‘Square the
Circle,’ ” which focuses on his accusation of collective intellectual dis-
honesty and/or scholarly incompetence on the part of dedicated and
competent scholars who have argued for the bubonic plague theory.
This clarification necessarily precedes discussion of the other issues
just mentioned.
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PART TWO
HOW S.K. COHN MAKES PHYSICIANS AND
HISTORIANS “SQUARE THE CIRCLE”
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CHAPTER TWO
THE ETHICS OF SCHOLARLY WORK
Introduction
Scholars who argue for revolutionary new theories in academic fields

where much consensual scholarly work has been performed by dedi-
cated and highly competent researchers must reject a substantial body
of previous work. Such rejection has the potential to lead modes of
argument that do not fulfill usual academic and methodological
standards.
Cohn’s monograph is a case in point. He sets the scene in opening
chapters titled “Scientists Square the Circle” and “Historians Square the
Circle,” in which virtually all medical and historical scholars who have
conducted serious research on historical plague epidemics and accepted
them as bubonic plague are scathingly criticized. The use of the idiom
“square the circle” has unfortunate connotations, implying that those
concerned are either intellectually dishonest or incompetent or both. It
is hard to imagine that competent scholars would handle their material
and apply methodology in such a way as to be open to the severe criti-
cism inherent in this phrase. Cohn also repeatedly strikes out at schol-
ars on subjects that have no, or at best peripheral, relevance to his
theory. His attack, for instance, on the Japanese medical researcher
S. Kitasato who discovered the plague bacillus at about the same time
as A.Yersin does not serve Cohn’s theory, and its unfortunate line of
argument is very different from the supportive and positive comments
made by leading expert medical plague researchers, for instance
L.F. Hirst and T. Butler.1
Cohn makes the most out of the confusion, uncertainties and great
range of opinions and suggestions made by researchers in the early
years of modern plague research around 1900, by using selective read-
ings of that literature to cast doubt on the research processes and the
validity of these early findings and, by implication, to strengthen his
1
Cohn 2002: 7–8; Hirst 1953: 106–9; Butler 1983: 22–4.
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26 chapter two
case for an alternative theory. However, as a historian, Cohn might be

expected to have been more understanding of the historical context of
those studies. In the late nineteenth and early twentieth century, hard
facts were few and tentative approaches and hypothetical notions were
justified. Gradually more hard facts and consensus emerged and there
was a better understanding of the epidemiological processes of trans-
mission and dissemination of plague. This process of accumulation and
systematization of knowledge in time formed a consistent and empiri-
cally well-founded theory of plague epidemiology and understanding
of the physical developments of the course of plague disease and its
characteristic clinical manifestations.
These developments also gave rise to a universal opinion among
plague researchers that the modern epidemics of bubonic plague they
studied were the same disease that ravaged late medieval and early
modern Europe. This unanimity presents a significant obstacle to
Cohn’s theory. For this reason, Cohn has no alternative but to discredit
in general terms researchers in the fields of plague medicine, epidemi-
ology and plague history. He vigorously accuses historians and medical
scholars of squaring the circle. How then, does Cohn belittle the com-
petence and, as it may seem, the intellectual integrity of so many schol-
ars who have made important contributions to historical or medical
plague research?
How Cohn Makes Medical Scientists “Square the Circle”
Plague research is blessed with several excellent standard works that

bring together and synthesize the vast corpus of medical and historical
studies on the disease written by outstanding medical scholars who
dedicated their professional lives to combating plague in the late nine-
teenth and early twentieth century during the so-called “third pan-
demic.” Since the outcome of their observations and studies are so
strongly at odds with the premises of Cohn’s theory, Cohn was obliged
to partially or wholly discredit their work. It is a scholarly duty to reveal
Cohn’s methods in performing this task. This will be achieved through
ample citations which will reveal Cohn’s procedure in detail. Hirst’s
standard work The Conquest of Plague is particularly dangerous to
Cohn’s theory because it is constructed along medical historical lines.
It contains powerful counter-arguments to Cohn’s theory and strongly
supports the notion that historical and modern plague epidemics were
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the ethics of scholarly work 27
the same disease: “there can be no doubt, however, judging from the
detailed descriptions that have come down to us, of the clinical identity
of the plagues of ancient and modern times.”2 Thus Hirst’s standard
work and his person3 are singled out for misleading and disparaging
assertions which can here be demonstrated only through the study of
representative quotations.
Cohn maintains, for instance, that Hirst’s “insistence that modern
and medieval bubonic plague were the same led him into self-
contradictions and other complications” and that his “lifetime thesis
[…] was brushed aside to explain how the fast-spreading, contagious
fourteenth-century and the slow-moving modern plague could be the
same.”4 This is not correct. Firstly, Hirst strongly and consistently
upholds the opinion that the Black Death and subsequent plague epi-
demics were bubonic plague, and does not at all believe that these epi-
demics were contagious in the interpersonal sense of the word
cross-infection (excepting cases of primary pneumonic plague).5
Secondly, since Hirst, as shown below in Part 3, strongly emphasizes
that bubonic plague spreads (and spread) over considerable distances
by (metastatic) leaps through the transportation of goods containing
infected rat fleas, especially grain, cotton, woollens, textiles, and over
short and medium distances often in luggage and clothing,6 he does not
at all have a problem with the spread rates of historical plague epidem-
ics when compared with modern plague epidemics that spread in the
same way by ship, train, and so on. Actually, Hirst devotes over 150
pages to this subject of mechanisms, patterns and rates of spread and is
not to be misunderstood, certainly not in the way asserted by Cohn.
Hirst is entirely clear on the question of spread rates: “All three pan-
demics spread along the main lines of communication in a similar way
at a similar rate; it seems improbable, therefore, that their epidemiol-
ogy can really be very different.”7 Thus, in strong contrast to Cohn’s
assertion on this point, Hirst argues for the identity of the so-called
Justinianic pandemic, the late medieval and early modern pandemic
and the “third” modern pandemic of 1894-c. 1940, and an important
2
Hirst 1953: 121; see also below.
3
See below: 46–54.
4
Cohn 2002: 19–20.
5
Hirst 1953: 331–4, 121–7, 189, 246.
6
Hirst 1953: 303–455.
7
Hirst 1953: 122.
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28 chapter two
argument to him is exactly the identity of the patterns and rates of

spread. Conspicuously, Cohn does not provide footnotes which would
make his assertions with respect to Hirst’s opinions testable according
to ordinary principles of scholarship.
According to Cohn’s theory the Black Death was a viral disease
which was spread effectively by interpersonal dissemination of the
contagion, while he asserts that modern bubonic plague epidemics
spread only exceedingly slowly by contact between contiguous rat col-
onies (see below). These assertions produce the implication that there
would be a great difference in spread rates between the late medieval
plague epidemics and bubonic plague. Cohn must misquote Hirst’s text
in order to suggest that Hirst brushed aside his long-held theory, and to
be able to provide an alleged explanation of what Cohn erroneously
claims that Hirst means, namely, that the plague epidemics of the Late
Middle Ages spread much more rapidly than “anything seen in Morocco
or any other plague epidemic of the twentieth century.” This assertion
is again made without a supporting footnote that would enable the
critical reader to check its validity. In the following citation from Cohn’s
monograph italics indicate an important phrase which Cohn had omit-
ted from his citation from Hirst’s text (Cohn’s footnotes are supplied in
brackets):
Hirst turned to the improbable Pulex irritans8 to account for the differ-
ences, now seeing this flea as an “important auxiliary in transmitting the
infection is most plausible for the period of the Black Death” in the late
Middle Ages. Such a flea as the late-medieval plague’s vector made it pos-
sible to explain away another discordant feature between the two plague
pandemics: earlier, characteristic of highly contagious diseases that
spread person-to-person, plague deaths clustered in households, while
twentieth-century plague shows no such tendency. [fn. 72: Hirst 1953:
246] Thus to maintain the identity between the two waves of disease,
Hirst was willing to forego the cornerstone of his life’s work, the central
importance of one rat-flea, X. cheopis, for explaining when plague reached
epidemic proportions among humans. [fn.73: Hirst 1953: 240, 244]9
Clearly, Hirst does not assert that Pulex irritans was generally an impor-
tant auxiliary in transmitting plague infection. As can be seen from the
phrase which has been restored to the quotation, he makes a highly
restricted comment or admission, restricted both with respect to level
8
The human flea, my footnote.
9
Cohn 2002: 21.
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of tenability, as indicated by the word “plausible,” and restricted with

respect to circumstance, namely to the Black Death. This view is pre-
ceded by a statement that explains and again underlines the highly
restricted relevance or perspective of his text on this point, which Cohn
neglects to cite or mention: “in the medieval and classical plagues” the
human flea could have played “a subordinate part in the spread of the
disease between members of the same household when present in
enormous numbers in the bedrooms of cases of septicaemic plague.”
The point is that Hirst in a chapter on “Interhuman plague,” and in the
context of an in-depth discussion of the possible role of the human flea,
also discusses over a number of pages assertions by the French scholars
G. Blanc and M. Baltazard to the effect that the human flea Pulex irri-
tans played a predominant role in outbreaks of plague in Morocco, and
that this also had been the case with the medieval plague epidemics in
the big cities of the time, though not in the countryside.10 In contrast to
Cohn’s dismissive style, Hirst, a gentleman scholar who studied at
Oxford, attempts to be as generous as possible with a position with
which he fundamentally disagrees. He is willing to consider the possi-
bility that the human flea could have played “a significant part” in the
Moroccan plague epidemics, because the human flea was present in
truly enormous and amazing numbers in the houses, but only in rela-
tion to severe septicaemic cases: “when their density is very high and
the blood in human cases contains many plague bacilli.”11 However,
Hirst is also very clear in his conclusion:
P. irritans occasionally spread plague from man to man in certain parts of
North Africa where this human flea is superabundant, though, even in
Morocco, it is highly probable that X. cheopis [i.e., the flea of the black rat:
my insertion] is the chief vector as elsewhere in the world today.12
It now also becomes clear that it is Blanc’s and Baltazard’s view he is
willing to consider as “plausible,” but only within highly restricted cir-
cumstances, namely in the Black Death, when the human flea was
present in great density in rooms and there were severely septicaemic
cases of human plague. Importantly, Blanc and Baltazard restrict their
assertions of the importance of the human flea in medieval plague
10
Blanc 1956: 548–9; Baltazard 1959: 519, 521; Benedictow 1993/1996: 234–6,
247–50; Benedictow 2004: 17, fn. 9.
11
Hirst 1953: 241.
12
Hirst 1953: 239–46.
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30 chapter two
epidemics to the big cities which at the time cannot have comprised
more than two per cent of Europe’s population. Clearly, they have noth-
ing in mind which challenges Hirst’s general opinion or which can con-
firm or support Cohn’s assertion as to the difference between historic
and modern plague epidemics. One should note that Hirst does not say
a word about spread rates in this context, neither in Morocco nor in the
fourteenth-century epidemics; it is not a problem or concern for him
precisely because he is of the strong opinion that the spread rates of
historic and modern plague were basically the same. It is Cohn who
must insist that that the Black Death spread very rapidly by interhu-
man transmission, because it is a necessary condition of his theory that
the Black Death was a viral infection. Actually, Blanc and Baltazard
disagree fundamentally with Cohn and agree with Hirst on a crucial
point that upsets Cohn, namely the superordinate importance of rats in
the epidemiology of historic plague, namely that:
The duration of the epidemics [in olden days] must have been dependent
on the existence of a large murine background. Indeed, if any proof of the
presence of R. rattus in the ancient world is required, it is furnished by
the very existence of plague.13
In addition, regarding my doctoral thesis, Cohn asserts disparagingly
that “In the spirit of Shrewsbury, Benedictow simply pushes the evi-
dence aside” and claims that I argue that “evidence of the plague itself
[…] is itself proof for Rattus rattus’s presence in medieval Iceland and
Norway,” referring to pages 159–60.14 However, on these pages no such
opinion is expressed, and indeed within the framework of my thesis
this would be a circular, and therefore fallacious, argument that would
undermine the validity of my efforts to identify the microbiological
agent of historical plague epidemics in the Nordic countries, which was
my academic mission. In fact in my thesis I discuss Blanc’s and
Baltazard’s work and cite the preceding quotation, which Cohn misat-
tributes to me. This exemplifies one of Cohn’s common argumentative
techniques: as will be shown also below, he attempts to discredit other
scholars by attributing to them opinions or arguments with which they
disagree.
It was indicated above that Cohn should be quite familiar with
Blanc’s and Baltazard’s work not only from Hirst’s quite extensive
13
Baltazard 1960: 261, 251. See also Baltazard, Bahmanyar, Mostachfi et al. 1960:
153–4; Blanc 1956: 546–8.
14
Cohn 2002: 53.
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discussion of it on pages to which he refers, but also from the quite

extensive discussion of it in my thesis.15 Thus Cohn should know that
Blanc’s and Baltazard’s studies in Morocco are based on just 90 plague
cases occurring in a clear pattern of endemic incidence in a small local
area.16 The notion that this material could be usable for comparison
with the Black Death with respect to pace of spread is erroneous on
elementary epidemiological and methodological grounds. The Black
Death and the small Moroccan episode are obviously not in pari mate-
ria and are unsuitable for the comparative purpose of attaining empiri-
cal knowledge of possible differences in spread rates. No such
comparison is made either by these two French scholars or by Hirst. It
is contrived by Cohn in order to create a fictitious criticism of Hirst’s
work. By erroneously attributing to Hirst the claim that he had observed
the same difference in spread rates that Cohn asserts to have found,
and then asserting that he avoided taking this fact into account, Cohn
can undermine Hirst’s standard work to clear the way for his own the-
ory. The considerable effort implied in constructing such an elaborate
text to this end is a remarkable feature of Cohn’s work. This also dem-
onstrates how much time and space is consumed in revealing the ways
he goes about arguing his case, and that any attempt to document all of
his tactics would require a series of monographs. Hence the necessity
of making a sufficient and representative sample.
Similarly Wu Lien-Teh’s and R. Pollitzer’s outstanding standard
works are dismissed by Cohn because the authors are convinced that
the Black Death and later plague epidemics of the past were bubonic
plague. Cohn asserts that Wu Lien-Teh “expressed doubts about mod-
ern and medieval plague as the same” in his important paper on the
first large Manchurian epidemic of primary pneumonic plague of
1910–1.17 Cohn does not provide a specific reference to page: several
re-readings of this substantial paper have failed to confirm his asser-
tion on this point. The reason is probably that this paper does not
provide an historical perspective, but relates directly, concretely and
specifically to this epidemic alone,18 which makes Cohn’s assertion on
this point untenable and misleading. The same is the case with Wu
Lien-Teh’s next paper, this time on the second Manchurian epidemic
15
Benedictow 1993/1996: 232–7, 247–51.
16
Blanc and Baltazard 1945. See also Benedictow 1993/1996: 162, fn. 233.
17
Cohn 2002: 22.
18
Wu Lien-Teh 1913.
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32 chapter two
from 1922–3.19 The first time that Wu Lien-Teh considers the Black
Death and modern plague from a comparative perspective is in his
monograph on primary pneumonic plague from 1926 and he is crystal
clear:
The fact that the Black Death does not quite correspond to the form of
infection as it is known to-day cannot eliminate the ample evidence that
it was plague. The descriptions of both the bubonic and the pneumonic
types, as given by contemporary observers, leave no room for doubt. We
shall not deal with the bubonic form, but it is perhaps necessary to
emphasise the large part this type played in the Black Death.20
This opinion is also clearly stated in his later work which was written
from a historical perspective.21 Thus Wu Lien-Teh never doubted, even
briefly, the identity of medieval and modern plague.
Another method employed by Cohn to argue his case emerges: he
implies that leading scholars of plague studies and authors of the stand-
ard works had briefly seen the light of his own theory, but did not have
the courage or competence to delve into it, but instead chose conform-
ity to established opinions and orthodoxy. They were the scientists who
squared the circle. This enables him to pretend that the basis or premises
of his own theory have been there for a long time for every open-
minded scholar to see and is therefore not only his personal brainchild.
This is true neither for Hirst nor for Wu Lien-Teh. Wu Lien-Teh, like
Hirst, is clear on the question of spread rates, arguing squarely against
any notion that the Black Death could have spread at a qualitatively
different pace than the modern epidemics of bubonic plague that he
(like Hirst) observed for several decades.22 This means, of course, that
they never observed that bubonic plague spread only contiguously
between rat colonies, as Cohn asserts, but observed instead that plague
characteristically spread by leaps over distances and developed spread
rates comparable to those of the Black Death (see below).
One should note that Hirst, Pollitzer and Wu Lien-Teh combined
superb qualifications: they combined a strong interest in plague history
with very substantial concrete knowledge of plague acquired in active
frontline service in combat of the disease and had, in the process, the
opportunity to make comprehensive observations of plague’s pattern of
19
Wu Lien-Teh 1922–3.
20
Wu Lien-Teh 1926: 3.
21
Wu Lien-Teh 1936a: 3–4, 9, 14.
22
Wu Lien-Teh 1936a: 3.
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spread and clinical manifestations in thousands of plague patients. In

the combat of an exceptional evil, they read voluminously, analyzing
and synthesizing all studies of plague they could track down and get
hold of, including historical studies. They were dedicated scholars and
researchers of the highest calibre. The fact that these excellent scholars
with their exceptional knowledge of plague were certain that the dis-
ease they used their professional lives to fight uncompromisingly for
decades was the same as the historical plague epidemics they encoun-
tered in historical contexts would normally, as had been the case prior
to Cohn’s study, elicit respect for their judgement.
In Cohn’s case, scepticism is also the watchword with regard to such
approval as is offered, because it comes at a price. As mentioned above
this is the case with the views of the Indian Plague Research Commission
(IPRC) on the mechanisms, pattern and pace of spread of bubonic
plague, a topic which will be discussed in a separate chapter below.
There are many other instances. Cohn asserts, for instance, in his usual
disparaging manner that the opinion held by the early plague research-
ers at the end of the 1890s “that the late-medieval and modern plagues
were the same hampered [their] understanding of their own plague”
and was an idée fixe. He goes on to state the following: “To their credit,
by 1906 the researchers of the Indian Plague Commission were willing
to put aside the past and state their findings no matter how opposed to
common knowledge of the late-medieval plague.”23 This unfootnoted
and unsubstantiated assertion cannot be confirmed. The facts are that
the preliminary fact-finding Indian Plague Commission was dissolved
in the autumn of 1905 and replaced by the Indian Plague Research
Commission. Thus, 1906 is the year when the newly formed IPRC
started to publish their findings in The Journal of Hygiene and had no
past to put aside. G. Lamb, Senior Member of the Commission, gives a
brief history of its formation in the preface and introduction to his
summary of its findings up to May 1907.24 Secondly, only two of the
Commissions members, namely Greenwood and Liston, published
comparative historical plague studies. They conclude, contrary to
Cohn’s assertion, on specific and tenable empirical grounds, specifi-
cally on the similarity of the peculiar pattern of spread according to
23
Cohn 2000: 41.
24
Lamb 1908: i–iv, 1–3. He includes in his summary studies which were performed
at the time but were published in subsequent issues of The Journal of Hygiene. He
then became member of the Advisory Committee.
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34 chapter two
variation in population density (see below), that the Black Death and
later plague epidemics were the same disease that they had studied in
India.25 No member of the IPRC expressed any doubt as to the over-
whelming similarity and identity of the Black Death and subsequent
medieval plague epidemics and the plague epidemics they studied in
India where there were millions of cases. This shows again that Cohn’s
approbation should engender the suspicion that the position he is
praising does not reflect the actual opinions or studies, but that Cohn
is attributing to others his own opinions in order to forward his own
theoretical agenda and make his position seem less isolated.
Hankin 1: Cohn’s Attack on Hankin’s Observation of Inverse Correlation

between Mortality and Population Density
E.H. Hankin was another leading British medical scientist who engaged
in the study and combat of plague and who argued for the identity of
the Black Death with modern bubonic plague in India. Hankin discov-
ered, among other things, that Indian epidemics of bubonic plague
caused higher mortality rates in villages than in urban centres and that
the Black Death in England appeared to follow the same pattern and,
thus, also was bubonic plague. For this discovery he is severely criti-
cized by Cohn.
This strange phenomenon, that mortality rates did not increase with
increasing population density, but on the contrary, decreased, is seem-
ingly at variance with the central tenet of epidemiology and must reflect
a very special or unique mechanism of dissemination.26 The observa-
tion of this unique characteristic is highly important because it may
expand epidemiological understanding of the particular process of
transmission and dissemination of an infectious disease and, in this
case, may serve as a sufficient criterion for identification of the disease
because it functions as a defining feature (see below). This represents a
serious threat to all alternative theories of the identity of historical
plague which are based on an assumption that the contagion was
disseminated by interhuman cross-infection, because cross-infection
is intimately associated with the opposite principle of increasing
infection rates with increasing population density, without exception.
25
Greenwood 1911b: 93–7, 150–1; Liston 1924: 900–1.
26
Hankin 1905: 48, 57–8.
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This topic of inverse correlation is so important that it will be discussed

in a separate chapter.27 Here the focus is on Cohn’s endeavours to dis-
credit Hankin as a scholar and to deny his important observation.
Hankin had an excellent scholarly background: he had been fellow
of St John’s College at Cambridge University before he joined the com-
bat of plague in India and became fellow of Allahabad University and
Chemical Examiner and Bacteriologist to the United Provinces and to
the Central Provinces in India. He was one of the pioneers of plague
study in India where he made important contributions to the under-
standing of the epidemiology and microbiological nature of plague in
the years around 1900.28 In his last work on plague published in 1905
he makes clear his view on the identity of medieval plague and contem-
porary plague in India. It is, so to speak, the final fruit and summary of
his work as a scientist who had joined the combat of plague in the labo-
ratory and in the field and in anti-epidemic organizational work. It
should be noted that Hankin’s paper was written before the important
discoveries made by the IPRC which were published in 1906–14. This
provides Cohn with the opportunity of making some cheap points at
Hankin’s expense, since he can dispense with the scholarly obligation
to consider Hankin’s work within the proper context of the history of
medical science and plague research.
In Hankin’s substantial paper, the part relating to the epidemiologi-
cal characteristics of the Black Death and its resemblance to and com-
patibility with the Indian plague epidemics is a small sub-chapter on
pages 57–8 titled “Resemblances of the Black Death to Indian Plague”.
It is untrue that Hankin “surveyed the late medieval and early-modern
sources” on plague epidemics in Europe and made further compari-
sons of this type. Cohn asserts disparagingly that Hankin without
any reason “presumed identity between these two epochs of bubonic
plague” and that this “led him to impose conclusions derived from
the present epidemiology of plague on the European past.”29 In the
following pages it will be demonstrated that these assertions are
groundless.
These allegations function as a prelude to a great effort to discredit
Hankin’s discovery of inverse correlation between mortality rates and
27
See below, chapter 8: 289–311.
28
Hirst 1953: 21, 130, 160, 293.
29
Cohn 2002: 16.
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36 chapter two
population density. Cohn goes on to state (I place his footnotes in

brackets):
With the new epidemiological discovery that modern plague mortalities
[in India] were inversely correlated with the population size of an infected
locality, Hankin stated boldly that the same was found for the Black
Death, asserting that mortalities had been high in English villages but
that that “no evidence of such depopulation exists for London or other
towns” [fn. 51: Hankin p. 58]—this despite Creighton’s analysis of wills
from the Court of Hustings published several years earlier that showed a
fifteen-fold increase in London’s mortality in 1348–9 [fn. 52: Creighton
p. 118].30
This is misleading in several ways. Hankin does not conclude with the
demanding concepts of “identity” or “the same” but with the far more
cautious concept of “resemblance.” Cohn also neglects to mention that
it actually was Hankin who discovered the strange inverse correlation
between population density and mortality in bubonic plague, namely
that bubonic plague caused much higher mortality in the countryside
than in towns of “Bombay Presidency.” Hankin discovered also that
this was the case with Indian plague epidemics in 1812 and 1836, and
established, thus, the outline of a consistent pattern which implies a
systemic causation.31 For this discovery, he deserves praise.
As a good scientist, Hankin wished to know whether this was a spe-
cific feature of plague in India or a more general and characteristic epi-
demiological feature. At the time, the scientific study of historical
plague epidemics was in its infancy. In order to obtain useful informa-
tion, he turned to Creighton’s general monograph on the history of epi-
demic disease in the British Isles of 1891 and found some support in
statements indicating extreme mortality and depopulation in the coun-
tryside, and lesser mortality in London and other towns. This is a cor-
rect understanding of Creighton’s text, which thus represents a threat
to Cohn’s alternative theory. In order to undermine the credibility of
Hankin’s assertion, Cohn refers to page 118 in Creighton’s monograph
asserting that Creighton claims there that his study of wills showed a
fifteen-fold increase in London’s mortality in the Black Death. This is
not correct: nothing to this effect is found on page 118. The incorrect
reference to page 118 provides an opportunity to avoid Creighton’s
30
Cohn 2002: 16–7, cf. 44.
31
Hankin 1905: 56–7.
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important specification on the preceding page of the types of informa-

tion obtainable by the use of wills as source material. According to
Creighton, wills are useful in obtaining information about the season
and duration of the Black Death, but he says nothing about using them
to obtain mortality data:
One of the best proofs of the season and duration of the Black Death in
London is got from the number of wills enrolled in the Husting Court of
the city in the succeeding months.32
Clearly, 118 years ago Creighton had the methodological conscious-
ness and scholarly insight that wills were unsuitable as sources for esti-
mating rates of mortality. There are several obvious and good reasons
why this should be so which Cohn ignores; for example, the will-
producing social classes constituted only a small fraction of the popu-
lation at risk and the size of the population at risk was not known.
However, there is another sufficient reason. My 2004 monograph on
the Black Death includes two substantial chapters on medieval demog-
raphy and medieval sources for demographic studies with particular
emphasis on mortality which function as an introduction to all mortal-
ity studies relating to the Black Death. Here it is made clear that wills
cannot be used for the study of mortality:
Wills reflect more the fear of death than death itself. A large proportion
of those who made wills in the face of an immediate epidemic threat to
their lives would be alive at the end of the day. Abrupt changes in the
number of wills relate to crisis mortality in an impressionistic and flimsy
fashion and the correlation between changes in the incidence of wills and
death rates is not quantifiable.33
Thus, Cohn misrepresents Creighton’s text on this point in order to
lash out at Hankin with a fallacy of methodology based on false and
misleading assertions that wills can be used and have been used by
Creighton as sources reflecting (f)actual death in order to produce a
mortality rate.
In fact, according to ordinary methodological considerations,
Hankin’s observation of resemblance between the Indian bubonic-
plague epidemics and the Black Death is valid but at a low level of ten-
ability because of the preliminary character of his Indian observations
32
Creighton 1891: 117.
33
Benedictow 2004: 272.
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38 chapter two
and the weakness of the comparative historical material he was able to

find. Since his observation is valid and at variance with epidemiologi-
cal orthodoxy on good self-explanatory grounds, it should be of great
interest to all open-minded and fair scholars. The question of the
inverse correlation between levels of mortality and population density
in plague epidemic is, as mentioned, thoroughly discussed below in
chapter 8.34
Hankin 2: A Brief Study of Cohn’s Technique of Argument
A further sample of the arguments and assertions that Cohn levels

against Hankin in order to belittle him as a scholar and person follows
here. That almost all arguments or assertions which Cohn attributes to
Hankin are false, can be illustrated by citing a paragraph of his text
with his few footnotes included in brackets.35 The text is divided into
ten constituent parts and rendered in italics, and each of these parts is
followed by my commentary. Significant points in Cohn’s text are
marked using a self-explanatory number-letter system:
(1) Following from the [1A] new discoveries made by the Indian Plague
Commission that [1B] the most destitute of India’s population seemed
to escape the plague, [1C] Hankin concluded the same for the late
Middle Ages,
(Comment on 1) All three elements constituting the first assertion Cohn
attributes to Hankin are factually erroneous. (1A) The Indian Plague
Commission made no such discovery and (1B) Hankin does not
make any assertion to the effect that the “most destitute” escaped the
plague, in fact it was obvious to him and to the Commission from
daily experience that this was not the case. On the contrary, Hankin
cites on the first page of his paper a colleague’s statement (which he
supports) to the effect that “the houses in the suburban villages near
Bombay which suffered severely from plague were not so over-
crowded as the houses in the slums of the city which were far less
severely attacked.”36 Hankin’s study of the peculiar property of
bubonic plague that there is an inverse correlation between mortality
rates and levels of population density, which is discussed in detail
below, follows from this realisation. It is, therefore, clearly apparent
34
See chapter 8: 279–88.
35
Cohn 2002: 17.
36
Hankin 1905: 48. Much the same perspective is implied by Hankin’s unequivocal
statement to the effect that “no definite relation has been observed between intensity of
plague (apart from its persistence), and badness of sanitary condition of dwellings.”
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that (1C) Hankin had not “concluded the same for the Late Middle
Ages.” As can be seen, Cohn provides no footnotes in support of his
erroneous assertions.
(2) seeing it confirmed by Simon de Couvin’s Black Death poem, which
alleged that tanners escaped the plague [fn. 53: “Hankin, ‘On the epi-
demiology of plague,’ p. 57.”].
(Comment on 2) Cohn refers here to the French ecclesiastic Simon of
Couvin who in 1349–50 wrote a Latin poem on the Black Death
inspired by the epidemic’s ravages in Paris, where he focuses on
astrological explanations but also provides descriptive epidemiologi-
cal and clinical elements.37 Since Hankin does not hold the opinion
which Cohn ascribes to him, that the destitute were not hit by the
Black Death, it is unsurprising that Cohn’s next assertion on his
behalf is also in error. It is simply untrue that Hankin cited this
source for confirmation of an opinion he did not hold. Instead,
Hankin refers to Simon of Couvin for support of an opinion he actu-
ally holds, namely that mortality rates were higher in the countryside
than in the towns: “According to Simon de Covino,38 who observed
the Black Death in Paris, Montpellier and probably other places, it
was especially severe in the smaller towns (suburbia).”39 As can be
seen, Hankin is uncertain about the correct translation of the Latin
word suburbia since he renders the original word in a parenthesis; an
alternative translation might be to take the meaning to be “villages in
the vicinity of/in the surroundings of urban centres,” which corre-
sponds closely to the use of the word “suburban” in the citation from
his colleague rendered in comment on (1B). Hankin says not a word
about tanners! Cohn’s unjustified criticism of Hankin’s work on this
point is apparently designed to challenge his scholarly competence
and methodological consciousness, and thus his conclusions. Cohn
refers to the correct page in Hankin’s paper where he comments
on Simon of Couvin’s statement, so there can be no doubt that
Cohn’s allegations are based not on a misunderstanding but on
manipulation of facts. Cohn is thus unable to confirm by an accom-
panying footnote with an appropriate indication of page that Simon
of Couvin actually wrote in his poem that tanners escaped the Black
Death.
37
Libellus de judicio Solis in conviviis Saturni, seu de horrenda illa peste, published by
Lettré 1840–1: 206–43, with introductory comments 231–6. For his biography, see
Renardy 1974: 273–92.
38
“Corvino” is the latinized form of “Couvin,” the name of a Belgian town.
39
Hankin 1905: 57: Et nimis immensum sensere suburbia damnum. It is a common
misconception that Simon de Couvin observed the Black Death in Montpellier.
However, it is unlikely that he observed the Black Death anywhere other than in Paris
where he had his benefice: see Renardy 1974: 279. It also seems unlikely that anyone
who observed the Black Death in Montpellier and had survived would move to Paris in
order to observe it again.
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40 chapter two
(3) True or false, [3A] tanners, almost invariably a guild occupation, [3B]
hardly comprised Europe’s most destitute circa 1348 as Hankin assumed
[3C] to make the past fit his present.
(Comment on 3) All three assertions in this sentence are untrue and are
based on Cohn’s unjustified assertion that Hankin used (3A) a tex-
tual element in the poem by Simon of Couvin on mortality among
tanners, that (3B) he was so incompetent that he believed that crafts-
men like tanners could be among the most destitute inhabitants of
Europe at the time of the Black Death, and even more disquieting
(3C) that Hankin manipulated this material in order “to make the
past fit his present,” or square the circle which is the disparaging
phrase that Cohn generally uses to describe the arguments of medi-
cal and historical plague scholars that modern and historical plague
are the same disease. On the contrary, Simon of Couvin emphasizes
that the poorest or destitute masses (vulgus, pauperrima turba) suf-
fered particularly high mortality in the Black Death and that it was
not high among the magnates, noblemen and knights (principibus et
nobilibus generosis/ Militibus),40 corresponding reasonably well to
what Hankin actually wrote. Cohn’s assertions with respect to
Hankin’s views in this regard all come from his own imagination; at
the same time, Cohn ignores aspects of Simon of Couvin’s descrip-
tion that run counter to his own alternative theory. Simon designates
the epidemic pestis inguinaria, expressing his view that the disease
had a clinical feature which overshadowed all other clinical manifes-
tations, i.e. buboes in the groin, a defining feature of bubonic plague
(see below). In addition, he refers to the characteristic intense pain of
buboes: nascitur inde dolor ignites in inguine sepe.41
(4) Using another new and unexpected recent finding—plague in India did
not follow trade routes as is normally the case with diseases that spread
person-to-person—
(Comment on 4) Frankly, Hankin’s statement is confusing. He does
indeed remark that plague in India did not show any “tendency to
spread along trade routes as such,”42 although the expression “as
such” indicates a possible reservation which Cohn omits. However,
this is not the main problem, which is that other contemporary med-
ical scholars and researchers in India hold entirely contrary views on
the matter. In his great treatise on plague which appeared the same
year as Hankin’s paper and which summarizes the Indian experience
in the preceding decade within a broad historical perspective,
Simpson flatly states that “plague travels by the most frequented
trade routes.” He points out that this was the case also with the Black
Death, subsequent historical plague epidemics, and also the present
40
Lettré 1840–1: 236; cf. 204.
41
Lettré 1840–1: 202, 232.
42
Hankin 1905: 56–7.
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pandemic, and Simpson goes on to enlarge on the Indian experi-

ence.43 As should be expected from Lamb’s presentation, the IPRC
held the same view in a number of papers on the spread of plague.44
Greenwood made a specific study of the spread of plague by railway
in the Punjab that confirmed the central importance of this means of
long-distance transportation of people and goods in the dissemina-
tion of the disease.45 Liston, another of the Commission’s prominent
members, summarized aptly its findings in this respect: “Infection
was disseminated along the main lines of communication by rail and
by ship.”46 Thus, it appears that Hankin is mistaken on this point and
he does not corroborate it by any reference in an accompanying foot-
note. He may have based this point on a non-specialist study of
plague in India written in the first half of the nineteenth century but
which remained unpublished until 1894, two years before the out-
break in India which is our focus here and before the start of scien-
tific study of the disease.47 However, it is also clear that Cohn is
mistaken when he characterises Hankin’s statement as fact, calling it
a “new and unexpected recent finding,” which confirms his peculiar
reading not only of the relevant plague studies performed before the
IPRC began publishing its works the following year but also of
Simpson’s treatise which he refers to twice in a form which suggests
that he was quite familiar with it.48 However, our focus here is on
Cohn’s use of Hankin’s paper.
(5) Hankin assumed the same for late-medieval plague
(Comment on 5) This is not true. Hankin makes no such assumption for
historical plague epidemics, and the statement on trade is made
exclusively in an Indian context, comprising the three nineteenth-
century outbreaks of 1812, 1836 and 1896. Within this context, he
emphasizes that “though it spreads with facility from a town or vil-
lage to a neighbouring village, it does not appear often to be carried
to great distances in epidemic form” and does not “spread along
trade routes as such.”49 In the subchapter on the “Resemblances of
the Black Death to Indian Plague,” he does not make any such com-
parison or present any such assumption with respect to the pattern
of spread which Cohn attributes to him.50 Clearly, Cohn’s assertion
on this point is incorrect.
(6) but for this he did not bother to cite any contemporary evidence. [fn.
54: “Ibid p. 56.”]
43
Simpson 1905: 194–5, 200–9.
44
45
Greenwood 1911a: 47–61.
46
Liston 1924: 950, 997.
47
Hankin, 50, 57.
48
Cohn 2002: 10, 15.
49
Hankin 1905: 56–7.
50
Hankin 1905: 57–8.
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42 chapter two
(Comment on 6) Cohn’s assertion on this point is not correct, since

Hankin does not compare the Indian plague epidemics and the Black
Death and subsequent plague epidemics in Europe with respect to
the role of trade in the dissemination of the disease, and it is for this
reason that he does not “cite any contemporary evidence” to this
effect. Probably, Hankin does not comment on this point because he
knows that in the Black Death and later European plague epidemics
the disease was most efficiently spread along the trade routes. Cohn’s
footnote is just plain wrong, since Hankin does not mention late
medieval plague epidemics on page 56 of his paper.
(7) Finally, Hankin rightly noted from chroniclers characteristics of
fourteenth-century plagues that had no parallels with the Indian
plague experience,
(Comment on 7) This is also untrue. Hankin does not make any use of
fourteenth-century European commentary on the Black Death other
than the citation from Simon of Couvin’s poetic work which has
been cited above in order to reveal Cohn’s false reference to the same
author. Hankin uses this citation, as shown above, to demonstrate
resemblance between the fourteenth-century epidemics and the
Indian plague epidemics, not dissemblance or dissimilarity. Thus,
Cohn again mischaracterises Hankin’s paper in order to clear the
way for yet another incorrect assertion, namely, that Hankin had col-
lected material from fourteenth-century chroniclers on the charac-
teristic features of plague epidemics that are incompatible with the
Indian plague epidemics. This enables Cohn (see below) to concoct
the false and disparaging assertion that Hankin had observed crucial
or important dissimilarities between fourteenth-century plague epi-
demics and the Indian epidemics of bubonic plague, but chose to
ignore them and pass by the obvious conclusion that they were two
different diseases. Cohn by this means contrives to make it obvious
to his readers that he (Cohn) has made the discovery that Hankin
should have made hundred years ago, but which through scholarly
incompetence or intellectual dishonesty Hankin chose to ignore.
(8) such as children as the principal victims of the second outbreak of
plague in Europe in the 1360s. [fn. 55: “Ibid. 64.”]
(Comment on 8) This is also fabricated evidence. Hankin’s only reference
to a medieval contemporary writer was clarified in the preceding
comments; he does not cite or refer to any commentary other than
Simon of Couvin’s (see above) and he cites him on the inverted cor-
relation between population density and mortality rates. He does not
write a single word about child mortality in the second plague epi-
demic (or any other late medieval plague epidemic) and could not
have done so also for the compelling reason that Simon of Couvin’s
account was written 1349–50 and cannot contain anything about the
epidemic in “the 1360s.” Again, Cohn falsely attributes to Hankin
(and to other scholars) his own observations, suggesting that the
facts had been there for a long time for any competent and honest
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scholar to see, but that it took his own genius to draw the correct
conclusions. Cohn’s reference to page 64 in Hankin’s paper is also
wrong: on this page, Hankin continues a discussion of the observa-
tion by P.L. Simond, the pioneering French epidemiologist, that
plague had a latent period of usually around twenty days between the
introduction of infection into a locality and the epidemic outbreak,
which he correctly points out is incompatible with interhuman
spread of a disease. This is a point Cohn must avoid mentioning,
since it is incompatible with his assertion that historical plague was a
viral disease spread by cross-infection. Hankin goes on to discuss
aspects of Indian plague epidemics in 1897–8. Thus, the cited
dependent clause in Cohn’s text is simply untrue. Cohn’s argument
with respect to child mortality in the second plague epidemic will be
discussed in a separate chapter below and will be shown to be
untenable.51
(9) Yet, despite discordances between the two plague periods,
(Comment on 9) This is a false assertion based on Cohn’s own misleading
allegations regarding the contents of Hankin’s text. Hankin did not
ignore any “discordances” between the two plague periods, but
argues in terms of resemblances between the Indian plague epidem-
ics and the late medieval plague epidemics (see also the following
point 10). The only “contrast” he mentions, which Cohn does not
find reason to cite, concerns the “extent of area attacked,” but he
explains this by arguing that “the present Bombay plague may be
regarded as intermediate between the Black Death and the Pali
plague.” Thus, Cohn’s use of the term “despite” is groundless as are
the alleged “discordances.”
(10) he concluded with confidence “all the known plagues of Western India
resemble the Black Death and the epidemics to which it gave rise.” [fn.
56: “Ibid. 58.”]
(Comment on 10) In this part of the quotation, Cohn manipulates Hankin’s
text and misrepresents his line of argument by omitting the explana-
tory continuation of the text, here rendered in italics:
Thus all the known plagues of Western India resemble the Black
Death and the epidemics to which it gave rise, in showing a high
degree of intensity at one time over a large area, and in the relatively
high rate of mortality that they produced in villages as compared with
towns. The two groups of outbreaks also resemble one another in their
power of spreading with facility from village to village.
Hankin also mentions other resemblances between modern plague in
India and the Black Death: “Correlated with the high degree of viru-
lence, there appears to be a certain similarity in the symptoms observed
51
Chapter 6: 212–68.
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44 chapter two
in these outbreaks,” which in Hankin’s use of the word indicates a

resemblance of level of virulence and a resemblance with respect to
clinical symptoms. Hankin argues using valid comparative methodol-
ogy, the systematic comparison of characteristic features or manifesta-
tions of these waves of epidemics which occurred centuries and
continents apart. He concludes that there were comprehensive resem-
blances, and no obvious dissimilarities, which permits him to identify
them as the same disease, namely bubonic plague. In my opinion it
would be fair to conclude that Hankin’s brief and pioneering compara-
tive discussion of plague in India and late medieval plague contains
valuable observations that constitute a reasonable case for a tentative
assumption of microbiological and epidemiological identity between
the two waves of plague.
Summing up, Cohn’s presentation and discussion of Hankin’s paper
do not meet reasonable standards of academic work, not because it is
amateurish but because such great effort and skill have been invested
into producing a grossly misleading presentation of its arguments and
of Hankin’s scholarly competence and integrity. This is very far from a
comprehensive analysis, but only a sample illustration of Cohn’s han-
dling of the observation of inverted correlation of density and mortal-
ity, a point of such great importance that it will, as mentioned above, be
discussed in a separate chapter below.
“The Ugly Americans”
Cohn’s American colleagues may ponder the following general critical

statement: “American researchers” in Vietnam “had learnt little from
earlier studies in India.”52 The American physicians and other medical
personnel who worked in Vietnam during the war had been sent there
to serve the military forces, not to make plague research. It so just hap-
pened that, to their amazement, they found themselves confronted
with a major epidemic of bubonic plague among the Vietnamese popu-
lation (for example 5,568 registered cases in 1967).53 Thus, they had to
52
Cohn 2002: 37. The criticism is primarily leveled at Marshall, Joy, Ai et al. 1967,
but see also the next footnote. I suspect that Cohn’s source of inspiration is Butler’s
statement that “American physicians in Vietnam from 1965–1975 were given opportu-
nities to rediscover the dramatic clinical presentations of plague”: see Butler 1983: 77.
This is, of course, a very different perspective.
53
Butler, Bell, Linh et al. 1974: S78; Butler 1983: 34.
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join a completely different war, to combat plague in order to protect

American servicemen from the disease, and also to help the civilian
population and do their very best to prevent or limit its spread and help
the diseased. Certainly, they were not sent there as plague researchers,
but they took on the responsibilities thrust upon them by fate, so to
speak. In my considered opinion they did an outstanding job, often
under dangerous and difficult circumstances. In the process, they col-
lected much empirical material and implemented a number of small-
scale research projects that confirmed and enlarged on our knowledge
of bubonic and pneumonic plague, plague in children, and so on.54 The
paper Cohn criticizes scathingly is a preliminary report in the form of
a small article of thirteen pages on the plague epidemics of 1965–6,
co-authored by six physicians and published the following year, with
the best of intentions, namely to make the experience and insights won
so far on this terrible disease in Vietnam more generally and usefully
known to health personnel. A number of valuable papers with this
same background were published subsequently until 1976. T. Butler,
who performed valuable studies of plague under these circumstances
in Vietnam, takes a very different and positive stance: “American physi-
cians in Vietnam from 1965 to 1975 were given opportunities to redis-
cover the dramatic clinical presentations of plague.”55 In his
much-praised 1983 monograph on Yersinia infections he gives a fine
and useful summary of the achievements in plague research by
American physicians in Vietnam at the time.
What is the reason for Cohn’s highly critical assertion in this case? Is
the fact that the American physicians in Vietnam consistently con-
firmed and supplemented the findings of the IPRC and the presenta-
tion of plague in the standard works of Hirst, Pollitzer and Wu Lien-Teh
really grounds for criticism? Could it be something like an accusation
of having “reinvented the wheel”? However, to the extent that these
American physicians performed their research independently of the
IPRC’s studies, which Cohn implies they did not know, would that not
serve on elementary methodological grounds to strengthen the validity
both of their findings and those of the researchers in India?
So it seems that there is a different reason for Cohn’s collective attack,
or maybe also an additional reason. At least since the 1920s, American
54
See, for instance, references in Benedictow 1993/1996: 252–6; Butler 1983: 34–9,
201–2; Burkle 1973: 291.
55
Butler 1983: 77.
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46 chapter two
medical scholars have continuously studied plague in the U.S.A, in the

laboratory and in the field. The Centers for Disease Control in Atlanta
has since the end of the end of the Second World War monitored
plague-related developments and supported research projects and
released international reports on plague. On the home page of its
“Division of Vector-Borne Infectious Diseases” this leading institution
of plague research in the U.S.A., six years after Cohn’s monograph was
published, unconditionally supports the notion that modern bubonic
plague and the plague epidemics of the Late Middle Ages were the same
disease caused by the same bacillary agent, namely Yersinia pestis, and
that it is transmitted by rat fleas. Obviously, these leading American
medical scholars of plague research were not impressed by Cohn’s argu-
ments. Is it really true that they hold this opinion for unscholarly and
unpersuasive reasons? In an ironic twist of research history, the com-
mittee which in 1991 was appointed to evaluate my doctoral thesis on
plague in the late medieval Nordic countries engaged Thomas Butler as
the leading expert on medical plague research in the world at the time.
He gave a very positive assessment of my thesis and its epidemiological
identification of these historical plague epidemics with bubonic
plague.
Cohn’s Accusations of Racism against J. Ashburton Thompson

and L.F. Hirst
There is, however, another aspect of Cohn’s academic “mass execution”

of previous scholars which is so outrageous that conscience demands
that we address it seriously: his accusation of several early plague
researchers of racism,56 specifically J. Ashburton Thompson, the
President of the Board of Health and Chief Medical Officer of the
Government of New South Wales, and also Hirst for endorsing
Ashburton Thompson’s opinions. Cohn’s composite role as accuser,
prosecutor, judge and jury is unacceptable and his bombastic convic-
tions of dedicated scholars are grave miscarriages of academic justice
which it is a scholarly duty to uncover and repudiate.
“Racism” and “racist” are words denoting the notion that one human
race is genetically superior to some other human race(s) or all other
races. Such notions are completely without basis in scientific knowledge
56
Cohn 2002: 39.
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or research, are conducive to dangerous political ideologies, and should

be unequivocally condemned. All other notions of human inequality
like ethnocentrism, chauvinism, xenophobia, and negative opinions
with regard to people of other religions, social classes, and so on, are
not racist, but relate to cultural and social notions of difference and
inequality. Such cultural notions are (regrettably) usual all over the
world today just as they have been in the past; among the native popu-
lations of India where they were systematized according to the notion
of cast, and found expressing in tensions between Muslims and Hindus.
There are very good reasons for relating to such notions with great
scepticism on the basis of a suspicion that they are prejudices and as
such detrimental to human relations and social exchange. However,
this does not mean that they are always and necessarily erroneous: it
should, for instance, be fairly obvious that different cultural notions of
the cause and spread of epidemic diseases can have very different func-
tional effects on those diseases’ powers of dissemination and mortality
in different societies based on different cultures and civilizations. Thus,
from the perspective of preventing epidemic disease and mortality it
can be argued on sound scholarly and scientific grounds that there are
important and even vital qualitative differences between the various
disease-related notions held by various civilizations or ethnic groups
at various times in history. Whilst racist notions are completely unsci-
entific and should be condemned in the strongest possible terms,
other notions of difference or inequality can be discussed within the
parameters of social science according to their functional aspects as
more or less tenable, correct or erroneous. This is at the heart of the
matter here.
Cohn cites a passage in a paper in the journal in which the Indian
Plague Research Commission published their own studies and also
those of other prominent scholars, namely The Journal of Hygiene,
where Ashburton Thompson presents the epidemiological observa-
tions and the anti-epidemic countermeasures applied in Australia after
plague slipped ashore in 1900:57
Plague has almost always appeared in countries inhabited by races for-
eign to the observer in their language and modes of thought, who were
of little instruction, of an education limited to ancient and immutable
conventions, and who lived for the most part under conditions which
57
Cohn 2002: 39, Ashburton Thompson 1906: 537–8.
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48 chapter two
unavoidably obscured the phenomena. It has thus often been impossible

to acquire that exact and complete knowledge of all the circumstances
under which the infection had been received by each person attacked,
which is the foundation of all investigations into the aetiology of disease
by the epidemiological method. [.…] At Sydney the conditions happened
to be much more favourable to its employment. The invaded population
numbered about half-a-million. It was not merely wholly white, of
English extraction and speech, and fully civilized, but intelligent,
instructed, and orderly, accustomed to direction and amenable to it.
The passage contains nothing at all indicating that Ashburton Thompson
considers that white people are racially, i.e., genetically superior to
native people in India or any other race or people. He makes the point
that the white (relatively) well educated population of British extrac-
tion in Australia accepted the various inconveniences associated with
the research efforts and strict anti-epidemic countermeasures which
were applied there, partly because there was a long tradition in European
culture that, for instance, diseased persons were taken out of their fam-
ilies and isolated in plague hospitals or wards. This meant that the
Australian sanitary authorities enjoyed a much more co-operative pop-
ulation than the population to which the British sanitary authorities
related in India. The native people(s) in India had a much lower level of
education and held very different cultural notions of the cause and
spread of disease and of relevant or acceptable countermeasures. For
these reasons, they resisted strongly and even violently comparable
research efforts and use of the same anti-epidemic measures in the
combat of plague in the early years of the plague epidemics. These
measures were certainly implemented with the best of intentions, not
because the British colonial authorities were “callous” as Cohn main-
tains. Clearly, this popular resistance impeded the huge efforts to pre-
vent plague from spreading, and had unfortunate effects.58 This is
reflected also in the first statement by G. Lamb, Director and Senior
Officer of the Indian Plague Research Commission, in the preface of
his summary of the results of the Commission’s first years:
In the early days of plague in India most strenuous efforts were made to
stamp it out by the means adopted in European countries in dealing with
epidemic disease, but these efforts failed and they too often led directly to
the misfortunes which they were designed to avert. When it was recog-
nized that it was impossible do deal effectively with the epidemic without
58
Simpson 1905: 67–8; Klein 1988.
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the help of the people themselves, a policy of persuasion and assistance

was substituted for the more rigorous measures, but this also failed to
prevent the extension of the disease, although in many places some
degree of success was achieved.59
Lamb makes it clear that the anti-epidemic measures introduced by the
British colonial authorities in India based on European experience and
culture were implemented with the best of intentions, to save lives by
stamping out a murderous disease, but failed because at the outset the
authorities did not recognize the importance of relating with sensitiv-
ity and insight to the Indian population’s cultures and mentalities.
There is no indication of the slightest element of racism in the scholarly
meaning of the word, as opposed to its use as an invective, only evi-
dence of deficient knowledge of relevant social anthropology. Thus, the
administrators learned a lesson from which the IPRC could benefit.
However, the alternative, avoiding efficient countermeasures that might
offend Indian sensitivities, also had weaknesses and, according to
Lamb, had cost lives. There is no dissonance between Lamb’s statement
on behalf of the IPRC and the views presented by Ashburton Thompson;
it is Cohn who has contrived a gravely misleading accusation.
Thus Ashburton Thompson’s observations and analysis appear cor-
rect and relevant. They are therefore supported by modern scholars, for
instance by I. Klein, which support exposed him to Cohn’s disparaging
assertions about his views.60 One might debate whether some of
Ashburton Thompson’s words have ethnocentric connotations, for
instance, possibly the concept of “civilization.” However, can we be cer-
tain that future generations will not consider with some ambivalence
our own choices of words, since the meanings of words develop over
time, changing connotations in a changing world with new social and
59
Lamb 1908: i.
60
Klein 1988. As for misleading assertions see, for instance, Cohn’s statement: “Yet
Klein, p. 754, still concluded that the reasons for the exceptional mortality from bu-
bonic plague in the early twentieth-century India resulted largely from overcrowding
and poor housing”; see Cohn, 2002: 30, fn. 28. In fact, Klein says the opposite, that
“plague dwindled and population grew amidst hunger and persistent poverty, misery
and environmental decay,” which according to ordinary understanding or interpreta-
tion should be taken to mean that plague in India declined despite worsening social
conditions. Instead, Klein advocates a very different theory, that the decline of plague
was due to biological adaptations by man and rats, with which one can agree or disa-
gree, but has nothing to do with Cohn’s assertion which is, therefore, misleading and
designed to devalue Klein as a scholar, since he does not agree with Cohn’s account of
plague in India.
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50 chapter two
political contexts? In order to illustrate the problem, I can mention that

in the Scandinavian languages the term “high culture,” “høykultur,” is
frequently used synonymously with civilization, a term that could, of
course, easily be denounced as containing an ethnocentric notion of
cultural superiority over tribal societies, and so on, or even as racist in
Cohn’s unscientific abuse of terminology. Actually, it is used more or
less consciously in its technical scholarly meaning in social science to
refer to cultures that have developed urban structures of settlement,
economic production and exchange in contrast to tribal or agricultural
societies.61 Is it really necessary for us to appeal to future generations to
relate to our choice of words with some lenience and good will and
seek a likely or possible positive interpretation?
As shown below, Cohn’s negative approach serves a purpose, namely
as a pretext to pass by in silence the observations on plague in Australia
presented by Ashburton Thompson which would undermine his own
theory of plague epidemiology. His contrasting kind words about the
IPRC’s attitudes towards the native Indian population serve to portray
himself as a reasonable man before ending with highly misleading
statements about the IPRC’s findings—which in fact conform entirely
with those of Ashburton Thompson (see below). The point is simply
that the British colonial authorities and their sanitary agencies learned
from the unfortunate early experience of their wholesale application of
epidemic countermeasures of European origin to make adjustments
that took into account the sensibilities and beliefs of the native Indian
populations.
Cohn also levels an accusation of racism, as mentioned above, at
Hirst, stating that he followed “Thompson’s racist version of events”
and goes on to select some words of a passage in Hirst’s monograph so
as to incriminate him as much as possible. In order to acquit Hirst of
61
The difference in the sociological meanings of the words “culture” and “civiliza-
tion” springs from the fact that the basic meaning of the term “culture” is “cultivation”
(of land, etc.), while the term “civilization” is based on the Latin word civitas with the
meaning “town” or “city”, or derived words like civilis which means “burgher” or “citi-
zen”, implying that the term “civilization” technically refers to cultures that have devel-
oped urban structures of settlement, economic production and exchange. “Civilization”
is a technical sociological term and does not as such contain qualitative connotations
relating to notions of superiority or inferiority of cultures, for instance, in relation to
tribal cultures based on agriculture, fishing or hunting and gathering that lack urban
formations or structures. The term “civilization” contains, thus, a valuable distinction
which makes it useful as an analytical sociological tool for understanding a specific
type of societal structures and their function in relation to various other types of
societies.
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this scholarly miscarriage of justice and make the true character of

Cohn’s accusations entirely clear I will cite both Cohn’s text and Hirst’s
original version, Cohn’s text first, with his selection of words from
Hirst’s text indicated in italics:
[…] 50 years later, a researcher in the last stages of the Indian Plague
Commission, L.F. Hirst, lost sight of this early twentieth-century history.
Instead, he followed Thompson’s racist version of events, concluding that
the Australians “enjoyed a considerable advantage over workers in Bombay”
because “investigation in Sydney had been conducted in the midst of a civi-
lised and homogenous community speaking the language of the
investigator.”62
I also cite the full passage of Hirst’s text, marking again for pedagogical
reasons the words Cohn selected with italics, words which he asserts
are “concluding,” although, as can be readily seen at a glance, are not
concluding. In fact, the passage continues after the end of Cohn’s cita-
tion, and Cohn’s mischaracterisation of the passage is not accidental:
His reports [i.e., Thompson’s] are models of cogent reasoning from unu-
sually precise epidemiological data. Thompson and his Australian col-
leagues enjoyed a considerable advantage over workers in Bombay for the
purpose of an exact investigation of the factors governing the spatial
spread of plague in a particular region. His observation on a series of
plague outbreaks in Sydney were conducted in the midst of a civilized and
homogeneous community speaking the language of the investigator and
already trained, during the course of an epidemic of smallpox, to co-
operate with the Department of Public Health: whereas in India the out-
look of the polyglot population was restricted by ancient tradition, and
the social conditions were such as to make it difficult if not impossible to
acquire that exact and complete knowledge of all the circumstances
under which the infection had been received by each person attacked,
which is the foundation of investigations into the aetiology of disease by
the epidemiological method.63
As can now be readily seen, Cohn has selected a few words here and
there and has inaccurately represented Hirst’s text with the purpose of
incriminating Hirst as racist, although the alert reader will readily dis-
cover that even the outcome of this dubious selection technique makes
the application of the terms “racist” or “racism” completely groundless.
The continuation of the passage after the end of Cohn’s selected words
shows clearly what Hirst had in mind, namely that the “polyglot” Indian
62
Cohn 2002: 39.
63
Hirst 1953: 144–5.
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52 chapter two
population(s) with their ancient and deeply rooted beliefs resisted and
prevented good research into the nature of plague epidemiology and
hampered efforts to contain the spread of plague.64 His line of argu-
ment is entirely based on comparative cultural and ethnological obser-
vations and inferences with rational implications for epidemiological
research and efficient countermeasures. Taken out of its context, the
word “civilization” might also in this case be thought to have been used
with ethnocentric connotations. However, seen within the full context
it becomes clear that Hirst, with his great experience from work in
India and Ceylon (Sri Lanka), agrees with Ashburton Thompson that
“investigations into the aetiology of disease by the epidemiological
method” were much easier to carry out when the investigators and the
population spoke the same language, and the population was trained to
understand and accept anti-epidemic measures on the basis of a long
cultural tradition of adapting to and understanding the reasons for
such sanitary measures and research projects. Thus, the gist of what
Hirst says is, as in the case of Ashburton Thompson, that European
civilization and populations of European extraction were much better
adapted to the implementation of research efforts on epidemiological
problems and efficient anti-epidemic measures than the population(s)
of the Indian civilization. This is not at all to say that Western civiliza-
tion as a whole was superior, only that this was the case in this specific
field of scientific medical research and anti-epidemic efforts at the time.
I would submit that this is true, and that it was at least for the most part
the adoption of Western scientific medicine and epidemiology that has
raised average life expectancy at birth in India from a maximum of
22–4 years as recorded by the Indian census of 1911 to the present level
of 66.46 years.65 There is not the slightest hint in the text that Hirst held
the notion that white Australians of British extraction were genetically
superior to Indians, and thus there is no justification for describing
him as a racist. Clearly, Hirst had the good of the Indian population in
mind and wished fervently to find ways to spare as many lives as pos-
sible and reduce human misery from plague disease.
Those of us who have not served heroically in the fields of combat of
plague but live comfortable and safe lives in the ivory towers of academia
may note with interest that Hirst, who had spent his professional life in
64
Cf. Hirst 1953: 418.
65
Coale and Demeny 1983: 33; www.cia.gov, World Fact Book 2010, s.v. ‘India’.
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active front-line duty in the combat of plague in India and Sri Lanka
(Ceylon), almost a generation later strongly supported and enlarged
upon this line of argument which was originally presented by Ashburton
Thompson. This type of argument consists of scholarly empirical obser-
vations and methodologically relevant considerations that can be dis-
cussed in an orderly scholarly way. If Cohn had not had such an
extraordinary agenda, he could have attempted to show in an ordinary
scholarly way why the constituent arguments were not relevant or sat-
isfactory, and in this way produce a case for asserting that the reason
for this discrepancy sprang from untenable racist notions. Since this
was not possible, Cohn attempts by means of misquotations, incrimina-
tions and accusations to degrade and eliminate from serious scholarly
consideration an excellent scholar of extraordinary merits. Hirst’s out-
standing monograph has obvious mortal implications for Cohn’s the-
ory, exactly because it conforms in its essence to the work of the IPRC.
Most importantly, Hirst was convinced that modern and medieval
plague epidemics were the same disease, that the plague he had studied
intensively in the field and laboratory and combated in India and
Sri Lanka and the historical plague epidemics that he studied were the
same. Hirst therefore constructed his monograph on plague as a his-
tory of the combat and Conquest of Plague from the Early Middle Ages
to the present day, presenting a vast amount of historical and modern
medical and epidemiological evidence. Thus, Cohn must decide how
to dispose of this prestigious plague researcher and author of one of the
he most respected works on plague. Cohn attempts to do away with
Hirst as a trustworthy and respectable scholar by discrediting him as
racist or, what is much the same, asserting that he followed and sup-
ported racist views.
In addition to Cohn’s false accusation of racism, based, among other
things, on misquotations, he also misrepresents other of Hirst’s central
views, for instance, those on the spread rates of medieval and modern
plague epidemics and on the means of dissemination (below). Cohn
ridicules Hirst for having “fabricated the story of an underground war
between Rattus rattus and the brown rat to explain the plague’s sudden
disappearance from Europe in the eighteenth century.” However, the
only fabrication is Cohn’s false reference to p. 141 in Hirst’s monograph
where nothing to this effect is stated.66 The reason is that Hirst holds a
66
Cohn 2002: 33.
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54 chapter two
very different and very sensible opinion, stating “It is quite possible
that advances in building construction and domestic hygiene during
the eighteenth century turned the ecological scale against the black rat
and encouraged the other species [= Rattus norvegicus] lurking in the
outskirts of human habitations to enter them.”67
How Cohn Makes “Historians Square the Circle”
In Cohn’s monograph, scholars and colleagues with opinions that differ

from his, that is, inevitably almost everyone who has worked in the
field of plague research, are scathingly criticised, often repeatedly. His
generally disparaging views of historians in this field of study is evident
in the name of his chapter “Historians Square the Circle,” a title imply-
ing that they are intellectually incompetent or dishonest or both. Here
a rapid succession of scholars are ridiculed.68 If their outstanding aca-
demic record cannot be denied, they are accused of excelling at con-
cealing what they really are doing: “To square the circle, Ann Carmichael,
who combines an expertise in medicine and medieval history [actually
in historical plague research, my insertion] was subtler than
Shrewsbury…,” and so on.69 And of course, she squares the circle again
a few pages later.70
There are quite a number of group executions: A. Zitelli, R. J. Palmer
and A. Carmichael are unceremoniously denounced because their
views on contemporary notions of the nature of epidemic disease,
which are the outcome of serious work and careful studies, undermine
a central premise of his theory.71 It is correct of Carmichael to under-
line that “medical commentary, characteristic of late-medieval plague
treatises, was formulated with good Galenic universalism.” This view
was based on the notion of miasma which can be understood as a
special type of airborne poisonous contagion. This notion was gradu-
ally developed into the concept of miasmatic-contagionistic epidemi-
ology, the notion that miasma was infectious and was transmitted
between people by contact (per contactum) or by touching objects
contaminated with miasma from a diseased person (fomites), or at a
67
Hirst 1953: 123–4.
68
Cohn 2002: 41–54.
69
Cohn 2002: 47.
70
Cohn 2002: 49–50.
71
Cohn 2002: 114–5.
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distance (ad distans) when a person exhaled miasmatic air which was
inhaled by another person. Over long(er) distances miasma attached to
persons, objects or goods that were moved by trade and transportation,
and therefore quarantine of ships and people coming from infected
places and intermission of trade were introduced early as countermeas-
ures to prevent the importation of contagion or miasma.72
Cohn’s counterarguments for dismissing Carmichael’s view are with-
out value. As proof of plague’s infectiousness he cites Ibn Khatimah:
“a well man did not remain long with a sick one without being
attacked by the disease.” Firstly, this does not disprove Carmichael’s
understanding that such observations or views reflect Galenic mias-
matic-contagionistic notions, since miasma was transmitted by con-
tact, also by contact with fomites, objects that a diseased person had
touched or used. According to modern notions of plague epidemiol-
ogy, any person visiting the house of a person diseased by plague would
most likely enter a house swarming with dangerous rat fleas and would
be at great risk of contracting the disease by flea bite(s) or of bringing
infective fleas with him back to his own house where the fleas would
seek out rat hosts and unleash an epizootic that after a period of around
three weeks would manifest itself in plague disease in the household or
in adjacent households. Cohn also cites the Muslim physician to the
effect that “in the neighbourhood of Almeria, where the clothing and
bed linen of the plague-infected were sold… all died almost without
exception.” This observation lends itself well to the same miasmatic-
contagionistic understanding, and also reflects reality according to
modern plague research in so far as clothing and bedding from persons
who had died from plague are liable to contain infective rat fleas. At the
end of the same passage, Cohn cites a fourteenth-century Dutch physi-
cian on contemporary practice in Italian city-states to the effect that it
was “better to burn the commodities of plague victims than to sell
them.”73 This point relates to the contemporary concept of fomites, con-
tagious objects infected by miasma, and makes no difference.
Carmichael’s view stands undefeated when seen within a proper schol-
arly context. Undaunted, Carmichael has risen from her academic
grave to haunt Cohn, disclosing the unfairness and serious weaknesses
of his argument in a fine review paper.74
72
See, for instance, Hirst 1953: 22–58.
73
Cohn 2002: 234–5.
74
Carmichael 2003: 253–66.
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56 chapter two
In his usual disparaging way, Cohn makes the following introduc-

tion to the intellectual “liquidation” of a large group of scholars:
It is difficult to know why historians and medical scientists have held on
so passionately to the notion that the Black Death and its successive
waves of pestilence must have been the same disease whose bacillus was
discovered in 1894.”75
Here Cohn asserts that historians and medical scientists have been col-
lectively blindfolded by passion and irrational sentiments and excludes
the possibility that they have, on the contrary, seen the light through
reason and competent scholarly work. He goes on to be more specific
both with respect to scholars and his views on their work:
For Robert Gottfried and Michael Dols […], Paul Slack […], Brossollet
and Mollaret […], and many others, the plague’s bacteriology is simply
indisputable; no argument need be made. [….] They then proceed to
impose their notions of the aetiology and mechanisms of transmission of
the twentieth-century bubonic plague on those of late-medieval and
early modern Europe. Worlds of rats and fleas, rat epizootics, and regur-
gitated bacilli are invented for 1348 and beyond with picturesque vignettes
without any grounding in the historical sources […].76
As can readily be seen, in the eyes of Cohn all of these fine scholars
“and many others” are irrational persons who hold scholarly opinions
based on passion rather than reason and they are collectively incompe-
tent or dishonest or both since they impose notions across centuries
and invent their evidence and contrive their conclusions without any
basis in sources. The “legal” basis for this awesome ruling in his private
court: because they do not agree with his theory that the Black Death
was caused by a hypothetical, hitherto unknown and long ago disap-
peared viral agent.
Cohn’s need for group liquidations of researchers can also be well
illustrated by his collective execution of E. Le Roy Ladurie, J. Aberth,
N. Cantor, P. Slack, O.J. Benedictow, and I. Klein,77 because they all,
actually correctly, argue their respective cases on the basis of the IPRC’s
well-researched finding that plague was spread over long(er) distances
in the guts of rat fleas transported in clothing, luggage, and in ship-
ments of grain, cotton and suchlike (see below).78 This group execution
75
Cohn 2002: 57.
76
Cohn 2002: 57.
77
Cohn 2002: 28–9.
78
This subject is quite exhaustively discussed below: 151–93.
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also reflects the highly problematic character of Cohn’s theory. Their

correct knowledge of the IPRC’s epidemiological findings unveils the
untenability of his theory of spread which is based on the false asser-
tion that bubonic plague spreads only by dissemination between con-
tiguous rat colonies, and therefore spreads much slower than the Black
Death and subsequent plague epidemics.
Cohn’s repeated attacks on this author’s doctoral thesis are, in my
view, based on gross distortions and misrepresentations motivated by
his desire to assert that I am squaring the circle.79 In the following chap-
ters, I will present and discuss a sample of his assertions about my doc-
toral thesis which I consider objectively untrue and also representative
of the way he argues his case. Here I will only make a couple of points:
Cohn states that my thesis “shows an impressive but highly selective
reading of the epidemiological material on modern plague.”80 He does
not indicate in what way my reading is selective, although such a seri-
ous accusation of biased collection and use of the scholarly literature
should obviously be documented just like any other scholarly argu-
ment in order to attain empirical status and some level of tenability or
credibility. As it stands, it is a groundless accusation and an academic
libel. The assertion is untrue. I started my work on plague with a scepti-
cal attitude to plague as an explanatory cause of late medieval depopu-
lation.81 It was therefore my ambition to read all relevant scholarly
literature on plague, the medical and epidemiological, the demographic
and historical studies, in order to be able to consider critically and
empirically the various views on the plague epidemics of the past and
penetrate as deeply into the matter as sources and science would allow,
albeit with a particular emphasis on relevance for identifying the
microbiological nature and epidemiology of the late medieval plague
in the Nordic countries. My thesis was the first monograph to result
from this ambition. Its bibliography contains a balanced and for all
practical purposes complete reading of modern medical and epidemi-
ological studies and standard works on plague, comprising some
730 studies all used actively in the text and referred to in the footnotes,
and the text contains 830 footnotes making it possible to check
the premise(s) of even the tiniest detail. Much of what I did not find a
79
Cohn 2004: 51–2.
80
Cohn 2004: 51.
81
Benedictow 1993/1996: 13–6, 125, 266–7.
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58 chapter two
practical evidentiary use for in my thesis has been employed in my two

subsequent monographs on plague, while hundreds of other studies
have remained unused for lack of relevance or quality. Taken together,
my three monographs on plague history contain 2274 footnotes, about
1500 bibliographical entries, more than 1000 individual studies if
duplication is deducted, and 1146 pages. This reflects my fulfilled ambi-
tion to read all the relevant scholarly literature and to maximize the
evidentiary status and empirical testability of my studies on plague.
For the same reason, it is easy for me to show, and for anyone inter-
ested in this unusual subject to ascertain, that the bibliography of my
thesis, which contains only studies referred to in the text or footnotes,
is far more comprehensive and balanced than Cohn’s bibliography
which exhibits glaring gaps. For instance, the works of Russian and
Soviet scholars and of the French researchers in Madagascar and
Morocco are completely missing as well as the works of Dutch scholars
in Indonesia and plague studies in Egypt, and so on. In short, I would
like to ask my readers to consult the bibliography of my thesis under
the names of, inter alia, Bibikova (and Klassovskiy), Klimenko, Vasil’yev
(and Segal), Fenyuk, Dörbeck, Alexander, Girard, Estrade, Brygoo,
Blanc, Baltazard, Van Loghem (and Swellengrebel), de Langen and
Lichtenstein, Petrie et al., and Wakil, and compare Cohn’s bibliography.
One could also note the remarkable paucity of plague studies by
American scholars in his bibliography (see also above). A likely expla-
nation could be that all these scholars consider that historical plague
epidemics were bubonic plague, or to be more specific, they consider
the similarities between the disease they study and historical plague
epidemics of the past so great or comprehensive as to warrant a conclu-
sion of identity. It is also easy to show that Cohn’s reading of the great
corpus of works by the Indian Plague Research Commission is quite
limited and selective and that he also misrepresents their studies in
order to defend his theory: this has already been shown above and will
be demonstrated more systematically below.
Cohn enters studies in his bibliography that are not mentioned in
the text, although there are very strong reasons why he should do so,
for instance, a paper by Greenwood, “Statistical investigation of plague
in the Punjab. Third Report,” which he dates to 1912, although any
scholar who has held this paper in his hand would know that it was
published in December 1911, which explains why it is not used in the
text, and why he does not mention the important “Second Report:
On the connection between proximity to railways and frequency of
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epidemics.” This can be seen as a small beginning of growing evidence

of Cohn’s selective reading of the IPRC’s works and his misrepresenta-
tion of their results.
Cohn has also missed my paper on a feature of bubonic plague which
is entirely unique to this disease and therefore can serve as a certain
premise for identification, i.e. as a defining feature, namely that mor-
bidity and mortality rates are highest in sparsely populated areas and
decrease with increasing population density; in that paper I show that
this was the case both in modern epidemics of bubonic plague and in
historical plague epidemics.82 Although he demonstrates that he has
read my doctoral thesis, he apparently missed the chapter on this sub-
ject titled “The Problem of Population Density,” which ends in a com-
prehensive conclusion written in bold type to indicate the importance
I attribute to it.83 This negligence allows him to deny the fact and criti-
cize Hankin for—correctly, as shown above— pointing out this impor-
tant and characteristic similarity between the Black Death and modern
plague, a point enlarged upon below in a separate chapter.84
In short, it is easy to demonstrate that Cohn’s reading of the modern
medical and epidemiological studies on plague is very deficient and
arguably “highly selective.” These are the reasons Cohn does not sub-
stantiate the purported selectivity of my reading of medical plague
studies. His reading of my thesis is also highly selective and his under-
standing of it is surprising and deserving of comment, for instance, his
interpretation of the significance of climatic temperature and rats in
the epidemiology of plague in the Nordic countries (see below).
In this context, it may be useful to describe some problems associ-
ated with another instance of how Cohn goes about arguing his case in
order to put down other scholars. In order to reveal my incompetence,
he discusses the statistical use of the Obituary of the Cathedral of Lund
in my doctoral thesis. He begins by presenting the Danish (at the time)
cathedral city of Lund (which he misspells “Lunn”), which is in western
Scania and faces Copenhagen on the other side of the Sound, as
Norwegian. This, despite the fact that in footnote 61 on the same page
51 I dutifully explain the geographical location and historical change of
hands of the region, which was not, however, from Norway to Sweden,
82
83
Benedictow 1993/1996: 177–80.
84
Above: 34–8, below: 289–311.
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60 chapter two
but from Denmark to Sweden: Scania has never been Norwegian terri-
tory, literally far from it. The point of departure is that my doctoral
thesis, in accordance with its title, Plague in the Late Medieval Nordic
Countries, relates not only to my Norwegian patria but also to the late
medieval plague history of the Nordic countries. In relation to the point
at hand I cite two fine studies of the Obituary of the Cathedral of Lund
by two Danish historians, namely by J. Kinch (1817–88) and by
Emeritus Professor E. Ulsig of Aarhus University,85 the leading special-
ist on Danish plague history today.86 Thus, it is simply untrue that
“Benedictow squeezes from a mere ten deaths records [sic] found in an
obituary of monks at Lunn a reading that is far beyond the statistical
probabilities of those records,”87 and so on. This is a characteristic and
instructive instance of Cohn’s distortions of facts. Obviously, I have
done nothing of the kind, I merely cite two studies by competent Danish
colleagues which I consider to be of high quality. Ulsig was first oppo-
nent when I defended my thesis in 1992 and he had no objections to
my citation and use of his own study or of Kinch’s.88 Likewise, I have
never seen comments on these studies by Nordic colleagues that have
any resemblance with Cohn’s allegations and therefore, by implication,
have collectively failed to recognize the crude statistical mistakes that
are so self-evident to Cohn. This should make it clear that the disparag-
ing words Cohn heaps on my work since it represents such a serious
threat to his theory are misplaced and that he is instead indirectly and
on false grounds disparaging Kinch and Ulsig as scholars. I have pre-
sented these studies again in my monograph of 2004.89
Cohn ends this chapter on historians (allegedly) squaring the circle
by generally disparaging historians working in the field of plague
research while singling out for special negative attention one of the
greatest scholars of twentieth-century historiography who, fortunately,
concentrated increasingly on the field of plague history and made tre-
mendous contributions, namely Carlo M. Cipolla:
Historians’ unbending attachment to the Black Death as the same as
modern plague illustrates with uncanny precision Cipolla’s observation:
“Paradoxical as it may sound, the lesson of history is that all too often
85
Kinch 1869; Ulsig 1991.
86
Benedictow 1993/1996: 51.
87
Cohn 2002: 52.
88
Ulsig 1994: 94–105.
89
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people find it easier to manipulate the facts to fit their theories than to
adapt their theories to the facts observed.”90
Cipolla had in mind, of course, people of the sixteenth and seventeenth
centuries who had to fight plague on the basis of proto-scientific, defi-
cient and misleading notions of the nature of epidemic disease which
affected the way they perceived the epidemic and the conceptual frame-
work within which they endeavoured to understand it. To assert, as
Cohn does, that Cipolla with his broad knowledge of the accumulated
wisdom of two generations of intensive modern scientific medical and
epidemiological studies of plague was a comparable victim of similar
misconceptions cannot be taken as a serious scholarly opinion. The
heart of the matter is again that Cipolla also considers historical and
modern plague the same disease. Does not the notion of “unbending
attachment” and its association with manipulation of facts imply intel-
lectual dishonesty on the part of historians in general and of Cipolla in
particular? Or can it be understood as an assertion of general gross
incompetence on the part of all scholars who have reached conclusions
different from Cohn’s own? Later Cohn belittles Cipolla again on as
poor grounds as here.91 These examples are only a small selection from
the first part of his monograph.92
It should be obvious what sort of need lies behind this profusion of
negative and disparaging characterisations and assertions, which col-
lectively degrade plague researchers of both the historical and medical
professions: “historians square the circle,” “scientists square the circle,”
“historians,’ unbending attachment to the Black Death as the same as
modern plague,” “historians and medical scientists have held on so pas-
sionately to the notion that the Black Death and its successive waves of
pestilence must have been the same disease,” “idée fixe,” and so on. Why
is it inconceivable that all of these historians and medical scientists
have reached their conclusions and opinions on the basis of dedicated,
serious and highly competent research and scholarship? What motive
could they conceivably have for squaring the circle in their field of
scholarly work? Is that not an accusation of intellectual dishonesty? Or
could they all really be grossly incompetent and therefore to be excused
of dishonesty?
90
Cohn 2002: 54.
91
Cohn 2002: 209.
92
Cohn 2002: 11–54, 114–5.
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62 chapter two
Why is it only Cohn who has understood the true nature of the Black
Death and plague in general? How can it be that all other scholars in
the field, physicians as well as historians, are collective victims of an
idée fixe, a suggestion with clear psychiatric connotations? Does not
Cohn really turn the scholarly usability of the notion of idée fixe on its
head? Is not a collective idée fixe a rather strange notion, especially
among scholars and trained scientists with their intellectual tools, sci-
entific methodology and long training for disciplined testing of the
tenability of scientific hypotheses? Is not an idée fixe much better
adapted as an analytical tool at the individual level of (psyco)analysis?
If this is correct, is this notion of idée fixe not much better adapted as
an analytical tool for understanding the individual scholar with ideas
which deviate sharply from those of everybody else, especially if this
individual scholar argues his case in a furioso way, disparaging more or
less all other scholars in this field of research (if he is not misleadingly
attributing to them his own notions)?
The Attack on Schofield (and Benedictow and L. Bradley)
In his study of the plague epidemic in Colyton 1645–6, a small town

of 1500 inhabitants, Schofield focused in exceptional detail on the
question of whether or not the pattern of mortality varied according to
size of family, and if it did, in what way, and what this could reveal
about the mechanisms of spread and the nature of the disease.93 It is
useful for several reasons to discuss Cohn’s unwarranted attack on
Schofield’s paper because these questions play a significant role in some
later discussions. In this attack, he also in his usual disparaging way
involves Bradley and me,94 while he forgets to include Slack who enter-
tains the same opinion.95 Schofield’s study is based on a full family-by-
family reconstitution of the population which requires meticulous
registration of all inhabitants in order to follow closely their individ-
ual and collective fates during the epidemic. This is gruelling time-
consuming work with the objective of performing a detailed empirical
analysis of the epidemic, which should make it clear that allegations of
93
Schofield 1977: 95–132.
94
Cohn 2002: 121.
95
Slack 1985: 177–8.
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arbitrariness are unfounded. Unfortunately, some long citations are

necessary to clarify the scholarly problems involved in this case.
Cohn makes the following three accusative and disparaging asser-
tions with the footnotes in the running text, and my enumeration in
brackets:
Curiously, Roger Schofield, “An Anatomy of an Epidemic: Colyton,
November 1645 to November 1646,” in The Plague Reconsidered, p. 102,
asserts the opposite: [1] that diseases such as bubonic plague cluster in
households but airborne infections do not. [2] His claim (and denial of
hundreds of years of common sense and epidemiological research) is not,
however, based on any new epidemiological findings; no note follows it,
but perhaps because of Schofield’s reputation as a demographic historian
and his quantitative skills, [3] others have followed blindly: see Bradley,
“Some medical aspects of plague” 11–24, ibid.; and Benedictow, Plague in
the Late Medieval Nordic Countries, p. 174.96
This passage contains three central accusations:
(1) Schofield’s view is obviously and self-evidently untrue and grossly
misleading and at complete variance with elementary principles of
epidemiology;
(2) Schofield’s view is not based on sources or fact but is arbitrary and
misleading;
(3) Bradley and Benedictow accept uncritically and therefore “blindly”
Schofield’s views because Schofield enjoys such high reputation as
a demographer.
Cohn asserts that his views are based on p. 102 in Schofield’s paper.
This page begins with the following statement:
Let us take as a first hypothesis the proposition that the more that the
chances of catching a disease depend on physical proximity to a localized
source of infection, the more deaths will be clustered by household or
family, so that some families will be affected whilst others, even near at
hand, will escape. In the case of bubonic plague, for example, we would
expect the chances of being bitten by an infected rat flea to be higher in a
locality where rats had just died of plague than elsewhere. Since the black
rat (Rattus rattus) generally stays close to human habitation, a person
would be more likely to be infected by a flea in a house where rats had
recently died, than by a rat flea hopping across either from a dead rat
96
Cohn 2002: 121, fn. 156.
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64 chapter two
lying in the gutter, or from someone encountered in the street. Similarly,

in the case of typhus, a person would be more likely to acquire an
infected louse from someone who had just died in the room in which he
was sleeping than from a casual encounter in the street. With airborne
infections, on the other hand, transmission occurs much more readily
as people breathe out infected droplets as they move around during
their normal daily activities. Thus diseases like bubonic plague and
typhus are likely to be associated with geographically clustered patterns
of death, while airborne infections, such as influenza, will show much
less clustering.
Clearly and obviously, Schofield establishes here a very interesting
working hypothesis on the basis of a sound and profound knowledge of
epidemiological tenets. This puts in perspective Cohn’s assertion that
Schofield’s view represents a “denial of hundreds of years of common
sense and epidemiological research.” Conspicuously, Cohn is not able
to find a single modern epidemiological standard work or paper for
support of his disparaging argument of “hundreds of years of common
sense and epidemiological research.” For about hundred years, scholars
have rejected the common sense of hundreds or even a couple of
thousand years of miasmatic epidemiology. The beginnings of bacteri-
ology, and therefore also the beginning of microbiology, was estab-
lished as late as in the last decades of the nineteenth century and for
obvious reasons epidemiological research in the sense of modern sci-
entific research begins at around the same time. There is no factual
basis for Cohn’s accusation: Schofield has not denied the tenets of
(scientific) epidemiology, but on the contrary, he has used them in
a creative and scholarly fashion in order to construct a fine tool for
intellectual analysis.
Schofield next prepares the ground for empirical testing of his
hypothesis and takes time for the pedagogical task of explaining some
elementary statistical principles of demographic distribution and the
usefulness of the binomial expansion for this purpose to his readers
who would tend to be historians without significant statistical
training:
If we want to discover whether deaths were in fact clustered in families in
a particular epidemic, we need to know what the distribution of deaths
by family would have been if they had occurred randomly throughout
the population […]. In order to calculate this distribution we need to
know the chance of dying and the size of the family. This immediately
raises the further question of whether the chance of dying in practice
varied according to the size of the family […].
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Comparison of the distribution of mortality according to family size

with a random distribution will reveal possible deviation, and if there
is deviation, the pattern of deviation should enable the identification of
social factors that affected the distribution of mortality.
After further methodological and epidemiological discussion on
pages 102–5, Schofield can finally address his material on the popula-
tion of Colyton which consists of 406 households containing 1513 per-
sons who suffered 298 deaths or a mortality rate of 20 per cent. Table 2
presents “Death rates by size of family, Colyton. Nov. 1645–Nov. 1646,”
and the material is here organized according to size of family from
1 person to 8+, the number of families according to each size, the
number of persons each size category contains, the number of persons
dying in each size category and the mortality rate for each age category.
This provides the basis for studying whether the chance of dying was
random or whether it was affected by family size. The conclusion to be
drawn from this material is couched in the careful language of an emi-
nent and disciplined scholar:
The balance of evidence would therefore seem to suggest that person-to-
person transmission of the disease in close physical proximity was not an
important element in the Colyton epidemic.97
In Table 3, the material is organized according to “Observed and
expected distribution of families, by size and number,” and Table 4
shows “Ratio of observed to expected frequencies ±(0.005),” and “No.
dying in family.” Schofield explains:
For every family size the number of families with extreme experiences
(no-one dying: everyone or almost everyone dying) was greater than
expected, and the number of families with some people dying and others
surviving was correspondingly far fewer than expected. There was there-
fore a marked tendency for deaths to cluster in some families and for
other families to escape the epidemic altogether […].
Thus in Colyton in 1645–6 an individual’s chance of dying in the epi-
demic was not independent of what happened to others in the same fam-
ily […] his chance of dying had little, if anything to do with the size of
household in which he lived […] this combination of a strong clustering
of deaths with little apparent association between mortality and house-
hold size, suggests that the Colyton epidemic is unlikely to have been
caused either by an airborne disease or by a contagious disease such as
dysentery. It also casts doubt on diseases, such as typhus, which are
97
Schofield 1977: 105–6.
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66 chapter two
spread by ecological factors, and the most promising candidate would

seem to be bubonic plague with the rat fleas as the significant vector.98
It is this result of Schofield’s combination of complete demographic
data, careful epidemiological analysis, and mastery of demographic
statistical methods that enrages Cohn because it adduces substantial
proof to the effect that historical plague was bubonic plague, and rep-
resents as such a mortal threat to all alternative theories. This explains
why the other advocates of alternative theories pass by Schofield’s paper
in silence, even when they cite other papers in the same book, as Scott
and Duncan do. This also puts in perspective Cohn’s assertion that
Schofield’s views were arbitrary: “His claim […] is not, however, based
on any new epidemiological findings; no note follows it.”99 The fact
is that Schofield’s views are massively documented and are based
on a very careful collection of empirical data through the total regis-
tration of the population according to the methodology of family
reconstitution.
Schofield’s observation fits well with the observations of the IPRC:
after the introduction of plague contagion in a rat colony, rats soon
begin to die and their fleas to gather on the remaining hosts, until the
rat colony is so decimated ten to fourteen days later that released rat
fleas have great and increasing difficulties in finding new rat hosts. In
this situation hundreds of dangerous rat fleas swarm in the proximity
of household members. Since bubonic plague is caused by great num-
bers of rat fleas released quite closely in time from dead rats, many
members of households or inhabitants of adjacent houses would con-
tract the disease at much the same time. This was also observed by
plague researchers in India: “[…] when two or more [plague] cases
occur in a house, they are attacked practically simultaneously as if from
a common source of infection.”100 For this reason, it is an epidemiologi-
cal misunderstanding when Cohn and Alfani in a recent paper on
plague mortality in early modern Milan and Nonantola maintain that
the fact that household members typically fell ill in a brief time consti-
tutes evidence that historical plague was a viral disease spread by drop-
lets.101 Instead it is evidence of rat-borne bubonic plague, as shown by
Schofield.
98
99
See above: 63.
100
Lamb 1908: 67; IPRC 1907i: 881.
101
Cohn and Alfani 2007: 178, 192–6.
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Cohn states disparagingly about Benedictow and Bradley that they

“blindly,” presumably meaning uncritically and incompetently, accept
and cite the epidemiological principles and findings of Schofield’s
paper. So again he levels accusations for incompetence and/or intel-
lectual dishonesty against historians. Are these accusations more ten-
able than those levelled against Schofield?
Benedictow presents the part of Schofield’s paper on clustering of
plague cases in Colyton on pages 173–4 of his doctoral thesis. This part
will be cited verbatim in its entirety so that the readers can see for
themselves and make their own judgement without making an extra
effort:
Schofield has explored new avenues to obtain insights about modes and
patterns of epidemic spread, and has devised methods of determining the
nature of epidemic diseases. In the case of Colyton (south-east Devon),
in which about 20 per cent of the population were lost in the epidemic of
1645–6, the source material did not allow any study of the territorial dis-
tribution or spread of epidemic mortality. Instead, he was able to demon-
strate that the pattern of deaths by family or household offered important
clues to the nature of the epidemic disease and its mode of transmission
and dissemination.
He first makes the important analytical distinction that “the clustering
of deaths in families, and the variation in the death rate according to fam-
ily size, are two logically separate aspects of epidemic mortality.” If the
chances of catching a disease depend on physical proximity to a localized
source of infection, as is the case with rat-borne bubonic plague, deaths
will be clustered in some households, whilst others, even in the immedi-
ate vicinity, remain unaffected. There should be no association between
the chance of being infected and household size. Airborne infections,
being transmitted directly between people as they move about during
their normal daily activities, show much less clustering, but a strong cor-
relation with household size (cf. Dijkstra’s demonstration of the pattern
of spread in Jordan of the influenza epidemic in 1918). Diseases spread
by human parasites, like exanthematic typhus (lice) or—according to
Biraben—bubonic plague by human fleas and lice, might be expected to
show a moderate clustering and a very strong association with household
size.
The conclusions were unequivocal. There was a “marked tendency for
deaths to cluster in some families, and for other families to escape the
epidemic altogether”; the “chance of dying had little, if anything to do
with the size of household.” This combination points to a disease with a
distribution which is largely determined by ecological factors, most prob-
ably “bubonic plague with the rat as the significant vector.”102
102
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68 chapter two
As a part of her dissertation on epidemic diseases in early renaissance

Florence, A. Carmichael carried out a study of the spread of plague in the
quarter of Santo Spirito during the minor epidemic of 1430. In my opin-
ion, the pattern agrees closely with the findings of Dijkstra, Woehlkens,
Slack and Schofield.103 The extreme local character of dissemination, the
clustering of deaths at first in one part of this traditional working class
district and even along certain streets within this small area, the cluster-
ing of plague deaths within some families even as the immediate neigh-
bours escaped unharmed, the slow progression of the epidemic, and the
impression that many streets seemed to begin to function as local plague
foci as the epidemic spread through the summer months, all point to the
same explanation. The maps showing the spatio-temporal progression
seem close to the maps of Dijkstra and Woehlkens. As Carmichael does
not make the important analytical distinction emphasized by Schofield,
that clustering of deaths in families, and variation in the death rate in
families of different sizes are two logically separate aspects of epidemic
mortality, she did not collect the information necessary to decide the
type of clustering she had registered. Her own epidemiological analysis
therefore becomes ambiguous.104 This illustrates the significant contribu-
tion of Schofield’s paper to methodology, he provides the instrument to
clarify the issue of clustering and to determine this social aspect of the
epidemic as the type of dissemination characteristic of rat-borne plague.
I ask readers to read this text carefully and consider whether it justifies
Cohn’s allegation that the author accepts blindly and uncritically
Schofield’s text (because of his “reputation as a demographic historian
and his quantitative skills.”)
In the case of Bradley, no such citation can be made. Cohn refers to
Bradley’s paper “Some medical aspects of plague” on pages 11–24 in
the same publication with a collection of papers on plague. However,
since this paper does not contain a word from or about Schofield’s
paper, it is impossible that Bradley in this paper accepts blindly and
uncritically anything from Schofield’s paper. It is again an unfounded
allegation.
Presumably, the crucial point is that Bradley published another
paper in the same book, his study of a plague epidemic based on a
complete family reconstitution of a parish population, namely the epi-
demic in Eyam in 1665–6. In this study, which is independent of
Schofield’s of Colyton, he reaches the same conclusion as to the nature
of the disease, namely that it exhibits the characteristic epidemiological,
103
104
Carmichael 1978: 74–92, 101–8.
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demographic and seasonal features of bubonic plague. Thus, Cohn

endeavours, as it seems, to discredit Bradley as a scholar without reveal-
ing to his readers that such a paper is published in the same book as
Schofield’s paper, and a fine paper it is.
In Part 1 of his monograph, Cohn clears the ground for his alternative
theory by criticising scathingly the work of various medical scholars
and historians in two separate chapters disparagingly titled “Scientists
Square the Circle” and “Historians Square the Circle.” As these titles
imply, Cohn asserts that the outstanding medical scholars who per-
formed great research effort on plague, many of whom also took a pas-
sionate interest in plague history, and the historians who have performed
comprehensive studies on plague epidemics in the past, have collec-
tively squared the circle. Thus, they have either been intellectually dis-
honest or incompetent or both and the outcome of their research has
been grossly misleading and untenable since it is incompatible with his
alternative theory. Such gross disparaging assertions on behalf of so
many fine scholars should meet with profound incredulity. Sadly, I
believe that it has been demonstrated here on a broad basis that Cohn’s
arguments are severely flawed and are grossly unfair to both medical
and historical scholars. The central aspect of the discussion as it unfolds
is reflected in the chapter’s title “The Ethics of Scholarly Work,” since it
is demonstrated that the means Cohn has employed are very question-
able and that it is simply not true that these medical scholars and histo-
rians have squared any circles. Instead, as dedicated and conscientious
scholars they have followed the tenets of medical and historical meth-
odology and made great and lasting contributions to the epidemiology
and medical knowledge of plague as a disease and to the history of
plague epidemics.
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PART THREE
BASIC CONDITIONS FOR BUBONIC PLAGUE
IN MEDIEVAL EUROPE
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CHAPTER THREE
RATS
Introduction: How to Study Rats in History
Advocates of alternative theories on the microbiological nature of

historical plague epidemics insist triumphantly that there was no
murine basis in the form of black rats in Europe at the time (see below).
They concede that there could have been a significant presence in
Southern Europe and along the Mediterranean coasts, especially in the
urban centres, but elsewhere in Europe, they maintain, there could
only have been an incidental and transitional presence caused by ship
transportation and they deny that the black rat could have had a per-
manent presence in Northern Europe. All of these scholars agree that
black rats play a crucial role in epidemics of bubonic plague. Thus, the
opposite is obviously true: if there were no or only a tiny presence
of black rats in medieval Europe restricted to the southern and
Mediterranean parts of the Continent, there could not have been epi-
demics of bubonic plague, or there could not have been more than the
occasional small outbreak in the southern parts of it. It is also generally
agreed that the brown (or grey) rat did not arrive in Europe until the
early eighteenth century.1 Consequently, if there were rats in medieval
Europe, they would have to have been black rats. This does not mean,
as the zoologist D.E. Davis asserts, that black rats are the cause of
bubonic plague.2 These rats have lived peacefully with human beings
for thousands of years. Rats are principally victims of bubonic plague.
As soon as their dead bodies start to loose temperature, their fleas
begin to desert them, fleas which have satiated themselves on septicae-
mic rat blood and can transmit the real cause of bubonic plague to
human beings, namely infective and lethal doses of the bacterium
1
See, Zinsser 1934/1985: 200; Hirst 1953: 123, 142; Twigg 1984: 75; Davis 1986: 456;
Audoin-Rouzeau 1999: 423, asterisked footnote. In a personal communication by
e-mail of 10 January 2006, Anne Kristin Hufthammer of the Zoological Museum of the
University of Bergen, Norway, has confirmed to me that this arrival date for the brown
rat is still generally accepted.
2
Davis 1986: 455.
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74 chapter three
Yersinia pestis. Methodologically, necessary conditions and causes are

very different matters and should also be sharply differentiated from
sufficient conditions and causes. Methodology is not Davis’s strong
suit, as will unavoidably be shown below.
Then there is the question whether or not the brown rat played a part
which may affect our understanding of medieval and early-modern
plague epidemics. In his “review” of my monograph on the Black
Death, Cohn rejects my view that, according to the IPRC’s reports, the
black rat was of paramount importance in the aetiology and epidemiol-
ogy of plague in India:
However, he [Benedictow] has read these reports selectively. For instance,
he maintains that the black rat (Rattus rattus) was responsible for plague
in the years 1346 through 1353 as well as during the 20th century, but the
Indian plague researchers found as many dead brown rats as black ones
in dwellings where infection was active.3
Cohn’s accusation warrants a closer look at the IPRC’s conclusion as to
the relative importance of the brown rat (today called Rattus norvegi-
cus, until 1910 Mus decumanus) and the black rat (today called Rattus
rattus, until 1910 Mus rattus):
In Bombay city Mus rattus and Mus decumanus both occur in prodigious
numbers, in the country villages, however, Mus decumanus is very rarely
found.
Mus rattus in Bombay is essentially a house rat […] it may almost be
said to be a domesticated animal.
Mus decumanus, as is well known, is a rat which lives for the most part
outside houses in sewers, storm-water drains, stables, etc.
Mus rattus is apparently much more common in Bombay than Mus
decumanus […].
It is necessary at the outset to insist upon the fact that in Bombay City
there is a Mus decumanus epizootic and a Mus rattus epizootic.
[…] there cannot be the slightest doubt that the place-infection of man
is intimately related to that of M. rattus […] that M. rattus is essentially a
house-rat and that it lives in close association with man. It necessarily
follows from this association that the place-infection of M. rattus must
correspond closely to that of man in the sense that both must be referred
to inhabited buildings.
We think it justifiable to conclude that the epidemic is directly attrib-
utable to the rattus epizootic.4
3
Cohn 2005: 1354.
4
IPRC 1907g: 743, 746–7, 752, 766–7.
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rats 75
This proves that IPRC researchers were of the opinion that the plague
epidemics were mainly or wholly a reflection of epizootics among black
rats; in the countryside where the brown rat was very rare, the epidem-
ics in the villages would be about entirely based on the black-rat epiz-
ootic. This demonstrates also that bubonic plague epidemics can
develop and spread on the basis of the black rat alone, a fact that under-
lies the conclusion that historical plague was bubonic plague. Also in
Mumbai where the brown rat had a substantial presence the epidemic
was predominantly based on the epizootic among black rats. As can
also be seen, the black rat was apparently much more common in
Mumbai than the brown rat, and since the brown rat was also largely an
out-of-door rat, its significance for the epidemic process would una-
voidably be relatively small. Cohn’s assertion that the IPRC found as
many dead brown rats as black rats in the dwellings of people in India
is spurious. This is confirmed by G. Lamb in his summary of the
Commission’s work to May 1907 which is an excellent source for reli-
able information on the Commission’s findings and views in the early
years.5 Clearly, Cohn misrepresents my view.6
Thus the relationship between the rat plague epizootic and human
plague epidemic in India must have been very much the same as in
historical plague epidemics, if they were indeed epidemics of bubonic
plague. Having clarified this point, we can now focus on the presence
and distribution of the black rat in medieval and early modern
Europe.
Leading plague researchers such as Hirst, Pollitzer, Wu Lien-Teh,
and J.J. van Loghem who studied the bubonic plague epidemics of the
first half of the twentieth century argue for a broad presence of the
black rat in medieval Europe. This view is based mainly on contempo-
rary medieval and early modern written sources which also contain
some drawings. Their view is also supported by peculiar epidemiologi-
cal features of the spread and seasonality of the epidemics that were
taken as reflections of a basis in rats and their fleas. In support of
this conclusion, they emphasized the interval between the first case(s)
and the subsequent endemic and epidemic developments, the latency
5
Lamb 1908: 22–3.
6
It is, however, not clear to me what point he is trying to make, since it is quite
generally believed, as mentioned above, that the brown rat did not arrive in Europe
until around 1700.
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76 chapter three
period which is a defining feature of bubonic plague,7 and the strong

tendency of epidemics to break out in the warmer seasons and disap-
pear or be substantially diminished by cold weather, which they
explained, on the basis of the findings of the IPRC and other scholars,
through the role of rats and their fleas.8 When Davis refers to Hirst’s
monograph and write “that a search for evidence to support these state-
ments [as to the presence and role of rats] produces nothing,”9 this is
not correct and also his reference to page 119 is wrong, since this mat-
ter is not discussed on this page. Further, his reference to a single page,
when in fact Hirst addresses the matter broadly over quite a number of
pages elsewhere in the monograph, can also produce an incorrect
impression, because Hirst has not taken this question lightly as Davis’s
remarks suggest (see below).
Since all medieval European references to house rats, both textual
and graphical, as a present type of animal clearly refer to black rats, the
discussion must address the question of whether or not black rats were
present in sufficient numbers and with a sufficiently widespread geo-
graphical distribution to constitute the basis for bubonic plague
epidemics.
Advocates of theories that historical plague epidemics were not
bubonic plague but were caused by some alternative microbiological
agent assert, as mentioned above, that there either were no rats at all
(so Scott and Duncan, with an incorrect reference to Twigg10 and
Gunnar Karlsson11) or that the presence of black rats was restricted to
a tiny and transient incidence in urban centres, “if it existed at all” (so
Davis and also Twigg, who first advocated this view, and who is sup-
ported by Scott and Duncan12). Cohn accepts that black rats were
present with some unspecified incidence, but maintains that they
were not involved in plague epidemics, since dead rats are not men-
tioned in such circumstances.13 On the first page of his monograph, he
declares that “No contemporary evidence links the Black Death or its
7
8
See for instance Hirst 1953: 121–9.
9
Davis 1986: 456.
10
Scott, Duncan and Duncan 1996: 18; Scott&Duncan 2001: 261, 262, 280–1, 357.
11
Karlsson 1996: 263–84.
12
Twigg 1984: 75–89; Davis 1986: 460. Scott and Duncan 2001: 55, 57, 108, 134,
317, 357.
13
Cohn 2002: 82.
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successive strikes in Western Europe to rats.”14 This view is based on

three main arguments:
(1) the paucity or absence of references to observations of dead rats in

contemporary sources relating to historical plague epidemics;15
(2) the climate in the northerly parts of Europe is too cold for black
rats, thus the frequent spread of plague epidemics must be seen as
proof that they were not bubonic plague;16
(3) Karlsson and Scott and Duncan maintain that they have proved
that plague epidemics in Iceland and the village of Eyam in
Derbyshire, England, respectively took place without the presence
of rats, which constitute proof that historical plague epidemics
were not bubonic plague.
Since the question of the presence of rats in Europe at the time of the
plague epidemics is important, these three main arguments by the
advocates of alternative theories should be discussed seriously and sat-
isfactorily, and this is the subject of this chapter. Karlsson maintains
that two fifteenth-century plague epidemics in Iceland were pure epi-
demics of primary pneumonic plague caused by some mutated form of
Yersinia pestis, the bacterium that causes bubonic plague, and that this,
in his opinion, was the general form of late medieval plague; his theory
will be discussed below in a chapter in Part 5.
In recent decades an important new source on the history of rats has
appeared, namely zoo-archaeology or more accurately archaeological
zoo-osteology, the study of animal bones found in archaeological exca-
vations. Bone material of rats constitutes material evidence of the pres-
ence of rats with strong evidentiary value. If such evidence is not found
or only incidentally found when looked for systematically, this will
constitute evidence to the effect that there were no rats in medieval
society or alternatively that there was only a tiny presence which can-
not constitute a basis for the large-scale spread of bubonic plague epi-
demics, and consequently, the view of the advocates of alternative
theories would be vindicated. However, if rat bones are found quite
14
Cohn 2002: 1.
15
Twigg 1984: 83, 111–2; Scott and Duncan 2001: 54–5, 359.
16
Davis 1986: 455–70; Twigg 1984: 57, 86–8, 99–100, 112, 218; Scott and Duncan
2001: 57, 261, 357.
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78 chapter three
frequently when looked for as an ordinary part of archaeological exca-

vations of human settlements, and with wide geographical distribution,
these advocates’ crucial argument on this point will, on the contrary, be
proven invalid. The osteological material and perspective will be pre-
sented in the last subchapter of this chapter on rats.
The Nature of Rats and the Frame of Reference of the Medieval Mind
Clearly, the basic observation with respect to the paucity of references

to rat mortality in plague epidemics in historical sources is correct,
although as for instance, J.J. van Loghem showed long ago, the silence
is not quite as systematic or complete as had been asserted.17 Twigg
considers over several pages and with considerable scepticism reports
of rat falls associated with bubonic plague.18 However, for several rea-
sons the implications and significance of the relative paucity of obser-
vations of dead rats in relation to historical plague epidemics is not
at all obvious. As we shall see, relevant studies on rat-plague epizoot-
ics associated with plague epidemics have not been considered, and
important methodological and source-critical problems have been
neglected.
In relation to this question, there is a crucial methodological point
which the advocates of alternative theories fail to address: the validity
of this argument depends on a premise to the effect that contemporary
sources should be expected to mention dead rats in connection with
bubonic plague epidemics, and that this should be quite a regular fea-
ture in accounts of those epidemics. Otherwise, this argument becomes
an inference ex silentio, an assumption to the effect that the failure of
sources to mention a phenomenon proves that it did not exist or occur,
which is a classic fallacy in the methodology of history and social
sciences.
Firstly, what medieval sources and medieval chroniclers do and do
not mention is a continuous source of disbelief and bewilderment to
modern scholars.19 Certainly, medieval man had a very different men-
tal frame of reference for the assessment of the relative importance
of various types of contemporary events from that of modern man.
17
See, for instance, Van Loghem 1918 and 1925. Cf. Wu Lien-Teh 1936a: 8–9.
18
Twigg 1984: 25–7.
19
Slack 1985: 34–5.
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In this context, it might suffice to mention that many chroniclers do

not mention the Black Death, although it can be shown that their city,
region and country were fiercely ravaged by the epidemic.20
Generally, modern historians find it difficult to accept that outbreaks
of mortal epidemic diseases were “determined by divine providence
and that their first cause was supernatural: epidemics were God’s pun-
ishment for man’s sin,” which was the usual opinion all through the
plague era.21 Also historians find it difficult to accept the reality or pre-
dictive value of the omens or portents of severe epidemics that contem-
poraries claim to have observed, for instance, the appearance of a man
mounted on a great black horse or a giant striding along, his head far
above the roofs of the houses, or the appearance in the night sky of
skeletons with swords, hearses, coffins, unknown comets and astrologi-
cal constellations. It is also difficult to accept the causative implication
in the assertion that the first victims of plague fell sick after people had
seen “a vision of a corpse or a dead body carried to the parish [church]
there to be buried,” and so on.22 Thus, medievalists have to recognize
and relate to the fact that medieval man, on the background of medie-
val culture:
(1) believed in types of epidemic manifestations and causation that
today will generally be rejected as superstitious or false;
(2) did not take the same interest in strict empirical observation, acute
analysis and accurate knowledge (in the scholarly meaning of these
terms) and, consequently, would not notice the same phenomena
as modern man;
(3) did not have the same view of what were important and memora-
ble contemporary events as modern man has.
Thus, all assertions as to what medieval man should be expected to
observe and record must be discussed according to medieval man’s
frame of mind and culture and be substantiated according to ordinary
20
See Benedictow 2004: 191–4, and fn. 9 on p. 192, 206–7.
21
Slack 1979: 10. In 1641, John Wright, Jr., published a book called Londons
Lamentation. Or a fit admonishment for City and Countrey, wherein is described certaine
causes of this affliction and visitation of the Plague, yeare 1641, which the Lord hath been
pleased to inflict upon us, and withal what meanes must be used to the Lord, to gaine his
mercy and favor, with an excellent sprirituall medicine to be used for the preservative
both of Body and Soule. See Cox 1910: 151.
22
See for instance Bell 1951: 1–3; Mullett 1956: 16; Slack 1979: 46; Slack 1985: 34–6,
87–8.
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80 chapter three
demands for evidence. If the assertion is that medieval chroniclers

should be expected to mention rat falls in connection with plague epi-
demics, such a subject should be shown to belong to the types of events
or topics that chroniclers would consider relevant to mention.
Empirical orientation increases with modernity, first slowly but
clearly from the Renaissance and the Early Modern Period. In order to
understand medieval and early modern sources one must understand
the frame of mind and understanding of the medieval and early mod-
ern people who produced them. To illustrate the significance of this
point: Jean de Venette (c. 1307–c. 1370), one of the most prominent
and commonly cited chroniclers on the Black Death, states that “the
most surprising fact is that children born after the plague, when they
became of an age for teeth, had only twenty or twenty-two teeth, though
before that time men commonly had thirty-two in their upper and
lower jaws together.”23 The fact is that young children have twenty milk
teeth, while adults have thirty-two teeth including four wisdom teeth.
The idea that plague should have caused such change is not only at
variance with modern genetics, but further, Jean de Venette could eas-
ily have tested and corrected it by examining the teeth of infants or
young children born before the plague and after the plague. This is,
then, an illustration of the weak empirical orientation even of educated
medieval people.
To illustrate the significance of the frame of reference for under-
standing the reality of observed phenomena, we may note that Anton
von Leeuwenhoek, who invented the microscope in the 1670s was the
first human being to observe microbes, but neither he nor other
researchers for 200 years to come persuasively connected such obser-
vations with the idea that such creatures could be causal agents of
epidemic diseases. They did not link this type of observation to an
explanatory idea of disease for the practical reason that they had no
frame of understanding and analysis, no theory, that could lead their
thoughts and reasoning to a microbiological theory of epidemiology.24
This puts in perspective medieval man’s great helplessness in under-
standing the nature and dynamics of epidemic disease. People observe
and explain and act according to what their frames of reference and
23
The Chronicle of Jean de Venette 1953: 51.
24
It is true that notions of germs had long been around, but this case history illus-
trates the lack of real interest in such ideas even after they became to some extent test-
able by microscopic observation.
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understanding permit or in the direction their thoughts are lead by

their preconceptions.
Thus, in this context, the beliefs and understanding of people in the
past in relation to the cause of epidemic disease and mortality must be
taken into account. The great majority, apparently the overwhelming
majority of medieval persons, believed that epidemic mortality was an
expression of God’s anger and punishment for their sins, and this view
was predominant far into the Early Modern Period.25 This belief would
not be conducive to observation of natural phenomena and alternative
rational interpretations. The limited number of learned persons who
had acquired knowledge of Hippocratic-Galenic medicine would have
understood epidemic disease as a reflection of the presence of miasma.
Miasma was corruption or pollution of the air by noxious vapours con-
taining poisonous elements that were caused by rotting putrid matter,
but could also be let out from the ground by volcanic activity or par-
ticular constellations of planets. Miasma was spread by wind and could
therefore spread speedily, it could enter persons by inhalation or
through the pores of the skin. Not until the Renaissance, in the decades
around 1500, was this theory of miasma expanded to include the idea
that healthy persons could be infected by touching infected persons or
objects contaminated by them with miasma (fomites), i.e., a miasmatic-
contagionistic theory of cross-infection and epidemic spread, although
the idea was for a long time not broadly accepted.26 In the words of
C. Creighton, the last champion of miasmatic theory in England, writ-
ing around 1890:
The virus of plague has its habitat in the soil, although it may be carried
long distances clinging to other things. In its most diffusive potency it
[miasma] is a soil-poison generated […] out of the products of cadaveric
decay; in its less diffusive but hardly less malignant potency, it is a soil
poison generated out of the filth of cattle housed with human beings, or
out of domestic filth generally […].27
Also, in its medieval form, miasmatic theory allowed in principle
empirical observation, but classical medicine’s enormous prestige and
medieval man’s weak empirical orientation (in the scholarly meaning
of the term) meant that chroniclers and physicians would rather inter-
pret what they saw according to the predictions of classical miasmatic
25
Slack 1979: 10; Slack 1985: 26, 28–9.
26
See, for instance, Hirst 1953: 222–72, and Creighton 1891: 326.
27
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82 chapter three
theory than believe their own eyes: several mention rat mortality in
connection with the Black Death, but together with mortality among a
combination of other animals that are not susceptible to the same dis-
ease, such as birds, horses and snakes.28 Since miasma seeped up
through the ground, it would also infect animals that spent much time
underground like moles, rats or snakes,29 and since miasma was spread
by wind, it was a logical corollary that birds would fall out of the sky,
bee hives succumb,30 and so on, and this type of miasmatic inference
took precedence over empirical observation. A typical example is pro-
vided by the account of the Greek historian Nikephoros Gregoras who
witnessed the Black Death in Constantinople:
[…] The calamity did not destroy men only but many animals living
with and domesticated by men. I speak of dogs and horses, and all the
species of birds, even the rats that happened to live within the walls of the
houses […].31
Since these accounts mention rat mortality in conjunction with mor-
tality of animals known to be refractory to bubonic plague infection
and insusceptible to the same pathogen, they are unusable as evidence
of reality and rat epizootics in time of plague, and are rather evidence
of contemporary culture and mentality and the presence of rats.
Lastly in this context, it seems appropriate to mention the almost
complete neglect of miasmatic theory by Scott and Duncan in their
monographs: in the first monograph the term does not appear in the
index, and in the popular version of the monograph of 2004 the word
miasma is not mentioned.32 They just assume that contemporary
notions of contagiousness can be understood in the light of the mod-
ern concept, presumably because this anachronistic approach serves
their line of argument. In their original paper of 1996, they mention
miasma, but apparently without understanding the concrete contem-
porary implications.33 An even more demonstrative instance of this
28
Hirst 1953: 127; Wu Lien-Teh 1936a: 8.
29
See for instance Creighton 1891: 173.
30
Twigg 1984: 215.
31
Cited by Bartsocas 1966: 395.
32
See also below: 613–9.
33
Scott and Duncan 1996: 19. Strangely, they do not seem to understand that,
according to the theory of miasma, it could be useful to put unslaked lime in plague
graves, since it would hasten the decomposition of the bodies and counteract the devel-
opment of miasma that could seep up through the soil and poison the air. The notion
that the use of unslaked lime indicates anthrax is an anachronistic interpretation based
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neglect is their citation from Daniel Defoe’s book on the Great Plague
in London where he describes in dramatic literary terms the notion of
miasmatic-contagionistic spread of plague by diseased individuals.
Whilst Defoe wrote this book in quite a journalistic way, hoping to
earn some money in a climate of renewed fear of a plague outbreak,
they present his account as proof of his great insight and judgment to
the effect that he describes modern ideas of infection. This provides
them with yet another opportunity to express their generally disparag-
ing views of historians and medical scholars (the italics are mine):
And yet for the whole of the twentieth century, going completely against
common sense, it was universally and unequivocally believed that all the
plagues were caused by a disease of rodents called bubonic plague, and
that the infection was transmitted to people from rats by fleas. Rats and
fleas are the established dogma of all history books today. What a pity
that little attention has been paid to Defoe’s observation.34
Characteristically, “Debunking History” is the disparaging name of the
chapter where this statement is found; the authors scorn historians
(and physicians) of plague research for collectively “going completely
against common sense” and for collectively being blind supporters of
dogmatic beliefs. Defoe was born in 1660; he was five years old at the
time of the year of the Great Plague, and his book A Journal of the
Plague Year was published fifty-seven years later. The assertion that
“Daniel Defoe had perspicaciously noted” the purportedly splendid
observations that they attribute to him is obviously untenable and mis-
leading and constitutes no reasonable basis for their disparaging
remarks against historians. Defoe was not a scholar or writer of popu-
lar science, but mainly a literary author with clear commercial motives
whose inaccuracies are legion. In fact, Defoe’s description of the conta-
giousness of diseased individuals is entirely compatible with and based
on contemporary miasmatic theory. Since Scott and Duncan have
apparently failed to note this, it seems that they do not have satisfactory
knowledge and competence in historical medicine and epidemiology.
The use of the term “common sense” as a superior substitute for scien-
tific observation is also noteworthy. Evidently all scholars who have
conscientiously and systematically applied scientific methodology and
on modern knowledge and usage. For the same reason, it was also usual to burn live-
stock which had died from murrain: see below: 580.
34
Scott and Duncan 2004: 165–6.
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84 chapter three
empirical observation to their work and made these the basis of their
results should have substituted it with “common sense.”
Cohn brushes brusquely aside sound studies of contemporary
notions of miasma in order to assert much the same (anachronistic)
understanding of medieval man’s notion of contagiousness as Scott
and Duncan.35 Carmichael has, as mentioned above, since taken Cohn
and also Scott and Duncan to task in a good review essay on this
point.36
Since bubonic plague, as shown above, is caused by great numbers of
rat fleas departing quite close in time from dead rats, many members of
households or inhabitants of adjacent houses would contract the dis-
ease more or less simultaneously. This was also observed by early plague
researchers: “[…] when two or more [plague] cases occur in a house,
they are attacked practically simultaneously as if from a common
source of infection.”37 Thus, the epidemic scene of bubonic plague
would readily lend itself to miasmatic and miasmatic-contagionistic
understanding under the assumption of simultaneous contamination
by polluted wind or multiple social contacts with a contaminated per-
son. Contemporaries entertained also notions that were closely linked
with superstition like the belief in the reality of the evil eye, that healthy
people were easily infected by the look of diseased persons. In connec-
tion with the Black Death, several chroniclers and commentators ven-
ture outside miasmatic epidemiology in this way, insisting that “merely
through looking, one person caught it from the other,” which can, of
course, support notions of great speed of spread and be taken as confir-
mation of miasmatic epidemiology.38
Since this chapter is not about contemporary notions of contagion
and the spread of epidemic disease, this subject cannot be developed
further here. However one should keep in mind that since, in contrast
to the claims of Scott and Duncan and Cohn, medieval and early mod-
ern man did not know that epidemic disease could be spread and trans-
mitted by insects, they had no alternative to the understanding of
contagion and transmission of disease offered by miasmatic theory (or
contamination by look).
35
See for instance Cohn 2002: 114.
36
37
Lamb 1908: 67; IPRC 1907i: 881.
38
See for instance Benedictow 2004: 236.
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rats 85
The Question of the Presence of Rats and the Methodological

Fallacy of Inference ex silentio
The advocates of alternative theories contrast the paucity or lack of

evidence of dead rats in historical plague epidemics with assertions to
the effect that this was a conspicuous feature of modern epidemics of
bubonic plague. However, these assertions are typically not accompa-
nied by references to corroborating scholarly studies, but reflect instead
what these advocates of alternative theories consider to be self-evidently
true, what must have been the case.
They all avoid asking the crucial methodological question: on what
grounds should people in the past be expected to observe intense rat
mortality or at least substantial numbers of rat falls preceding the
outbreak of plague epidemics and running concurrently with the
epidemics as they unfolded? These researchers are thus committing
a methodological fallacy, the fallacy of inference ex silentio, which is
to infer from silence in the sources that a phenomenon or event did not
exist or occur.39
Twigg, who generally functions as the pioneer of alternative theo-
ries, presenting seemingly important arguments that are eagerly picked
up by others, is also the first advocate of alternative theories who com-
mits this fallacy of inference ex silentio. He claims that
if rats were present when bubonic plague arrived in 1348 there would
have been heavy rat mortality, a fact well known and commented upon
by people in endemic plague areas, and as this would have been experi-
enced by the English then that fact alone would have been an important
feature of the times. So far as I can find there was no occasion when this
was recorded in the British Isles in 1348–50.40
This statement contains unsubstantiated and therefore arbitrary asser-
tions as to what people at the time must have seen and what they should
have commented on in writing. It contains also an arbitrary argument
of fact in so far as Twigg asserts that heavy mortality of rats during
plague epidemics was a “fact well known and commented upon by peo-
ple in endemic plague areas” which is left unsupported by any corrobo-
rative evidence or references in the text or in accompanying footnotes.
The lack of support is not accidental or fortuitous, for these assertions
39
Cf. Benedictow 2004: 192 and fn. 9.
40
Twigg 1984: 111–2.
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86 chapter three
as to what people should have seen are misconceived (as we shall see),
but they do have a function: they clear the ground for using them as the
basis for inference ex silentio that concomitant rat plague did not occur
in medieval plague epidemics.
When Cohn states on page 1 of his monograph that “No contempo-
rary evidence links the Black Death or its successive strikes in Western
Europe to rats,”41 also he commits an obvious fallacy of inference ex
silentio, because he claims that such accounts or “links” should have
been made by contemporaries without addressing the question of why
contemporary people should be expected to note the role of rats and
record it in writing. Cohn commits this fallacy of methodology again
when he states: “To date, no one has found a description of a rat epiz-
ootic preceding or accompanying a plague in late-medieval or early
modern Western Europe.”42 He believes that this provides him with
another occasion to denigrate historians, stating: “As for the absence of
rats associated with the medieval plague, historians have asked us to
believe that their ubiquity made them invisible, even though they were
noticed in moments other than plague.” He then goes on to cite “the
English chronicle of Henry V” where it is related that the besieged
inhabitants of Rouen were so desperate from hunger that they ate “all
thair cattis, hors, houndis, rattis, myse.”43 Obviously, these two situa-
tions are not in pari materia, they cannot be compared in this regard:
the English chronicler has a motive to mention rats, he wished to
emphasize the English victory, and thus said that the French citizens
were forced by the brave English besiegers to degrade themselves by
eating animals usually never touched for food. This does not imply that
contemporary chroniclers generally had a motive for mentioning dead
rats in connection with plague epidemics if they were bubonic plague.
However, it does contain evidence that (black) rats were present in this
north-western French city in numbers making them usable for supple-
mentary nourishment, and this was evidently acceptable as true by all
readers of the chronicle, which is at variance with the insistence of the
advocates of alternative theories that only tiny numbers of rats were
incidentally and transitorily present in these parts of Europe, a point
Cohn does not reflect on.
41
Cohn 2002: 1.
42
Cohn 2002: 22.
43
Cohn 2002: 82.
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rats 87
The fact that Twigg is unable to support his assertion that people
usually observe heavy mortality among rats during plague epidemics
casts sinister shadows over Scott and Duncan’s repeated assertions to
the same effect in their monographs, for instance, that
Since bubonic plague is a disease of rodents, the arrival of an outbreak is
frequently presaged by rats dying in the streets […].44
It has been regularly reported that the start of an outbreak of bubonic
plague spreading to humans is presaged by rats dying in the streets; in a
small village perhaps just a few, in a large South African township per-
haps many barrowloads. And yet it is generally agreed that there is no
mention in any of the accounts of rat mortality during the epidemics in
the age of plagues in Europe.45
Thus Scott and Duncan also claim that dying or dead rats in the
streets were a regular feature of bubonic-plague epidemics. However, it
is a very conspicuous feature of this assertion of a fact purportedly
based on frequent or regular observation that it is supported only by
one reference to purported observations in a South African township.
This is obviously very weak support for a sweeping comparative asser-
tion on a purportedly central feature of contemporary bubonic plague
as well as historical plague epidemics, actually they refer to it at least
four times.46 Obviously, even if it were correct it is not an adequate
basis for the crucial generalizing claim of the high frequency or regu-
larity of this phenomenon. However, as we will see below, it is not
correct.
Scott and Duncan cross the line into this fallacy again in their sec-
ond monograph of 2004 when they state disparagingly of historians:
it is generally agreed that there is no mention in any of the accounts of rat
mortality during the epidemics in the age of plagues in Europe. One
comment was that “Historians have noted that contemporary accounts
omit any mention of rat mortality,” but they have chosen to ignore this
important point.47
Since they do not provide footnotes or literary references in support of
their statements and assertions in the second monograph, it is impos-
sible to know the identity of the person represented by “one comment
44
Scott and Duncan 2001: 359, cf. 54–5.
45
46
Scott and Duncan 2001: 54–5, 65, 359; Scott and Duncan 2004: 176.
47
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88 chapter three
was,” if this assertion has any basis in reality at all. The disparaging
remark on historians is, according to the form of the citation from their
text, clearly their own, implying that in their view historians in this
field of study are generally intellectually dishonest, since they purport-
edly have collectively chosen to ignore an obvious and important, even
crucial fact, and that historians, with their “eyes shut wide open”, have
made this choice in order to protect their untenable theories on the
microbiological nature of historical plague.
It is possible to uncover the basis of these assertions from informa-
tion supplied in their first monograph of 2001. Here, Scott and Duncan
assert that dead rats were swept up by the barrowload in a South African
township and that “dead rats littered the streets of an eastern metropo-
lis,” citing “Annotation 1924” and “Liston 1924.”48 This is taken almost
verbatim, references and all, from A.B. Christie’s general textbook on
infectious diseases. Strangely, they insist that their assertion is based on
the first edition of Christie’s textbook, published in 1969 which does
not contain a chapter on plague; nor does the second edition of 1974.
However, the third edition of 1980 contains a non-specialist chapter on
plague, quite flawed, as will be seen.49 This chapter contains the account
they cite and also important information which they neglect to men-
tion in conjunction with their repeated assertions that dead rats were
collected by the barrowful in the streets.
Christie’s account of plague in South Africa is inconsistent, even
insouciant. He mentions the purported observation in the South
African township twice: on page 758, he uses the wording “dead rodents
have been collected ‘by the barrowful,’ ” and two pages later he states
that rats “may be swept up by the barrowful in a South African town-
ship.” It is this second assertion that Scott and Duncan have chosen to
contrast with the lack of similar information in relation to historical
plague epidemics in Europe and as proof that these epidemics could
not have been bubonic plague. However, one page later, Christie
notes that in South Africa “167 outbreaks with 372 cases and 235 deaths
have been recorded,” revealing that outbreaks comprised, on average,
2.2 cases with 1.4 deaths, which means that plague did not occur in
epidemic form but only in weak endemic form. This is a pattern that on
its own raises very serious doubts that it could be associated with open
48
Scott and Duncan 2001: 65, cf. 55.
49
Below: M400–5.
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rats 89
mass death of rats in a township. Then Christie adds that “apparently

plague has not spread in South Africa via the R. Rattus and X. cheopis
combination.” This constitutes sufficient grounds for rejecting the idea
that these tiny plague episodes can be associated with dead rats, observ-
able or not, and have any significance for the understanding of histori-
cal plague epidemics. It can be shown that Scott and Duncan knew
these basic facts, but placed them at safe distance from their assertions
that rats were collected by the barrowful.50
In support of their various assertions on this point, Christie/Scott
and Duncan refer to “Annotation. Reservoir of plague in South Africa,”
published in The British Medical Journal, 1924, page 875. However, in
this “Annotation” not a word is said about rats, nor is the word barrow-
ful used, and in particular, nothing is said about collection of rats or
other rodents according to this gauge or any other measure. Instead, it
mentions that wild rodents called gerbilles play the main part in con-
stituting a weak plague focus in South Africa. Rare human cases of
plague are mainly associated with plague among these rodents or occa-
sionally with some other wild types of rodents. Gerbilles avoid “human
habitation,”51 a fact which explains the miniscule incidence of human
cases of plague and also associates the incidence of such cases with
rural localities and makes it difficult to relate observations of great
numbers of these plague-dead rodents to townships. However, sud-
denly or inadvertently Scott and Duncan mention that all “367 [sic]
human cases” “were confined to the villages,” in short, human cases
occurred episodically and were not associated with townships, streets
and urban structures but with rural society and African village-struc-
tures.52 This shows that they were aware that there were only incidental
cases of plague in South Africa. The assertion that rats were collected
by the barrowful in a South African township is false. It is this false
assertion of the observation of barrowloads of plague-dead rats in
South African townships which allows Scott and Duncan to construct
a contrast with the lack of similar information in historical plague epi-
demics in Europe and to consider the difference as proof that the his-
torical epidemics could not have been bubonic plague. The fictitious
character of the first half of the comparison invalidates the comparison
and the inference. One should keep in mind that the other half of the
50
51
Wu Lien-Teh 1936b: 197.
52
Scott and Duncan 2001: 50. No source reference given.
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90 chapter three
comparison is also unsupported by evidence, a point that will be dis-

cussed below.
The brief statement about rats that “litter a street of an eastern
metropolis” given by Scott and Duncan is intriguing. They refer to a
paper by Liston; however, the statement and supporting reference are
taken directly from Christie.53 Unfortunately, Liston’s paper consists of
lectures and is unannotated. It contains one passage that could possibly
be the source of Christie’s/Scott and Duncan’s account: “It is stated that
as many as 20,000 dead rats were collected in a short time in certain
quarters of Hong-Kong, and that 1,500 were obtained from a single
street.”54 One should note two aspects of this account: firstly, the unspe-
cific nature of the opening words may indicate a reservation or a sec-
ond-hand origin, and secondly, nothing is said to the effect that rats
littered the streets, only that dead rats were collected, also the second
part of the passage fits into this framework. All standard works on
plague have been searched for corroboration of this information,
but nothing was found bearing directly on Liston’s remarks even in
the standard work published by the National Quarantine Service,
Shanghai Station, by the outstanding scholars Wu Lien-Teh, J.W. Chun,
R. Pollitzer et al., Plague. A Manual for Medical and Public Health
Workers. Some remarks in the historical introduction could be of inter-
est. It is related that a person called Dr Mary Niles “tells of a Chinese
official at Canton” who in 1894 offered to pay out of his own pocket
“ten cash” for every dead rat brought to him and collected over 35,000
in the course of a few months. On elementary source-critical grounds,
the incidental and uncertain nature of this piece of information is quite
obvious and it does not relate to the metropolis specified by Liston.55 It
is mentioned in an early standard work on plague that in 1901, thirty
men were employed in Hong Kong to collect rats, and “a private firm of
30 coolies employed in sorting, and one of whose duties was to collect
dead rats from the godown when required,” and that in another firm
rats were dying in the store-room and two men were engaged in remov-
ing them.56 Conceivably, this could be the background of Liston’s
remarks, but if so, it cannot be considered evidence bearing upon the
point, at least not significant evidence: both cases relate to attempts at
53
Christie 1980: 760.
54
Liston 1924: 950.
55
Wu Lien-Teh 1936a: 21.
56
Simpson 1905: 217.
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reducing the rat population by payment for dead rats or organizations

for the collection of dead rats in Canton and Hong Kong. It is not stated
that the rats were picked up in the streets, and thus many may not have
died by plague, but could have been killed for cash or were picked up
or caught in godowns, store rooms or other storage facilities.
To my knowledge, evidence of mass deaths of rats is at best sparse
or almost non-existent not only in relation to historical epidemics
of plague but also in relation to modern epidemics, which explains
that only Scott and Duncan attempt to refer to such evidence, errone-
ously as has been shown. Accounts of purported observations of mass
death of rats in plague epidemics in India in the 1830s are mentioned,
but these observations were not available in the form of scientific
studies.57
Taking a closer look at the few accounts or assertions of observations
of widespread rat mortality associated with bubonic plague epidemics,
it becomes clear that they are not based on scientific studies but on
reports written on obsolete miasmiatic premises, are presented in an
untestable or inaccurate form, have the character of hearsay or rumour,
or relate to special circumstances that do not clearly imply widespread
or mass occurrence of dead rats in streets or other types of open public
spaces. It appears impossible to corroborate on the basis of scholarly
studies that easily observable mass mortality of rats has occurred either
in connection with modern epidemics of bubonic plague or with his-
torical plague epidemics. There is a conspicuous paucity of relevant
evidence on this point and its problematic nature must be underscored.
This raises the question of why this should be so.
Ars Moriendi Rattorum: Where Have all the Dead Rats Gone?
Modern plague research started with the outbreaks of plague in Canton

and Hong Kong in 1894 which showed that the disease had retained
its ability to cause enormous mortality;58 it had also retained its great
ability to spread from commercial hubs by ship to countries abroad,
as had been demonstrated with enormous vigour by the Black Death.59
In a few years, plague was transported to India, Australia, Indonesia,
57
Hankin 1905: 55. Cf. Simpson 1905: 43, 46.
58
Hirst 1953: 103; Yersin 1894: 662.
59
Benedictow 2004: Map 1, p. xviii–xix, 60–229.
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92 chapter three
Madagascar, Egypt, the U.S.A., countries in South America, and so

on. This menacing development was taken very seriously: national
health organizations were mobilized, eminent medical scholars with
relevant qualifications were organized into plague research commis-
sions equipped with fine medical laboratories and ample assistant per-
sonnel, generous grants financed comprehensive studies of the disease’s
microbiological, medical and epidemiological properties in order to
develop efficient anti-epidemic countermeasures at a time when no
medication effective against the disease was available.60
The black rat or Rattus rattus, alias the house rat or ship rat, was
quickly singled out as the (main) carrier of the disease. It was pointed
out at the very start of modern plague research, in Yersin’s small paper
of 1894 summarizing his early findings in Hong Kong, that “it is prob-
able that the rats constitute the main vehicle.”61 Soon it was also sus-
pected that its usual rat flea was the agent of transmission both between
rats and from rats to human beings. The Indian Plague Research
Commission (IPRC) concluded early on that “the epidemic is directly
attributable to the rattus [rattus] epizootic” and that “the rat-flea [of the
black rat] and the rat-flea alone is the agent of transmission of the
plague bacillus from rat to man.”62
However, the pioneering plague researchers who started their work
around 1900 when little scholarly work had been carried out on rats
were soon confronted with an intriguing problem, namely the scarcity
or even absence of observed rat falls both under ordinary circum-
stances and during plague epidemics. In their endeavours to acquire
indispensable knowledge of the behavioural patterns of rats, especially
severely ill or moribund rats, they had to perform much basic work.
The IPRC implemented comprehensive studies of natural rat mortality
in relatively isolated villages outside Mumbai and in the Punjab. Despite
considerable efforts and opening up of rat holes and burrows, so few
rats were found that they had to acknowledge that the findings could
not “represent the normal rat mortality and it may, therefore, be inferred
that the large majority of rats which die from normal causes die in inac-
cessible places.”63 The IPRC were not unprepared for this conclusion.
60
Hirst 1953: 101–6, 296–300; IPRC. XXII. 1907g: 724–5; Lamb 1908: i–iv; Brygoo
1966.
61
Yersin 1894: 667. My translation from French.
62
IPRC 1907g: 743–62, 767, 777; Lamb 1908: 54.
63
IPRC 1907h: 854; IPRC 1907j: 908; Lamb 1908: 24.
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In 1906, J. Ashburton Thompson, published, as mentioned above, a

paper summarising Australian research after bubonic plague had
appeared in Sydney in 1900. In this paper he also addresses this phe-
nomenon and the insights gained by the health authorities under his
leadership. He contends that the reason that some scholars thought
that there were plague epidemics in India without a basis in rat-plague64
was that a proper search had not been performed.65 “Systematic detec-
tion of rat-plague is in reality a difficult business,” he points out. It was
not until a “rat intelligence staff ” had been trained and acquired practi-
cal experience in the search for plague rats that they were regularly
found in the individual houses in which plague cases had occurred,
work that started in 1904. Several reasons for this phenomenon were
indicated; apparently the basic or crucial reason is that “Rats eat each
other in nature.” When rats become seriously ill or dying and cannot
defend themselves, they try to hide away as best they can in order not
to be eaten more or less alive by their fellow rats when they are no
longer able to defend themselves. They tend to die out of sight in
obscure and relatively inaccessible places. Therefore, finds or reports of
sick rats that had come into the open, “could be counted on the fingers.”
Ashburton Thompson goes on to enlarge on his findings:
They do die in unusual places, and so regularly that we feel justified in
regarding the discovery of three or four carcases at a similar stage of
decomposition under floors, or in, or on the tops of cupboards, etc., dur-
ing known presence of an epizoötic as probable evidence of death from
plague. In ordinary, as is very well known, rats generally die out of sight
[…]. Even when poison has been laid discovery of several dead bodies in
such situations should arouse suspicion.66
This makes it clear why it is so important for Cohn to dismiss the find-
ings of Ashburton Thompson by falsely labelling him racist (see above),
that is, because they represent a grave threat to one of the pillars of his
theory, and why Ashburton Thompson’s observations are generally
passed over in silence by the other advocates of alternative theories of
plague.
The IPRC had ample occasion to observe that rats eat dead rats and
rat flesh. In their experimental godowns, the Commission observed
that dead or dying rats were eaten: “that of 12 rats proved to have died
64
See Hankin 1905: 64, 66.
65
The paper was written before the IPRC had commenced publication of its work.
66
Thompson 1906: 548, 550–1. Cf. Hirst 1953: 147–8.
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94 chapter three
of plague, the carcases of nine were more or less eaten,” that the “car-
cases of four inoculated and seven uninoculated were found to have
been eaten, several almost completely,” and “in godown No. 9, many of
the carcases were eaten.”67 They also carried out experiments by feeding
rats highly infected viscera of dead plague rats or “the whole carcases of
their plague-infected comrades” which were readily eaten.68
The IPRC made also thorough studies of rat-plague epizootics in
selected localities in Mumbai and the Punjab. Again their findings were
very similar to those reported by Ashburton Thompson. In 1908, Lamb,
the leader of the IPRC, summarized their findings:
In proportion to the severity of the epidemic the number of plague-rats
found was very small, notwithstanding the very thorough and extensive
search made. The experience both in Sion Koliwada [Koliwada is the
northerly part of the village Sion outside Mumbai] and in the Punjab vil-
lage of Dhund in this respect points to the danger of concluding that
plague-rats are absent from an infected locality unless a very thorough
search is carried out.69
A couple of years later, the IPRC noted the same observation during
their study of plague at Belgaum, a small town situated roughly 400 km
slightly southeast of Mumbai, where the role of rats was very much in
focus and a great program was launched to trap as many rats as possi-
ble. Some 39,460 were trapped, while in contrast
the number of dead rats obtained being very small indeed […].
Undoubtedly, too, rats may be dying in a house without the inhabitants
being aware of the fact. Rats not infrequently die in their burrows, or
under cover of boxes or sacks, or amongst rubbish or even in the roofs of
the houses.70
A sprinkling of dead plague rats was found in India and China. The
reason for this appears mainly to be that the black rat is an excellent
climber which finds Indian and Chinese housing well suited for mak-
ing their nests in the ceilings, and when seriously ill, the occasional rat
would fall down on the floor.71 Plague researchers working in an
Egyptian village noted that “Dead rats were picked up from the floor of
67
IPRC 1910a: 316–7, 318, 321, 324, 326, 331.
68
IPRC 1907a: 373–81; Lamb 1908: 33–6.
69
Lamb 1908: 18, cf. p. 24.
70
IPRC 1910c: 453–4, 456, 469.
71
Pollitzer 1954: 296.
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most of the rooms, having fallen presumably from the beams of the
ceilings.”72
Ashburton Thompson’s strong emphasis on the point that local expe-
rience in the habits and haunts of rats was essential in order to con-
duct successful surveys of rat-plague was a lesson carefully noted by
later plague researchers. In 1911, the Department of Public Health of
the Egyptian Government appointed a team of British and Egyptian
experts on plague research to study plague in Egypt. They made a very
thorough study of the rodent populations in selected areas. As soon as
plague broke out in a village, the team would move in, see to it that the
population was evacuated, and start their investigations. “We first
trapped the empty village but did not capture any rats, nor were any
dead one seen. This result was puzzling in view of the considerable
number of human plague cases.” However, they caught truly extraordi-
nary numbers of rat fleas inside the houses which indicated the recent
death of a considerable number of rats. The explanation was uncovered
when two of the houses were torn down and “the rat burrows were
exposed and traced. A regular system of nests and burrows existed at
the bottom of the walls with free communication at their junctions, an
arrangement that indicated continuity along the whole length of each
block of houses.”73
When plague broke out in Colombo, Sri Lanka, in 1914, W.M. Philip
and L.F Hirst were sent to investigate the epidemic. Keeping Ashburton
Thompson’s advice in mind, they organized an anti-plague staff and set
out to uncover the underlying plague epizootic. The description of the
difficulties they met with and how they resolved them on the basis of
modern knowledge, technical means and a scientific approach high-
lights the improbability that medieval populations in times of plague
could be expected to observe recurring significant rat mortality that
would lead to suspicion of a connection with the human plague epi-
demic. To begin with Philip and Hirst
found few dead rats in the open and conspicuous evidence of a rat epiz-
ootic was lacking. In order to reveal the presence of dead plague rats it
was usually found necessary to open up rat burrows and thoroughly dis-
sect the tiled roofs of houses or to force surviving infected rats out of
their burrows by pumping Clayton gas fumes into their holes. As the
72
Petrie, Todd, Skander et al., 1924: 129.
73
Petrie, Todd, Skander et al., 1924–5: 129–30.
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96 chapter three
anti-plague staff gained experience, the correlation between rat and

human plague in space and time became closer and closer.74
This presentation of the rat-related plague studies in Sri Lanka by Hirst
and Philip and the final citation are taken from Hirst’s standard work
on plague and can serve as yet more evidence of why Cohn felt that he
had to do away with this work, and hoped that by labelling him racist
(see above) he could make scholars turn away from his work. Twigg
gives such a skewed presentation of Hirst’s and Philip’s work in Colombo
that the central point is completely obscured.75
This subchapter on the behavioural pattern of dying rats and the
great difficulties of finding rats having died either from normal causes
or from plague unless a highly competent and very thorough search
has been implemented can be closed with the observations of Dutch
scholars in Java and their concluding remarks. J.J. van Loghem and
N.H. Swellengrebel met with the same curious absence of rat falls and
almost had to completely tear down native huts in order to reveal the
rat nests and the presence of dead rats. After great efforts, they learned,
among other things, that the house rats made their nests in the hollow
bamboo frames of the huts and also of the beds; rat nests were found in
the roofs, between the walls and in the internal wall covering made of
thin bamboo sprouts, and so on, and in these places they also found
rats dead from plague.76
The results of research on rats in plague epidemics in the first dec-
ades of the twentieth century are aptly summarized by the Dutch medi-
cal scholars C.D. de Langen and A. Lichtenstein:77
The most important argument adduced by the opponents of the “Rat-
Flea-Man” theory of the distribution of plague is that in various epidem-
ics no rat plague has been observed, or the epizootic has only developed
after the epidemic has started. A really critical examination of the data in
these cases shows in every instance that no sufficient search was made for
the preceding rat plague. In some cases the mere fact that among 100 rats
caught in traps no rat plague could be demonstrated was accepted as suf-
ficient proof that there was no rat plague present! How very difficult it is
74
Here I cite the succinct summary by Hirst 1953: 148, of the original text in Philip
and Hirst 1917: 542–5.
75
Twigg 1984: 112.
76
Van Loghem and Swellengrebel 1914: 467. See also the photographs in the
appendix.
77
De Langen and Lichtenstein 1936: 185–6.
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rats 97
to demonstrate even a very widespread rat epizootic has been shown in

Java where, in spite of the most diligent search, no rat plague could be
found, until van Loghem easily demonstrated the wide distribution of
the disease among the rats by splitting open the bamboos used in build-
ing portions of the native houses.
The “Rat-Flea-Man” theory as it has now become sharply defined in
Java, regards the rat plague as an epizootic disease conveyed by fleas […]
it follows that rat plague must always precede human plague; this has
almost always been capable of demonstration in Java after a careful
enough search has been made.
At the same time, Wu Lien-Teh pointed out:
Modern examples could be quoted where not only the population at large
but even the medical men believed rat plague to be absent and yet the
presence of an epizootic was demonstrated by a proper search.
And he goes on to underline what all the advocates of alternative theo-
ries of plague collectively have neglected to take into account: “In old
Europe many factors militated against such discoveries.”78
Against this background, the question must be asked: on what
grounds should people in the past be expected to have observed intense
rat mortality or at least substantial numbers of rat falls preceding the
outbreak of plague epidemics and running concurrently with the epi-
demics as they unfolded?
In the preceding subchapter, I showed that the assertions of the
advocates of alternative theories that the paucity or lack of historical
evidence of dead rats during historical plague epidemics proved that
the epidemics could not have been bubonic plague were methodologi-
cally flawed, and have the character of inference ex silentio. In this
subchapter, material has been presented that demonstates in the clear-
est possible way the invalidity of their inferences ex silentio: dead rats
were not seen during historic plague epidemics simply because it is
very difficult to find dead rats, not because they were not present.79
Finally, it must be permitted to ask how so many studies and com-
ments on this rat-related problem can have been overlooked by the
advocates of alternative theories if a proper study of the relevant works
on plague research published in leading journals and standard text-
books had been performed.
78
Wu Lien-Teh 1936a: 8–9.
79
Cf. Benedictow 2004: 192, and footnote 9.
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98 chapter three
Zoobiological and Zoogeographical Arguments on the Question of

Significant Presence of Black Rats in Medieval Europe
A central argument concerning the presence of the black rat in Europe

is based on the idea that its geographical distribution is determined by
the fact that the species originated in a warm region, Burma and India,80
the North African or Arabian parts of the western Mediterranean as
well as the eastern Mediterranean81 or more vaguely that it had an
“Oriental origin.”82 Twigg and Davis who are zoologists assert in abso-
lute terms that this origin means that black rats are tender and warmth-
needing animals and that the climate in the northerly parts of Europe
is too cold to be compatible with a significant and widespread presence
of this species; at the most there could have been a more or less spo-
radic incidence due to importation by ship from Mediterranean ports.83
Consequently, historical plague epidemics in these regions must be
some other epidemic disease than bubonic plague. This argument is
embraced by Scott and Duncan and Cohn, presumably because it helps
clear the way for their alternative cases.84 In this subchapter, I will
therefore address this question as a subject suitable for serious discus-
sion. Some priority will be given to Davis’s paper on the matter, since it
appears that this is the most influential work in this connection, and
also to Twigg’s discussion of this topic, as both are zoologists and oper-
ate in this field with some scholarly prestige.
Some of the arguments have considerable illustrative powers. Twigg
enthusiastically cites a remark by G.M. Thomson who, in a work on the
North-West Passage, asserts that the Black Death “struck Greenland
even more savagely than Europe.”85 Thomson is neither an historian
nor an archaeologist and has no competence on medieval history and
no competence on Nordic history, yet Thomson’s assertion permits
Twigg to conclude: “It is highly unlikely that Rattus rattus was present
there at that time and I can find no records of this species in Greenland
in modern times either.” By implication historical plague could not
have been bubonic plague. Also this argument is embraced by Scott
80
Pollitzer 1954: 282; Russell and Russell 1983: 102; Twigg 1984: 86.
81
Zinsser 1934/1985: 198; Davis 1986: 456.
82
Hirst 1953: 126.
83
Twigg 1984: 80, 86–7, 100–1; Davis 1986: 455–70.
84
Cohn 2002: 53; Scott and Duncan 2001: 261; Scott and Duncan 2004: 174–5.
85
Twigg 1984: 86–7.
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and Duncan who maintain repeatedly that the fact that the Black Death
ravaged Greenland and Iceland constitutes proof that it could not have
been rat-borne bubonic plague.86
In fact, Nordic scholars, both historians and archaeologists, have
taken substantial interest in what happened to Greenland’s Norse pop-
ulation and why it disappeared. This research has been thoroughly and
comprehensively summarized in English in a fine paper by J. Berglund.87
It is also succinctly summarized in English by the Finnish scholar
J. Vahtola: “In the late Middle Ages the entire Norse population [in
Greenland] disappeared. There is no evidence that epidemics of plague
or any other disease caused the desertion.” The main explanation of the
desertion is ecological: “Recent investigations have demonstrated con-
vincingly that the fertility of the soil was ultimately destroyed by cli-
matically caused erosion and overgrazing of pastures and meadows. In
the face of incipient starvation many of the people may have moved to
Iceland.”88 This is exactly what is stated on the matter in my monograph
on the Black Death.89 Twigg’s and Scott’s and Duncan’s assertions are
without foundation in relevant scholarly studies.
For the same reason, Scott and Duncan maintain repeatedly that the
Black Death raged in Iceland.90 On this point the Icelandic annals are
entirely clear: “This disease did not come to Iceland.”91 Scott and
Duncan state also that the Black Death crossed “the Baltic to Norway,”92
an impossible feat of geographical dissemination. As a matter of fact,
the Black Death did not even spread across the Baltic to Sweden (or
from Sweden across the Baltic).93
At the heart of Davis’s line of arguments is a series of interacting
methodological fallacies. He presents some selected information from
modern studies on the brown rat and the black rat and claims that,
although most of this information relates to the brown rat, “enough is
known of Rattus rattus [the black rat] to permit conclusions about [the
rat] populations at the time of the Black Death.”94 This is an obvious
86
Scott and Duncan 2001: 6, 81, 98, 108–9, 357. Scott and Duncan refer to the
uncritical and poor work of Kohn 1995.
87
See the fine summary by Berglund 1986: 113–34.
88
Vahtola 2003: 567–8, 576.
89
90
Scott and Duncan 2001: 6, 81, 98, 108–9, 357, 374, 376.
91
Islandske Annaler 1888: 276. Lawman’s Annal: “Þessi sott kom ecki aa Island.”
92
93
Benedictow 2004: 170–8; 196–7, 209–10.
94
Davis 1986: 459.
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100 chapter three
instance of fallacious methodology. Historical periodisation is not for-

tuitous, but reflects historians’ general view that historical processes
have changed societal structures so profoundly over time that they are
relating to qualitatively different social formations or societal struc-
tures. This means that a condition found in one historical period can
only provide the basis for a working hypothesis to the effect that it also
was the case in another historical period and functioned or interacted
in much the same way within different social structures. It is a fallacy
of methodology to make inferences across the boundaries of historical
periods without due consideration to historical and societal changes
and a clear argument as to why a specific factor should nonetheless be
able to operate the same way in the specific case under discussion.95
Methodologically, interperiod comparisons or approaches have the
character of analogies or parallels which can prove nothing but can
serve to construct working hypotheses, while proof requires evidence
in the form of empirical data relating to the historical social formation
under study. For this reason, observations on aspects of one social for-
mation generally cannot be projected into some other social formation,
they can only serve as a base for working hypotheses to the effect that
these specific parts of social reality have not changed with the struc-
tural societal transformations. If the case were otherwise, if one could
legitimately and freely project aspects of one social formation into
other social formations, one could legitimately show that medieval
society was identical or similar to Early Modern society or even mod-
ern society. Therefore, only evidence specific to the period under dis-
cussion can be used for evidentiary purposes with respect to any topic;
if there is no evidence, the historian has lost.
It should be obvious that the biotopes and ecological niches and
environments of rats have changed profoundly and fundamentally, and
that there is no profound similarity in these crucial respects that will
permit argument for historical similarity over these historical periods.
Here we may mention the dramatic zoological effects of the introduc-
tion of the brown rat in Europe in the eighteenth century on the living
conditions of the black rat. Because the brown rat was much stronger
and more aggressive, it drove the black rat out of its usual habitats and
caused its extinction in many countries and regions (see below). One
must also take into account the intensive and fundamental changes of
95
See for instance Benedictow 2004: 387–94; Benedictow 2006: 133–42.
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rats 101
human society with respect to types and distribution of settlement and

of building structures and of mentality and culture also in relation to
animals and insects, which in modern Western society are strongly
aligned against the presence of rats and insects in immediate human
proximity. These methodological and sociological remarks should suf-
fice to uncover the fallacious and untenable character of Davis’s
approach.
However, these are the premises that allow Davis to conclude as fol-
lows (the enumeration of his assertions is mine):
Application of this information to rat populations of the Middle Ages
produces the following scenario. [1] Rattus rattus may have persisted in
towns, especially grain ports, but the number of buildings with rats was
small and the number of rats was stationary. [2] The [rat: my insertion]
population in a particular town disappeared in few years but might again
become established as a result of new introductions. [3] These character-
istics held for northern France, Scandinavia, and the British Isles, but
[4] in the more southern Mediterranean region of France Rattus rattus
may have lived in small numbers in rural areas.96
All four assertions contained in this citation on the presence and role
of rats in medieval society are only speculative or hypothetical. They
could legitimately be working hypotheses that could be tested and
potentially corroborated through the gathering of evidence. However,
Davis has adduced no evidence, and thus, proved nothing. Conversion
of working hypotheses into assertions of fact and also inference across
the dividing lines of historical periods are fallacious.
Another typical instance of a methodologically flawed argument is
Davis’s absolute assertion that the black rat
lives in trees and roofs of houses […] they rarely if ever inhabit burrows,
tunnels in the ground, or aquatic habitats. Thus references to rodents liv-
ing in burrows or swamps exclude Rattus rattus.97
A number of citations and references has been presented above which
demonstrate the burrowing abilities and habits of the black rat in con-
nection with the difficulties of finding rats dead from plague.98 The
inherent anachronistic flaw in Davis’s assertion becomes immediately
apparent when these assertions are related to Pollitzer’s presentation
96
Davis 1986: 459–60.
97
Davis 1986: 456, 457.
98
Above: 91–7.
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102 chapter three
and discussion of rats, where it is stated that “in the absence of Norway
rats, R. rattus may live on the ground floors or even underground.” The
point is that in the presence of the bigger and stronger brown rat which
aggressively fight the black rat for territory, the black rat which is an
“excellent climber, prefers to shelter in the upper parts of buildings.”99
The same perspective is found in the IPRC’s remarks that
in contrast with Mus rattus [= Rattus rattus] in Bombay, the Punjab rat
burrows extensively […]. It is almost certain that the rat-burrows in the
Punjab villages are very extensive, ramifying beneath and opening up
communication between several contiguous houses.100
A Punjab village may be looked upon for our present purpose as being
honey-combed with rat burrows which ramify in all directions.101
Mus rattus, although typically a climbing rat [in Mumbai], is able to bur-
row, e.g., in beaten earth floors. We have frequently made this observa-
tion and in one instance (in Parel village [outside Mumbai]) have seen
exceptionally large and numerous holes and burrows in the earthen floor
of a store-roome for grain from which many Mus rattus had been
trapped.102
In Mumbai where the brown rat is usual, the black rat prefers to live in
the upper parts of buildings, in the Punjab they are typical burrowing
rodents, since the brown rat “is not found in the villages of this
Province.”103 The IPRC noted that black rats were burrowing exten-
sively in Belgaum (see above) both outside and inside houses where
there were no brown rats.104 Again it can be readily seen that Davis just
projects into the past the modern situation and the behavioural effects
on black rats of the intensely competitive presence of the stronger and
more aggressive brown rats, a constellation which did not exist in the
Middle Ages or for a long time thereafter. The question of the burrow-
ing of black rats will be discussed below in connection with the history
of black rats in the Nordic countries and finds of medieval skeletal
remains.
From an epidemiological perspective it is also important to note
Pollitzer’s point which serves to underline the erroneous character of
99
100
IPRC 1907j: 905.
101
Lamb 1908: 13.
102
IPRC 1907g: 746.
103
IPRC 1907a: 376.
104
IPRC 1910c: 456.
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Davis’ assertion, namely that “the available evidence shows that

X. cheopis has an affinity for rats living underground rather than for
those sheltering on higher levels of the houses.”105
Another important question relates to the issue of the density or
numbers of rats in relation to the density or numbers of people in an
area, because this relationship concerns the necessary conditions for
effective spread of bubonic plague epidemics. Twigg and Davis endeav-
our to play down the relative number of rats as much as possible in
order to undermine a necessary condition for efficient spread of
bubonic-plague epidemics.106 The central point which they faile to take
into account is that the presence of rats in modern cities and settle-
ments tends to be strongly affected by counter-measures by sanitary
authorities and extermination campaigns. When Davis studied the rat
population of Baltimore in 1947 he estimated their numbers at 200,000,
one rat per five inhabitants. However, three years earlier the number
had been estimated at 400,000 rats; the rat population in the meantime
had been greatly reduced by counter-measures. Thus, again their argu-
ments are based on the fallacy of anachronistically projecting the out-
come of modern studies into the Middle Ages. Pollitzer’s following
statement is a useful guideline to the question of relative numbers:
“There is reason to assume that in less well-sanitated cities, and in
smaller settlements in general, the number of rats equals or even
exceeds the number of people. This is presumably the rule on farms
(Tice).”107 The IPRC’s study of the rat infestation of Parel village dem-
onstrated beyond doubt that the numbers of black rats in the houses far
exceeded the number of human inhabitants.108 In Belgaum, the IPRC
trapped a number of rats higher than the human population without
exterminating the rat population, so the number of rats clearly exceeded
the number of inhabitants.109 I have noted with some interest that
the responsible municipal authority in Oslo (Norway) cautiously esti-
mates that today the number of rats equals the number of people,
despite their efforts at extermination.110 Generally, from the High
Middle Ages and through most of part of the Early Modern Period
105
106
Twigg 1984: 88–9.
107
108
IPRC 1907h: 844–54.
109
IPRC 1910c: 457.
110
Tollefsen 2005: 7.
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104 chapter three
about 85–95 per cent of European populations lived in the countryside

on holdings and tenancies of various sizes, each according to local cus-
toms with two or more buildings in which colonies of black rats would
like to settle: a dwelling house, barn, storehouse, stable, cowhouse, and
in addition a cottage to accommodate aging parents and not infre-
quently “undersettles” (sub-tenancies).111
In the opinion of Davis, it is an important argument that ports can
usefully be compared to islands and
in order to understand the establishment and persistence of Rattus rattus
over time we can follow some principles of island zoogeography. A port
can be assumed to have the characteristics of an island because, on the
land side, numerous barriers of habitat and frequent hazards prevent rats
regularly from spreading far from the wharves. A spread of up to a kilo-
metre or so can nevertheless occur.112
Davis asserts that commercial hubs like Venice, Florence, Genoa,
London, Bruges or Lübeck can from a zoogeographical perspective be
usefully compared to (more or less isolated) islands. In order to defend
this position, Davis resorts to assertions about ports that fly in the face
of the amassed knowledge regarding the functions of urban centres in
general and specifically also of medieval urban centres, from Max
Weber’s classic sociological study of pre-modern cities113 to R.S. Lopez’s
classic monograph The Commercial Revolution of the Middle Ages, 950–
1350, Pound’s great summary of medieval economic history, and all
serious work that has been published on the subject in the last genera-
tion. Urban centres do not function geographically as islands in any
significant respect but, on the contrary, as centres of communication
lines that radiate out from them and also meet in them. Along these
communication lines by land or sea or rivers a great variety of goods
are transported and people travel with them or with a great variety of
baggage and motives. Microbiological agents, insects and animals will
imperceptibly move with goods, people, luggage or clothing. The com-
prehensive commercial activities of ports and economic hubs were very
well suited for the distribution of rats at various distances through the
transportation of many types of goods, merchandise, and commodities
over land or sea or along rivers by various types of vehicles or vessels or
111
See, for instance, Astill 1988: 51–2.
112
Davis 1986: 457–8.
113
Weber 1966, Lopez 1976, Pounds 1974.
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even pack horses.114 One could consider the implications of the IPRC’s
observation: “We have seen rats dive, as it were, into bags containing
bran and disappear, so that the bags could be moved without any evi-
dence of the presence of the rats within. M. rattus [= Rattus rattus, the
black rat] from its habits is particularly liable to be transported in this
way […].”115
Davis’s central argument is based on the untenable notion that black
rats could spread over land only by individual locomotion, by moving
on their feet. According to ordinary scholarly methodological princi-
ples, Davis should be obliged to explain to his readers the empirical
grounds which permit him to state that in medieval urban centres
“A spread of up to a kilometre or so [by black rats] can nevertheless
occur.” It is the basic flaws of his theory that force him to found his
arguments on such absurd notions as ports as islands suitable for the
study of the functions of “the principles of island zoogeography.” In the
end, he has to admit that “Factual support for these applications of
island geography are regrettably meagre.”116 However, he proceeds
unaffected to go on arguing his theory as if this were not the case, which
allows him to conclude triumphantly that he has proven that there
could only have been an incidental presence of the black rat in the
northerly parts of Europe, the concept of proven here being released
from its strong evidentiary associations.
This line of argument is supplemented by further arbitrary asser-
tions to the effect that because “towns, the ships and the docks were
small, we can assume that the rate of extinction was high” and that
“persistence of populations of rats would have required frequent arriv-
als of ships from the Mediterranean, where rats were widely distrib-
uted.” In methodological parlance, the concept of “assumption” applies
when there is an evidentiary basis that constitutes sufficient ground
for making an inference in relation to some part of reality, and this
evidentiary basis is more demanding than in the case of other words
implying lower levels of tenability such as “plausible” or “possible” or
“hypothetical” or “speculative.” When the evidentiary basis is not pre-
sented, as in this case, the appropriate terms would be “speculate” or at
best “hypothecate.” According to the principles of methodology, each
114
Pollitzer 1954: 294; Pollitzer and Meyer 1961: 452; Shrewsbury 1971: 29.
115
IPRC 1908b: 255.
116
Davis 1986: 458.
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106 chapter three
of these assertions is a speculative working hypothesis that requires

corroborative evidence in order to cross the dividing line between
speculation or hypothesis and valid statement on reality at some level
of tenability, however slight. Eventually, this point also occurs to Davis
since he states that from “these principles we can construct a hypo-
thetical history of rats in Europe.” However, he immediately leaves the
methodological implication of this characteristic, concluding in terms
requiring a significant empirical basis: “The available evidence indi-
cates that Rattus rattus was rare and erratically dispersed both geo-
graphically and temporally at the time of the Black Death.”117 However,
no evidence to this effect has been presented.
This unsubstantiated history is based on the speculative view that
black rats could not uphold an autonomous widespread presence. Finds
of rat bones force a small admission to the effect that black rats may in
Roman times have been spread from the Mediterranean region by ship
transport to ports in Western Europe in a continuous process that
secured a small and continuous presence of the black rat in ports.
According to Davis, the decline in shipping with the break down of the
(Western) Roman Empire and the beginning of the Middle Ages meant
that ports became so small that “it resulted in the extinction of rats in
most cities of the north” and “the size of remaining ports were not ade-
quate to maintain large rat populations.” This is plainly serial specula-
tion that can provide premises for any hypothesis. It is also an expression
of ignorance: there was no direct shipping between Mediterranean
ports and Western Europe in Roman times and up to the end of the
thirteenth century, rats would have a local origin and a continuous
presence. It ignores also the widespread finds of rat bones from Roman
times far from ports in many parts of Europe (see below).
Davis goes on to argue that the “increase in shipping and the size of
ports in Columbian times released an avalanche of rats which has been
reduced only in recent decades.”118 Around 1500, the size of Europe’s
population was close to the late medieval minimum after the ravages of
the Black Death and subsequent plague epidemics. The intensity and
volume of international trade, the size and ramifications of banks, and
so on, were vastly greater around 1300 than around 1500, as were the
size of populations and volume of general economic activity. This is the
117
Davis 1986: 468.
118
Davis 1986: 458–9.
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rats 107
reason Lopez writes about the commercial revolution of the High

Middle Ages, and I write about the plague history of the Late Middle
Ages. If there was to have been an avalanche of imported rats into
northwestern Europe, the High Middle Ages up to 1350 would have
been the period of pre-eminence. Davis’s arguments are without basis
in the economic and demographic history of the Middle Ages.
This leads Davis to a peculiar conclusion: “Evidence for this chronol-
ogy is meagre, but it offers a plausible explanation of changes in rat
populations.”119 Since he has not presented any empirical evidence in
support of this chronology of rat history, and even characterizes it him-
self as a “hypothetical history of rats in Europe,” it is not “meagre,” it is
non-existent. Methodologically, this relates to the fact that the concept
of “plausible” relates to a level of tenability which requires sufficient
evidence to position it between the level of possible and the level of
likely. Davis appears unwilling to accept that what he really is doing is
constructing an explanatory model on entirely speculative and hypo-
thetical grounds. He also appears unable to accept the fact that a model
is an intellectual tool that proves nothing, but which in the hands of a
conscientious scholar can be useful for the collection, organization and
analysis of empirical material.
In addition, Davis’s knowledge of plague disease is unsatisfactory. It
is not true that “most cases during the Black Death were of pneumonic
plague” and that this “is now documented.”120 He refers for support to
Biraben 1975: 86, where the opposite is maintained, namely that there
could have been some episodes of primary pneumonic plague, but that
“everywhere else it appears in the bubonic form with secondary pneu-
monic or haemorraghic manifestations.” In the immediate continua-
tion of this statement, Biraben also makes it clear that these epidemics
of bubonic plague which dominate the scene “are arrested or dimin-
ished by the cold season,”121 Davis is aware that primary pneumonic
plague “occurs all year round,” he knows also that bubonic plague is “a
disease [typically present: my insertion] in late summer,”122 and he has
seen Biraben’s strong evidence to the effect that the Black Death was
119
Davis 1986: 459.
120
Davis 1986: 460–1. See Benedictow 2004: 27–31, 233–41. Davis does not differ-
entiate between primary and secondary pneumonic plague, but has apparently pri-
mary pneumonic plague in mind.
121
My translation from French.
122
Davis 1986: 460.
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108 chapter three
bubonic plague, which does not accord with his assertion on the pre-
dominance of primary pneumonic plague.
This puts in perspective Davis’s assertion that “fall and winter epi-
demics were surely not the result of the transmission by fleas from
rats.”123 In the accompanying footnote he refers to (1) Gras 1939: 305,
(2) Simpson 1905: 159, (3) Gasquet 1893: 43, and (4) The Indian Plague
Research Commission 1907: 324–476. I will comment on these refer-
ences below in paragraphs marked by corresponding number. First,
it must be pointed out that he calls the IPRC the “Indian Advisory
Commission,” which reflects his confusion of the scientists who made
the research and wrote the papers or reports with “The Advisory
Committee” which was responsible for controlling the quality of the
papers and arranging for their publication. Lamb makes painstakingly
clear the difference between the Advisory Committee and the Research
Commission in his summary of their work up to May 1907: “It was
arranged that reports of the work done by the Commission should be
published by the Advisory Committee in the Journal of Hygiene.”124
Since it can be shown that Davis has not read the papers contained in
these pages (see below, paragraph 4), this confusion may be taken to be
a consequence of Davis’s hasty look at the title on the opening page of
this sequence of papers in the Journal and its last page in order to pro-
duce a seemingly normal reference. This is not, as will be shown, the
only case.
(1) Gras’s paper is a study on the Black Death in the small Burgundian
town of Givry on the basis of the only surviving complete parish regis-
ter in Europe from the time of the epidemic. However, according to
this study, the first victim of the Black Death died 17 July, the epidemic
slowed down sharply in October and petered out in the first half of
November, and in the second half of November three final cases are
registered on the 19th.125 This is not a case of a “fall and winter” epi-
demic, but instead in conforms to Biraben’s general account of the sea-
sonality of the Black Death in France. Clearly, this reference is also
fictitious.
One should note that rat fleas are typical fur fleas (and not nest
fleas),126 which means that they spend much of their adult lives in the
123
Davis 1986: 467.
124
Lamb 1908: ii–iv.
125
Gras 1939: 305–6.
126
IPRC 1908b: 245–6, 258; Liston 1924: 997; Pollitzer 1953: 321; Pollitzer and
Meyer 1961: 461; Busvine 1976: 37.
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rats 109
fur of their hosts, enjoying there a relatively warm microclimate even

in chilly or cold weather and ample feeding opportunities. This explains
why plague epidemics can produce cases in chilly or cold autumnal
weather, although at a rapidly diminishing rate, until the depletion of
the number of rat fleas and the reduction of septicaemia in plague-
infected rats caused by cold weather stop the epidemic or it manifests
itself by only occasional cases. The idea that plague epidemics must
stop abruptly with the advent of chilly or cold weather is untenable.127
(2) Simpson 1905: 159, does not relate to the Black Death or the
subsequent late medieval or early modern plague epidemics. This page
is the first in a chapter on “Variation in Virulence of Plague Epidemics”
which has nothing to do with Davis’s subject. Consequently, this is also
a fictitious reference. Evidently, Davis has again arbitrarily picked some
pages in order to produce a false impression of a normal reference in a
footnote.
(3) Gasquet 1893: 43, relates to the Black Death in Avignon. The
course of this epidemic cannot be followed closely, but the epidemic
continued during the winter months. It is generally agreed, especially
on the basis of the clinical descriptions of Guy de Chauliac, the pope’s
personal physician, that this phase of the epidemic was predominantly
primary pneumonic plague or rather a mixed epidemic.128 Since this is
a unique case, as no other case of an epidemic of primary pneumonic
plague or more likely a mixed epidemic is known, it does not at all sup-
port Davis’s assertion that the Black Death was at least predominantly
primary pneumonic plague. Much has been written on the Black Death
in Avignon after 1893.
(4) Davis’s reference to IPRC 1907: 324–476, comprises not one but
ten studies which all have in common that they do not relate to the
subject in question and do not, consequently, contain support for his
assertion which therefore is arbitrary.
On the same page, Davis asserts that “Human plague can occur
without involvement of Rattus. For example in India only eight of forty
local epidemics had obvious mortality of Rattus.” In the accompanying
footnote, Davis provides three references to scholarly works in support
of his assertion, all of which need close and sceptical scrutiny: (1) Hirst
1953: 121; (2) Martin 1913: 63; and (3) Hirsch 1883, Vol.1: 494–544.
I now comment on each of these references:
127
See below: 396–8.
128
Benedictow 2004: 97–8, 236–8.
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110 chapter three
(1) Hirst 1953, 121: Hirst’s monograph is devoted to the study of the
history of human combat of bubonic plague. He does this in a broad
and in-depth historical perspective of the development of medicine
and epidemiology and concludes with a strong case for the rat-flea the-
ory of bubonic plague. Every scholar who has read this outstanding
standard work on bubonic plague will immediately recognize that
Davis’s reference is fictitious. Far from providing support for Davis’s
assertion, Hirst argues strongly against it. On page 121, which is sited
by Davis, starts Chapter VI on the role of “Rats and Plague”; the
subchapter starting on this page relates to “Rats and the First Two
Pandemics.” Thus, this chapter does not relate to the third pandemic
and developments in India in this period. On page 121, Hirst begins by
emphasizing very strongly the early resistance among scholars to the
rat-based rat-flea theory of bubonic plague.
(2) It is on the following page, Hirst 1953: 122, that Davis had the
luck to find his next reference, namely Martin 1913: 63. Here Hirst
states that “the paucity of records directly and clearly associating human
plague with mortality among rats in medieval literature has led some
authorities, including Sir Charles Martin and Professor Jorge, to postu-
late the human flea as the chief transmitter of the bubonic element of
the Black Death.” This view asserts the importance of interhuman
spread of plague which begins from rat plague but then continues inde-
pendently of rats by cross-infection, a view with which Hirst entirely
disagrees and against which he argues intensively over many pages.
Davis has, thus, made a misleading reference to Hirst’s monograph in
support of his own view. He makes no reference to Hirst’s comprehen-
sive discussion leading to his conclusion on the fundamental role of
rats and rat fleas in the epidemiology of bubonic plague among human
beings, including in India. A huge number of studies have appeared
after Martin published his study in 1913, among them quite a number
relating to the possible role of the human flea, and they affect the ten-
ability of Martin’s opinion. Many of these studies are used and referred
to by Hirst. Certainly Hirst disagrees, this is at the heart of his mono-
graph: the role of fleas is discussed in the following chapter, the ques-
tion of interhuman spread in Chapter IX, and the spatio-temporal
patterns of plague epidemics in Part III, Chapters X-XII. In fact, even
the most ardent supporters of the human-flea theory, namely G. Blanc
and M. Baltazard, do not maintain that the Black Death or subsequent
plague epidemics were in the main spread by the human flea, only that
it could be of importance in the great cities of the Middle Ages, which
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rats 111
means that at most 2 per cent of Europe’s population would be at risk,

and the hypothesis of little consequence even if it were tenable.129 The
main reason that the human-flea theory is untenable is that plague sep-
sis in human beings is generally far too weak to infect fleas sufficiently
for development of blockage other than in sporadic cases.130
(3) Davis’s third and last reference in support of his view on this
point raises immediate scepticism, namely that to August Hirsch’s two-
volume Handbook of Geographical and Historical Pathology of 1883,
which is an English translation of the two-volume German edition
of 1860–4. This work is surely much too old to contain scientifically
tenable information on the matter. I have taken a look at the origi-
nal German edition and also the second edition of 1881–6 (three vol-
umes) which are the versions owned by the University Library of Oslo.
In the first edition, bubonic plague is presented in Volume 1, in a chap-
ter of twenty-three pages, which fits very poorly with the fifty pages to
which Davis refers. This chapter does not contain anything to the effect
that involvement of rats was observed in only eight of forty plague epi-
demics in India. Since the presentation of plague in the original first
edition starts on page 192, it may seem quite impossible that this chap-
ter in the English translation should start on page 494, at which point
the original German edition is in the middle of a 312-page discussion
of chronic diseases. One could also take into account that the proper-
ties of the English language make translations from German shorter,
not longer.131 Hirsch’s work is, of course, unscientific, based on the the-
ory of miasma in both editions, and it contains no reference to bubonic
plague later than 1850.132 This makes it clear that the author could not
consider any theory of bubonic plague involving bacteria, rats and rat
fleas as agents, carriers and transmitters of bubonic plague among
human beings. Hirsch has of course not had the opportunity to learn
from and take into account the modern scientific studies performed by
Ashburton Thompson, the IPRC or van Loghem and Swellengrebel
who discuss the behavioural patterns of rats and revealed that epizoot-
ics among rats were, in fact, at the basis of epidemics of bubonic plague.
129
Benedictow 1993/1996: 228–37. Cf. Benedictow 2004: 17, fn. 9.
130
Benedictow 1993/1996: 243–63.
131
In the much expanded second edition, the chapter on bubonic plague runs from
page 349 to page 384.
132
Hirsch 1860: 211. The chapter on bubonic plague in the second edition of 1881
contains a few later references to plague epidemics, but not in India.
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112 chapter three
Davis’s reference to Hirsch is fictitious; Hirsch’s book cannot be the

source of his assertion that only eight of forty plague epidemics in India
exhibited evidence of involvement by rats.
The real basis for Davis’s assertion is taken from Hankin’s paper of
1905. Here Hankin summarises a report by Planck relating to the
Garhwali area where plague tends to be “endemic” in the Annual Report
of the Sanitary Commissioner for the North-West Provinces and Oudh
for the year 1876.133 While Davis presents his assertion as if it were
based on scientifically tenable research, for instance Hirst’s monograph,
it can now be seen that the basis is another proto-scientific report writ-
ten many years before the establishment of bacteriology and therefore
also based on the miasmatic theory of epidemic disease and without
notions of any role for rats or insects. On the basis of relevant scholarly
studies, the question of why rat falls are such rare sights during plague
epidemics has been quite extensively discussed above. This makes it
clear that Davis’s assertion could not be based on valid evidence.
Importantly, Hankin uses the term “endemic,” which means sporadic
cases, so that in this context the term “outbreak” does not refer to epi-
demic plague and a large number cases. This means that the role of rats
would not be obvious because of the sporadic and endemic incidence
of the plague cases, in addition to the other factors cited above. The
report Davis refers to is not relevant for the understanding of epidemic
plague.
Davis asserts in seriousness that the human flea might have been
involved in the dissemination of plague, because they “can transmit the
bacillus that appears in saliva and human feces.”134 Human fleas like
other types of fleas are ectoparasites, bloodsucking insects, and do not
ingest human saliva both because they do not have access to it, and
because it would not be useful as nourishment or as a necessary basis
for the production of eggs which unconditionally requires blood.
Certainly, human fleas are not dung insects and will not touch human
faeces with their proboscises.
Davis asserts also that “Buboes can occur in cases of pneumonic
transmission and cannot be construed as proof of transmission by fleas
that infest either rats or humans.”135 In support of this statement, he
133
Hankin 1905: 49–50, 66.
134
Davis 1986: 461.
135
Davis 1986: 461.
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rats 113
refers to the following standard works on plague, namely Wu Lien-Teh

1936b: 409, Hirst 1953: 29, Pollitzer and Li 1943: 161/212–6136 none of
which works contains anything that supports his assertion, neither on
the indicated pages nor elsewhere. They are fictitious references.137 Wu
Lien-Teh’s standard work on primary pneumonic plague makes it clear
that the pneumonic mode of infection does not give rise to buboes.138
Davis goes on to present other misleading statements on plague.
He asserts, for instance, that the Black Death “travelled across or
around the Alps in the winter.”139 This is not correct, the Black Death’s
advance into the Alpine area stopped with the advent of cold autumn
weather which extinguished its epidemic manifestations, and it did not
re-emerge until the advent of spring temperatures when it started pen-
etrating into Southern Germany. Its spread in this region was also tem-
perature-dependent, requiring temperatures of the warmer seasons,
which can be easily explained by a rat-based and flea-transmitted
disease.140
Davis asserts also that in “Europe the spread of plague was rapid,” its
“speed and intensity was remarkable” and incompatible with spread rates
characteristic of contiguous spread between rat colonies. His empirical
examples of rapid spread of the disease are that it travelled to:
(1) Paris in six months, and to
(2) southwestern England by December; it spread to
(3) northern Norway (Bergen and Trondheim) in a year;
(4) it permeated all of England within months.141
The enumeration is mine, and my comments below are marked by cor-
responding numbers. Davis does not mention the point in time of the
start of epidemic spread from the chosen point of origin and the time
of its arrival at the chosen destinations. Neither does he clarify his con-
cepts of speed or rapidity by providing his readers with his criteria and
explaining why he considers these characterizations suitable. As will be
136
The discrepancy in the page numbers is due to my use of the version published in
Chinese Medical Journal 1943: 212–6, while Davis refers to a somewhat shorter version
published at the same time in Journal of Infectious Diseases 1943: 160–2.
137
Neither does Wu Lien-Teh mention such cases in his monograph on pneumonic
plague. Wu Lien-Teh 1926: 241–73.
138
Wu Lien-Teh 1926: 184–7.
139
Davis 1986: 460.
140
141
Davis 1986: 460–1.
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114 chapter three
seen, they are not only arbitrary in form but also erroneous and con-
fused in fact.
(1) The first outbreak in France was noted in Marseilles 1 November
1347, and the outbreak in Paris was noted at the end of August, which
means that ten months passed between the arrival of the Black Death
in France and its arrival in Paris. However, the part of the Black Death
that spread northwards from the original epicentre at Marseilles killed
its first victim in Givry in Burgundy on 17 July (according to the parish
register), which means that in mid-July the epidemic was more than
300 km from Paris as the crow flies, and much further by ground trans-
port. It also means that by the end of August it would have moved only
about 60–70 km further on its way northwards and still be several hun-
dred km away along the main roads to Paris.142 The crucial point that
Davis has missed is that the Black Death was shipped out of Bordeaux
to Rouen in Normandy in time to cause a recognized outbreak there in
June and could cover the much shorter distance thence to Paris in time
for an outbreak at the end of August, a spread rate that would quite
likely have been hastened by ship transportation up the R. Seine.143 The
basic problem here is that Davis does not recognize the importance of
metastatic leaps which will be comprehensively discussed below in the
next main chapter.
(2) Davis’s assertion that it is an example of remarkable speed of
spread that the Black Death could spread from Melcombe Regis
(Weymouth in southern England), where it broke out shortly before 24
June 1348, to southwestern England by December is intriguing, since
the Black Death started in southwestern England. It has long been
known that by the beginning of August most of the tenants of Frome
Braunch in Somerset had died and that peasants had died on other
manors in the area. It has also been long known that the Black Death
broke out in Bristol on 15 August, shortly afterwards in Gloucester
(and that it had broken out in coastal towns of the Pale in Ireland by
early August).144 The reason Davis again is so out of line with historical
plague research and reality here is that he does not recognize the cru-
cial importance of metastatic leaps in plague epidemiology and he has
poor knowledge of the relevant historical studies.
142
For spread rates in this part of France, see Benedictow 2004: 106, 230.
143
Benedictow 2004: 72–3, 96–108.
144
Benedictow 2004: 126–8, 130–1, 143–4.
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(3) As a Norwegian scholar who has specialized on plague history

and who has written his doctoral thesis on the late medieval plague
epidemics in the Nordic countries and a complete history of plague
epidemics in Norway (1348–1654),145 I do not understand what Davis
means when he states that the Black Death spread to “northern Norway
(Bergen and Trondheim) in a year” and one should take into account
that Norway is a very long country, over 2000 km long. Bergen is situ-
ated on the western coast of southern Norway and is only slightly more
northerly than Oslo, while Trondheim (Nidaros at the time) is situated
in central Norway. In short, these two cities are not situated in north-
ern Norway, literally far from it. There are no sources on the history of
the Black Death in northern Norway or even north of Trondheim/
Nidaros; all medieval Norwegian sources have been published and I
believe that I have identified every source that could have a bearing on
the history of the Black Death in Norway. The history of the Black
Death in central Norway north of Trondheim and in northern Norway
is unknown and may remain so, although the new scholarly discipline
of paleomicrobiology holds out promise of microbiological identifica-
tion of Yersinia pestis in archaeologically datable plague graves.146
Obviously, this part of Davis’s statement reflects great historical
and geographical confusion or disorientation, and what Davis has in
mind may therefore just be confused and disoriented. The only possi-
ble realistic interpretation I can make is that the Black Death spread to
Bergen and Trondheim in a year, taking into account these cities’ cor-
rect geographical position. In this case, the facts on the ground are that
the Black Death was introduced to Bergen directly from England, prob-
ably by a ship transporting grain from King’s Lynn; the disease broke
out in Bergen some time in the second half of August 1349, and was
transported by ship thence to Trondheim where the outbreak appears
to have been in full development at the end of September. At the time,
the usual duration of a voyage from Bergen to Trondheim (or vice
versa) was a fortnight.147 Obviously, these developments cannot sup-
port an argument that the Black Death spread so rapidly that it could
not have been bubonic plague. There is nothing in the pattern of spread
which is at variance with the normal assumptions of the spread rates of
145
For the history of the Black Death in Norway see Benedictow 1993/1996: 73–102;
Benedictow 2002: 46–96; Benedictow 2004: 146–58; Benedictow 2006: 83–163.
146
See below: chapter 11: 249–58.
147
Benedictow 2002: 67–80; Benedictow 2004: 102, fn. 20.
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116 chapter three
bubonic plague if the erroneous assertion that bubonic plague spreads

only between contiguous rat colonies is discarded and we take into
account metastatic spread over long(ish) distances by ship and by land
and over short and intermediate distances by the agency of human
beings transporting rat fleas in clothing, luggage, or goods (see below).
The average daily spread rate along the main roads was about
1.25–1.5 km.148
(4) It would have been a proof of remarkable speed of spread if it
were true that the Black Death “permeated all of England within
months,” actually it would have been a remarkable feat for any conta-
gious disease whatever its mechanisms of dissemination and transmis-
sion, especially under medieval conditions of communication and
transportation. However, this assertion is without basis in research.
The Black Death broke out in Melcombe Regis shortly before 24 June
1348 and petered out in northern England in the late autumn of
1349.149
The Significance of Evolutionary Theory and Adaptation by Selection
Despite the agreement among advocates of alternative theories of

plague that black rats are too warmth-needing to establish more than a
sparse and transient presence in the northerly parts of Europe, it has
been easy to demonstrate that this view has been argued in ways that
makes it untenable on source-critical and methodological grounds.
The lack or paucity of references to dead rats in contemporary accounts
of plague epidemics does not support the assertion that there were no
dead rats; instead this inference is a fallacy of methodology. This makes
it clear that the argument that black rats are too warmth-needing to
have a significant presence in the northerly parts of Europe has a prin-
cipally explanatory character. This explanatory function can only be
relevant and activated when it has been empirically proved that rats
were, in fact, absent or few and far between in these parts of Europe
and such an observation needs explanation. Consequently, it is also a
fallacy of methodology to use this explanatory potential as factual evi-
dence to prove the absence or approximate absence of rats, as all these
advocates of alternative theories do. Instead, the methodological status
148
Benedictow 2002: 35–40, 319–20; Benedictow 2004: 151–3, 157–8; Benedictow
2006: 91–5, 107–8, 113.
149
Benedictow 2004: 126–31, 138–42.
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of this notion is that of a working hypothesis that must be corroborated

by evidence in order to assume the character of valid assertion with
some level of tenability.
It has also become clear that this argument is methodologically
problematic in yet another respect: the plague epidemics of the past
could in principle provide the basis for a hypothesis that they repre-
sent a reflection of a broad presence of black rats and, consequently,
that the epidemics were bubonic plague. These two legitimate hypoth-
eses are diametrical opposites, a fact which demonstrates that up to
this point in the discussion nothing has been precluded: it is univer-
sally agreed that there must have been at least a tiny sprinkling of rats,
not necessarily enough to generate epidemics of bubonic plague.
The crucial question is how these two hypotheses can be empirically
tested.
Twigg and Davis and other advocates of alternative theories assert
that in the Middle Ages there could only have been autonomous or
self-maintaining small rat colonies in Mediterranean ports, and possi-
bly also in some rural districts. In the ports of northwestern Europe
there were no rats or only a tiny and transient population of rats which
could not reproductively maintain itself and establish itself there per-
manently, and their presence was dependent on a trickle of new rats by
ship from Mediterranean ports. As pointed out above, regular direct
voyages between Mediterranean ports and northwestern Europe did
not begin until quite late in the thirteenth century. On logical grounds
alone there could not have been any rats in these parts of Europe before
that time if the assumptions of the advocates of alternative theories
were tenable. Instead, the implication is that there was a continuous
presence of rats. It has been shown above that negative assertions in
this respect are not empirically based but are speculative notions or
working hypotheses awaiting corroboration. In this connection,
another methodological point should now be mentioned, namely that
the methodological requirements for proving that some phenomenon
did not exist or taken place tend to be rather more demanding than for
adducing positive proof of a phenomenon or event.
The argument asserted by advocates of alternative theories that since
the black rat originated in a warm region means this species is too
warmth-needing to have a significant and continuous self-maintaining
presence in the northerly parts of Europe is based on a very narrow
view of the question: it neglects to consider the possible significance of
evolutionary theory and the process of adaptation and development of
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118 chapter three
species by natural selection. In the words of Pollitzer, rats are “extremely

fertile.” They reach sexual maturity long before they have completed
their growth, when they are about three months old. The females have
a sexual season extending for about nine months of the year, during
which they are “in heat” at intervals of about ten days, the period of
gestation is about twenty days, parturition tends to be immediately fol-
lowed by “heat” so that a female can be impregnated a few hours after
the birth of a litter. This means that there are many litters during a year
and the number of young per litter is, on average, 5.4–6.150 The mortal-
ity rate of sucklings is quite high, but this also means that the forces of
evolutionary selection are intensely at work, making for relatively rapid
adaptation to changing circumstances.151 The view that a species with
such enormous fertility and brief generational cycle as the black rat
should not be able to adapt to various biotypes, ecological niches, and
climates, is obviously untenable. Clearly the advocates of alternative
theories accepted this hypothesis without careful consideration simply
because it agreed with their theories.
The heart of the matter can easily be put in perspective. The Vikings
brought horses to the Shetlands and to Iceland when they began to set-
tle there at the end of the eighth century and in the 860s ad respec-
tively.152 Within a few hundred years, these horses developed into the
Shetland pony and the Iceland pony characterized by considerably
reduced size, a rough coat, and a long mane and tail as evolutionary
adaptations to the new environments. Thus, new, smaller and hardier
breeds of horses had come into being in these islands as early as the
High Middle Ages. When horses with only a tiny fraction of the fertil-
ity of rats and much longer generational cycles can adapt so readily to
new and difficult climatic and ecological circumstances, the complete
rejection by all advocates of alternative theories of plague of the possi-
bility that rats could have any such adaptability becomes the more
remarkable. Can it really be true that rats arriving in the northerly parts
of Europe would not develop by the process of evolutionary selection
into a hardier breed with size and coat adapted to the climate? Does not
such a surprising assertion demand a specific and empirically based
150
IPRC found an average of six foetuses in 975 pregnant rats in the Punjab, IPRC
1907j: 907, and 5.4 in 4841 pregnant rats in Belgaum in Bombay Presidency. IPRC
1910c: 457. See also Liston 1924: 998.
151
Pollitzer 1954: 290–1. Cf. IPRC 1907 g: 750.
152
Lamb 1995: 173–4; Sawyer 2003: 106, 112.
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defense? Do not the bare assertions that this is excluded or improbable

in the case of rats and the complete absence of empirical arguments to
this effect represent a fallacy of methodology? Would it not be logical
to consider adaptation by degrees, as black rats were transported north-
wards in Europe over the centuries, which would introduce a long-term
evolutionary perspective?
M. McCormick emphasizes that to assume that “only human sup-
port can sustain rat populations outside a Mediterranean ecology is to
underestimate rats’ adaptability.” He underlines this point by referring
to the fact that burrowing black rats are found thriving in subantarctic
conditions on Macquarie Island, latitude 54.30° S, longtitude 159° E,
not far from Antarctica. Black rats are also living in the chilly and windy
north Atlantic climate of the Shiant Islands in the Hebrides (Scotland).
Interestingly, the zoologists who studied these black rats in the Shiant
Islands, in stark contrast to Davis and Twigg, state firmly and uncondi-
tionally that “Rattus rattus was once widespread throughout the UK.”153
The black rat was also present until recently on Lundy Island off the
northwestern coast of Devon,154 having survived from the Middle Ages
in the absence of the brown rat.
Size is important for the survival or improvement of the competitive
situation of rats (as for other animals). According to the same evolu-
tionary reasoning, McCormick emphasizes that “the size of modern
black rats might be a misleading criterion, since substantially larger
ones are documented in medieval Corsica.”155 This is also the case with
finds of medieval rat bones both in England, Norway and Sweden
(see below).
Correspondingly fleas which have much higher fertility and shorter
generational cycles than rats, would readily adapt by selection—fleas
might, in the words of Bacot, “adjust itself to the varying conditions of
climate experienced in its geographical distribution.”156 This is also
underlined by Pollitzer:
As shown by its wide geographical distribution, X. cheopis is able to adapt
itself to a considerable range of climatic conditions. It is, as have been
153
McCormick 1998: 22–3; Key, Fielding, Goulding et al. 1998: 228–33. Under ordi-
nary circumstances, I would have tended to think that these studies would have been
of interest to Icelandic scholars.
154
James 2001: 12, and pers. comm. These rats have subsequently been
exterminated.
155
McCormick 2003: 3.
156
Bacot 1914: 449–50.
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120 chapter three
previously noted, the common rat-flea in Manchuria and is also the

prevalent species in the tropical section of Brazil.157
Another error at the heart of the arguments of Davis and Twigg is that
they project anachronistically into the Middle Ages the modern situa-
tion of black rats. In modern Western society, black rats arriving in the
northerly parts of Europe or North America by modern means of
transportation directly from warm countries are not only poorly
adapted to the new environments; further, their situation with respect
to having the opportunity of going through a process of evolutionary
adaptation is very different from what it was in historical European
societies, for three important reasons:
(1) they are mercilessly fought by the larger and more aggressive brown
rat which did not arrive in Europe before the eighteenth century;
(2) modern buildings and settlement structures are poorly suited for
the establishment of colonies of house rats;
(3) modern man has a very hostile attitude towards rats in their
habitations.
These three factors cause too high mortality rates among these rats to
allow adaptation by selection before they are exterminated. In these
circumstances, their presence will be dependent on fresh arrivals by
ship, according to the model constructed by Davis and Twigg, but
applied anachronistically by them to the Middle Ages. Rats have a rich
and complex history which is structured according to a number of evo-
lutionary developments and a plethora of social, economic and cultural
factors in the human societies on which they depend. To project the
situation of black rats in modern Western society back into the Middle
Ages is obviously fallacious.
The inherent dangers in neglecting to address the theory of evolu-
tion by natural selection for a species can also be demonstrated in rela-
tion to rats in several ways with profound theoretical and empirical
implications. It has been shown, for instance, that black rats in the
northerly parts of Europe could have had several different origins.
Since both Twigg and Davis refer to Hirst’s monograph of 1953, it may
be instructive to cite his statement that “the fossil remains of a very
similar species [to black rats: my insertion] have been found near
157
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Geneva, in Lombardy, Bohemia, and Crete in Pleistocene strata, and

numerous bones among the pile dwellings of Mecklenburg.”158 Thus,
several finds of fossils of animals very similar to the black rat have been
made from a pre-historical period starting more than a million years
ago and stretching to about 10,000 years ago, covering several very cold
periods or ice ages. This suggests that the black rat or rather a closely
related species may have been present continuously in Europe, retreat-
ing with expanding glaciers and following in the wake of their with-
drawal much like reindeer, bears, wolves and many smaller mammals.
This notion is supported also by the fact that numerous bones of this
rat or a similar rat have been found in excavations of human settle-
ments in northeastern Germany from about 4000 to 2500 years ago.
This can be taken to indicate the continuity of a species of rat very or at
least quite similar to the black rat which was well adapted to life in
northerly climatic zones. It also suggests that this rat rapidly found a
new and attractive environment or ecosystem with the advent of human
beings and their housing, settlements and economic activities, espe-
cially farming and animal husbandry with their corresponding prod-
ucts and outbuildings. As pointed out by Hirst, this indicates that “rats
were associated with man since his first cultural beginnings, since the
time when he first began to store large quantities of cereals in grana-
ries.” Since this provides evidence of a species of rat which is quite
closely related to but not identical with the black rat, it may usefully be
taken as evidence of the black rat’s adaptability by evolutionary selec-
tion to northerly climates and environments, and evidence that black
rats have adapted to northerly climate at least once, and quite likely
twice in the past. The material is too small to constitute proof of the
continuous presence of this species of rat from the Pleistocene or the
Bronze Age to the Middle Ages, or of its early and continuous associa-
tion with man. However, this evidence may serve as the basis for a well-
founded working hypothesis calling for further investigation.
Davis and Twigg would have been right in their view that the black
rat and its accompanying fleas would quite likely not have survived in
the northerly parts of Europe if specimens were picked up in India and
dropped there by parachute. However, if a long time perspective and
conditions for adaptation are introduced in an evolutionary model
which lets rats and their accompanying fleas start from southern
158
Hirst 1953: 126. Davis 1986, refers erroneously to page 121.
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122 chapter three
Europe and gradually spread northwards over centuries, both black

rats and their fleas would easily produce variants or biovars adapted to
the new conditions. It is therefore a fallacy of methodology and evolu-
tionary theory to assume, without empirical evidence, that black rats of
modern India and black rats in the northerly parts of Europe in the
Middle Ages or Early Modern Period were biologically identical in
the sense of having the same biological adaptation to environments,
biotopes and climates. This is a valid argument also for a comparison of
black rats in southern Europe and northern Europe at the time. This
perspective will now be tested against the sources and material
evidence.
The presence of rats in Europe at the time of the Black Death is the
focus here. In consideration of the large time spans in question, we
must take into account the possibility that there may have been another
later independent introduction of the black rat, representing a second
or third introduction, and another subsequent evolutionary process of
adaptation. If it were correct that it was too cold in the northerly parts
of Europe to allow a broad presence of black rats and that nonetheless
the same disease ravaged this part of Europe as southern Europe, this
would constitute independent and sufficient proof that the Black Death
must have been some disease other than bubonic plague. Consequently,
evidence on the presence of rats in Europe, especially the northerly
parts of Europe in the preceding centuries, would be of pivotal
importance.
Rat Bones: Material Evidence of the Presence of Rats in the Middle Ages
In Europe, rat bones older than ca. 300 years must be remains of the
black rat. Twigg argues that it is reasonable to dismiss the significance
even of archaeological finds of rat bones in medieval layers on the
grounds that the “Black rat in temperate latitudes today lives only in
the warmer parts of towns and it is likely that it has always done so” and
adds that “Rattus rattus is essentially a sedentary animal, therefore in
temperate climates its occurrence in towns where it does not leave the
warmth of buildings is a fact of great significance in the aetiology of
bubonic plague and one we should remember when viewing past epi-
demics of that disease.”159 As shown above, this type of argument is
159
Twigg 1984: 80, 88.
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fallacious. It represents an attempt to make an argument which is

at variance with the elementary methodological principle that all
scientific and scholarly arguments must in principle be open to
falsification.
Twigg also attempts to undermine the significance of finds of rat
bones in layers of medieval remains on the basis of two other premises,
namely that (1) the brown rat is known for its prowess in burrowing,
and (2) the bones of the black rat and the brown rat are quite similar
and their remains are therefore often difficult to separate. For this rea-
son, he holds that finds of rat bones in archaeological excavations of
medieval sites do not constitute evidence of the medieval presence of
the black rat, but could reflect the burrowing capacity of the brown
rat.160 However, Twigg does not take into account any limit to the depth
to which brown rats were apt to burrow. It is therefore important to
emphasize that brown rats’ “burrows for shelter and nesting rarely
exceed 18 inches (approximately 45 cm in depth),” and that they will
only dig deeper in order to “gain access to food-supplies.”161 Since there
is not much food to be found in medieval strata even for rats, burrows
of the brown rat will normally be significantly shallower than 45 cm,
and will, consequently, often or normally not reach medieval layers
that will tend to be deeper, especially in urban and village environ-
ments where deposits from daily life tend to increase the ground level.
Another point is that rat burrows tend to be archaeologically traceable
and their origin identifiable.162 For this reason, finds of rat bones in
medieval layers will normally be remains of black rats and only excep-
tionally come from a brown rat, and then under circumstances where
this will tend to be recognizable. The brown rat is normally larger than
the black rat, also the size of the bones provides some useful if not deci-
sive indication of the type of rat. While it is true that the burrows of
brown rats may occasionally have penetrated into medieval layers, and
that this should be taken into account, finds of the remains of rats in
medieval layers are now so numerous that the great majority of them
must be of the black rats. Different types of evidence and arguments
can be accumulated to produce a solid case for identifying rat bones
found in excavations of Roman or medieval sites as medieval remains
of the black rat.
160
Twigg 1984: 78, 80.
161
Pollitzer 1954: 286; he cites US Public Health Service, Communicable Disease
Center (1949).
162
Rackham 1979: 112–20.
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124 chapter three
The main conditions of source-criticism and the significance of finds

of rat bones must also be assessed in a historical perspective. Zoo-
osteological studies of finds in archaeological excavations are recent
features of archaeological work, having been taken up beginning in the
1970s; this is especially the case with small bones. Earlier studies of
small bones are so few that they can be considered exceptional, for
instance, finds of two-thousand-year-old rat bones in Pompeii.163 This
also means that while excavations up to about 1970, and to a large
extent also later, have undoubtedly made significant contributions to
our knowledge of the past, they have also destroyed much valuable evi-
dence for the study of bones, insects, and plants, and so on, which could
help to form a more complete picture of human environments and
ecology in the past. Much of medieval Oslo was destroyed when the
first railway was built in the early 1850s and also in the subsequent
decades as the railway network was expanded; as late as around 1970,
excavations of some remaining medieval sites were performed without
sieving for small bones (such as rat bones).164 Wars have also been
destructive, especially the mass aerial bombardments and massive use
of artillery along the front lines and in urban battles which are charac-
teristic of the Second World War. Archaeological excavations tend also
to be performed in urban centres or at the manors and castles of the
rich and mighty, whilst peasant houses and settlements have attracted
much less interest and are often much less amenable to such studies.
Black rats are nimble climbers and like to nest in the roofs or ceilings
of human housing where they are safer from predators like cats, and
also because warm air rises from the hearth and produces better living
conditions there. This means that their bones and their nests will often
be long gone or be dispersed in a way that will make finds very unlikely.
Black rats are also, as mentioned, burrowing animals, and they have
been burrowing away from human habitation also in the Nordic coun-
tries (see below). They could have burrowed within medieval and early
modern houses with beaten earthen floors until it became usual to
build houses with timbered floors as in the Nordic countries or with
tiled floors as in the more southerly parts of Europe, and subsequently
and gradually also on low stone foundation walls, a process that appears
163
MacArthur 1952: 209.
164
Lie 1988: 159. I thank Professsor Egil Mikkelsen, Director of the Historical
Museum, University of Oslo, for useful comments on this point in a personal commu-
nication by e-mail 25 January 2010.
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rats 125
to have started in many places some time in the sixteenth century and
to have been largely completed by 1800. This meant that the black rats
increasingly had to focus on nesting in roofs or ceilings, outbuildings
and burrows which increased their vulnerability, especially after the
arrival and growth of the brown rat populations.165 One should note
that it was usual in the past that live-in farm workers slept in the
outbuildings, especially in stables and cowhouses where the dense
housing of large animals produced a significantly higher temperature
which also would be attractive to rats, as would the opportunities for
finding food.
Unfortunately, in the large regions of the Nordic countries charac-
terized by detached or semi-detached peasant holdings, houses have
over many centuries and even millennia been reconstructed or replaced
on the same or partially overlapping sites (tofts). In the villages of man-
ors, especially in medieval Denmark, the lords in the process of so-
called equalization organized the holdings into units of equal size more
or less unhindered by customary rights typical of, for instance, con-
temporary English manorial economy. This makes it unlikely that
medieval rat burrows will be found in such sites, or that such finds will
be exceedingly rare.
The fields from the Viking Period and the Middle Ages are also
largely long gone, having been reworked many times and in recent gen-
erations by heavy machinery which crushes burrows in the ground or
works so deep into the soil that burrows will be destroyed. And of
course archaeologists rarely study undisturbed fields of the Viking
Period or the Middle Ages, so rat burrows in the fields near human
habitation will remain undiscovered. Another factor is that undis-
turbed fields or tofts over such a long time will tend to be unrepresenta-
tive for some of the same reasons that have made them unattractive for
re-settlement. For all of these reasons, the chances of finding medieval
rat bones or rat burrows may appear small, but such finds would be
more likely in urban centres than in the countryside for reasons that
may not have anything to do with the territorial distribution of black
rats in the past. Consequently, the incidence and number of archaeo-
logical finds of rat bones should be expected to be small, but will
increase as archaeologists more often look for small bones of animals
and take a more complete interest in human environments of the past.
165
Benedictow 2002: 250, 276–8.
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126 chapter three
The substantial number of finds of rat bones from the Middle Ages that
is now available for analysis and their wide distribution across Europe
is therefore a surprising result of archaeological investigations in this
regard.
The source-critical problem of the representativeness of archaeologi-
cal finds of rat bones can also be illustrated in another way on the basis
of the report that B. Hårding, the former Swedish osteologist, produced
on the study of bone material found in excavations of the original area
of the small town of Sigtuna (north-west of present-day Stockholm)
which developed beginning in about 975 a.d. An area of about 1,100 m2
was excavated, bone material was collected from about 400 m2, but
small bones from small mammals were only searched for with adequate
methods in a sample of eight squares of 2×2 m, a miniscule fraction of
the excavation area. Since the osteologist nonetheless found twenty-
two rat bones of which fifteen could be identified with certainty as
black rat,166 it would be inadequate to conclude that these bones repre-
sented just a few rats; instead it would be more realistic to infer that
black rats were ordinary animals in the small town at the time, in the
late Viking Period and the early High Middle Ages.
As new archaeological finds of rat bones were steadily reported over
the last decades, patterns of development and spread became observa-
ble. I produced the first preliminary overview of finds up to 1991 in
the medieval Nordic countries and northern Europe in my doctoral
thesis.167 The first full inventory of finds was published by F. Audoin-
Rouzeau and F.-J. Vigne in 1994.168 After this date, more than thirty
new finds from about twenty ancient and medieval sites169 have
been recorded and presented in a broad historical perspective by
M. McCormick in 2003,170 a paper that appeared when my typescript
on the history of the Black Death was with the publishers. However, in
my monograph I give a broad account of such finds in the chapter “Rat
History.” McCormick and I independently reached the same crucial
conclusions about this material, although I have chosen to ignore the
166
Hårding 1992: 0–1 (sic), 4, 27.
167
Benedictow 1993/1996: 157–60. The writing of the dissertation was finished in
1991, it was defended in 1992 and was published in a slightly revised form in 1993 and
reprinted in 1996.
168
Audoin-Rouzeau and Vigne 1994: 125–45. Cf. Aduoin-Rouzeau 1999: 220–6.
169
McCormick 2003: 6, fn. 7.
170
McCormick 2003: 1–25.
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rats 127
question of geographical origin of the black rat as being peripheral to

my subject.
A useful point of departure is the numerous finds of rat bones in
Roman imperial territories in the West and also in its northern territo-
ries. McCormick summarizes finds of rat bones in sixty-five sites from
the Roman period up to the eighth century. Several finds of the skeletal
remains of black rats dating back to Roman times have been found in
Italy, they are widespread in Roman Gallia/Gaul (France), have been
found near Amsterdam and in Valkenburg in the Netherlands, in
southern Belgium, in Roman Austria and are widespread in Roman
Germania all the way to about the city of Cologne (a Roman military
camp called Colonia = settlement) in the northwest.171 In Switzerland,
skeletal remains of two black rats have been found in excavations of a
Roman villa near the city of Bern, the remains of one rat in the Roman
town Augusta Raurica, present-day Augst, and the remains of a rat dat-
ing to the 4th–8th century have been found near Geneva.172 Many of
these finds come from rural inland regions, and only a few from ports.
In England, several finds have been made of the skeletal remains of
the black rat dating back to the time of the Roman occupation, namely
in York and London, at a Roman settlement (Gorhambury) near
St Albans roughly 35 km north of London, in Wroxeter (Shropshire),
and of two rats from the first century a.d. in a Roman villa in
Beddingham situated inland in East Sussex. Remains of three rats
found in Walton, Aylesbury, in Buckinghamshire, the very heartland of
rural England, have been dated to the 5th–7th centuries, and may
therefore be from the late Roman period or transitional early Anglo-
Saxon England; subsequent finds at this location up to the 9th–12th
centuries reflect a presumably continuous presence. These finds are
widely distributed in the northeast, southeast, central and western
parts of England, respectively. They are certainly not restricted to ports
or to cities, which are the case only with the finds in London and York.
The devastating implications of these findings for advocates of alter-
native plague theories are demonstrated by the complete silence on
these finds by Scott and Duncan in their monographs of 2001 and 2004.
This permits them to maintain that “the black rat had not spread to
northern Europe by the time of the plague of Justinian [540–1]” and
171
Armitage, West and Steedman 1984: 379; Audoin-Rouzeau and Vigne 1994: 129;
McCormick 2003: 6, fn. 7.
172
Stampfli 1965–6: 454–5; Audoin-Rouzeau and Vigne 1994: 129, 134–5.
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128 chapter three
that the black rat may have arrived in England in the Middle Ages, but
“a variety of dates have been suggested.”173 In support of these asser-
tions they refer to Matheson’s book of 1939 and Shrewsbury’s mono-
graph of 1971, again seeking refuge in obsolete works in relation to an
important point. In the later popular version of their monograph, they
express the same opinion and again pass in silence by all the finds of rat
bones from Roman England and Northern Europe.174
Despite the fact that animal bones, especially of small animals, have
attracted the interest of archaeologists and osteologists only in recent
decades,175 it has been shown that the black rat was widely dispersed in
Roman Europe, from Italy to England, to “Belgium” and the Netherlands
and all over Roman Gaul in the west to the Roman military settlements
on the borders with the Germanic tribes along the R. Rhine and the
R. Danube. The pattern of finds in time and space indicates that the
black rat was spread over Roman Europe by the movement of the legions,
by their long logistical train of wagons with sufficient food stuffs to
support 4000–6000 men in each legion over time, and through the
market-oriented network that was established by the Roman Empire.
This is one of the important observations that McCormick and I made
independently.176 This is really not surprising in view of the fact that
there was no commercial (or military) sailing from the Mediterranean
to western and northwestern Europe, and legions and goods moved by
land from Italy to Britain, to Gaul and Roman Germania.
Up to 1984 when Twigg’s monograph was published there had been
six finds in England of skeletal remains of the black rat dating back to
the Early Middle Ages, and also one find in Ireland. As mentioned
above, at Walton, Aylesbury, finds were made dating back to the 5th–
7th centuries, the late Roman period or transitional early Anglo-Saxon
England, while other finds at this location date to the 9th–12th centu-
ries, indicating a continuous presence. Twenty-seven finds dating back
to the 11th–15th centuries with a wide territorial distribution in
England have also been made.177 After 1984, many new finds of
remains of rats have been made in England from Anglo-Saxon times
173
174
Scott and Duncan 2004: 174–5; Davis 1986: 463–4.
175
McCormick 2003: 6.
176
McCormick 2003: 9; Benedictow 2004: 22.
177
Armitage, West and Steedman 1984: 381; Rackham 1979: 112–20; Audoin-
Rouzeau and Vigne 1994: 129–35; McCormick 2003: 6, fn. 7.
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and subsequent periods of the Middle Ages. They show a wide distri-
bution in the country, as far north as the Brough of Birsay on the west-
ern tip of the main island of the Orkneys where they dated back to the
9th–12th centuries.178
Nonetheless, Scott and Duncan state that
Dr Twigg has continued with his careful study of the black rat in England
during the age of the plagues and has collated overwhelming unpublished
evidence that it did not spread to rural areas.179
This raises a number of questions: How can Twigg maintain that the
black rat only had had a sporadic incidence in English ports in the
Middle Ages and later, when the material skeletal finds on the ground
prove a much longer history of wide distribution back to Roman times,
also in inland regions, when he shows knowledge of several of the stud-
ies that present this evidence?180 How can Scott and Duncan refer to
“overwhelming” unpublished evidence collated by Twigg which con-
firms that rats did not spread to rural areas in the face of substantial
published empirical zoo-osteological evidence to the contrary? How
could Twigg collect and collate “overwhelming” evidence bearing on
the matter which is unknown to archaeologists and osteologists who
would have had to produce it? And why is this “overwhelming” mate-
rial still not published?
Fortunately, Scott and Duncan mention two arguments based on
Twigg’s unpublished material which afford the opportunity to test its
quality or tenability, especially since these arguments must be assumed
to have been selected for their importance and evidentiary powers.
Conspicuously, these arguments have no relation to zoo-osteology or
finds of rat bones, which presumably would be the only powerful mate-
rial evidence in this case. Instead, these two supposedly important
pieces of evidence relate to (1) changes in the design of dovecots in the
1720s and (2) changes in the design of storage facilities for grain in
1730s, which purportedly constitute proof of the normal absence of the
178
James 1999: 20–1; James 2001: 12; Audoin-Rouzeau and Vigne 1994: 129–31;
McCormick 2003: 7–9. McCormick’s information is not as well arranged and easily
surveyable as that of Audoin-Rouzeau and Vigne and therefore not easily structured
and summarized at the level of finds, but is updated and contains more valuable per-
spectives and analyses.
179
180
Twigg 1984: 80–1.
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130 chapter three
black rat back in English history. It is also asserted that these two devel-
opments reflect the contemporary spread of the brown rat which
arrived in England in 1728 or 1729. These two arguments contain sev-
eral elementary methodological fallacies. The notion that observations
regarding technological developments in the third and fourth decades
of the eighteenth century can prove anything about reality in Roman,
Anglo-Saxon, medieval or Early Modern Periods in England is obvi-
ously untenable. The argument that the advent of the brown rat in 1728
or 1729181could be the cause of widespread change in the construction
of dovecots in England in the 1720s is obviously also an anachronistic
assumption of causation and as such fallacious. The idea that a tiny and
growing number of brown rats which probably numbered in the hun-
dreds and was distributed over a tiny area in the course of the 1730s
could affect how grain was stored in England in the 1730s reflects the
same temporal problem of causation but also again the fallacious
anachronistic implication that it would have evidentiary relevance for
a discussion of the presence of black rats in preceding historical peri-
ods. The explanatory potential of the modernization of mentality and
culture in the early phase of the Industrial and Scientific Revolutions
should also be considered. This could make it clear that these authors
will have to device a methodologically tenable research strategy that
will uncover material with unambiguous evidentiary and explanatory
powers relating concretely to the historical process in question. To my
knowledge, a generation later Twigg has still not published his pur-
ported material, the outcome of his “careful study of the black rat in
England,” although Scott and Duncan characterize these two argu-
ments as “splendid pieces of scholarship.”
In conclusion, it can be emphasized that despite the fact that animal
remains have only quite recently attracted the interest of archaeologists
and osteologists,182 it has been shown by numerous finds of skeletal
remains that the black rat was widely dispersed in England in Roman
times and was distributed all over the country in the Middle Ages. The
difference in the incidence and distribution of finds between these two
historical periods is probably due to two facts, firstly that there are
fewer physical remains from Roman England than from medieval
England that can be examined and, secondly, that Roman remains have
181
Shrewsbury 1971: 9.
182
McCormick 2003: 6.
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rats 131
attracted relatively greater interest from English archaeologists and to a

greater degree had been excavated before they started to take interest in
small bones, and relevant skeletal material has inevitably been destroyed
en masse.
From the Roman border provinces, the black rat could easily have
been spread further into Germanic and Slavic territories through trade.
Actually, remains of black rats dating back to late Roman centuries
have been found in the excavation of a Germanic settlement at Wal-
tersdorf in eastern Germany near present-day Berlin, and in Slavic set-
tlements in present-day northwestern Poland (Smuszewo) and on the
eastern side of the Gulf of Gdansk (Tolkmicko). There has also been a
find in Szczecin (Stettin) dating from the 4th–8th centuries. Thus, it is
not surprising that numerous finds of skeletal remains of the black rat
dating back to the early medieval period have been made in northern
and northeastern Germany, and in Poland, including sites on the Baltic
Sea.183 In the most important commercial centre in Northern Europe in
the Early Middle Ages, namely the town of Haithabu situated north of
present-day Hamburg, several finds of skeletal remains of the black rat
have been made.184 From this important commercial centre black rats
must have been distributed into the Nordic countries by ships—the
black rat is not only the house rat but also the classic ship rat. Again, a
long temporal process of spread and adaptation is indicated.
The lines of trade and communication extended much farther
around Northern Europe: Franks and Frieslanders traded with the
Nordic countries in the Early Middle Ages and the Vikings sailed all
around Western Europe trading and plundering as they saw fit. In the
880s, the Norwegian merchant Ottar who lived in northern Norway,
visited King Alfred the Great of Wessex in England. He told the king
about Norway and the other Nordic countries, an account that was
included in the geographical section of the translation of the Roman
author Orosius’s History of the World, a project in which the king
eagerly participated. Ottar’s account produces a vivid picture of trade
by ship that in the ninth century interconnected the whole of Northern
and northwestern Europe in a commercial network along which black
rats, the classic ship rats, would almost inevitably have been widely
distributed.
183
Teichert 1985.
184
Reichstein 1974 and 1987.
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132 chapter three
Against this backdrop, it is unsurprising that finds of black rats in

the Nordic countries date back to the Early Viking Age. Recently the
archaeologist B. Wigh published a monograph on excavations at Birka,
an urban centre which developed in the second half of the eighth cen-
tury on an island in the big L. Mälaren west of present-day Stockholm.
Within a chronology of stratigraphic phases he reports that the remains
of a rat were found in phase 3 covering the period c. 810–30 a.d., thir-
teen remains of four rats were found in phase 4, a stratum pertaining to
c. 830–45 a.d., the remains of another rat date back to the subsequent
phase 6, the period c. 860–900, and from phases 7–8 covering the
period 900–50 twenty-four bone fragments of black rats were identi-
fied,185 before the town disappeared around 975.186
Finds of skeletal remains of the black rat dating back to the end of
the Viking Age around 1050 have been made in other urban centres, in
Lund187 near the western side of the Sound, and in Sigtuna situated on
L. Mälaren north of the former town of Birka and northwest of present-
day Stockholm. As mentioned above, twenty-two bone fragments of
rats of which fifteen were identified with certainty as black rat have
been found in a special study of a tiny part of the excavation area in
Sigtuna. Within this area, the bone fragments were quite dispersed and
presumably represent several specimens. These finds suggest that black
rats were ordinary animals in the urban environment of the time.188 In
all three cases, the presence of the black rat in these urban centres
occurred quite early in their developments, and they may have been
present about as early as urban growth first started, which appears to
have been the case in Birka. The appearance of rats in the first phase of
the formation of new urban centres in the Viking Period indicates that
rats at the time were widespread and usual on board ships and were
easily spread to new ports that would act as epicentres of spread inland
with the further distribution of goods by boats or pack horses.
Also the remains of two rats datable to 1220–60 have been found in
Lund.189 Large numbers of skeletal remains of the black rat dating back
185
Wigh 2001: 29, 54, 125–6.
186
A small first excavation at the location was performed in the early 1870s and
among the finds were the remains of a rat, but since the find was not handled according
to modern standards nothing more can be said than that it dates from the ninth or
tenth century. See Wigh 2001: 29, 125; and Audoin-Rouzeau and Vigne 1994: 129.
187
Bergquist 1957: 98–103.
188
Hårding 1992: 27; Hårding 1993: 25. Cf. Wigh 2001: 125.
189
Bergquist and Lepiksaar 1957: 11–84.
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rats 133
to the thirteenth century and the late medieval period have been found
in excavations in Stockholm.190 Excavations of a settlement on the
Baltic island of Öland unearthed the remains of three rats dating back
to the 11th–13th century.191 In excavations in Visby in Gotland Island,
G. Malmborg, the osteologist at the University of Gotland, has in recent
years found many remains of the black rat from the 13th and 14th cen-
turies. In a personal communication, he states that he finds it improb-
able that the black rat was not spread to all parts of the island in the
medieval period, and suggests that the brown rat did not arrive until
around 1800.192 Remains of two black rats from the decades around
1400 have been found in Hälsingland,193 a completely rural region
along the Baltic coast in northern Sweden, namely in the royal bailiff ’s
fort at Faxeholm,194 after only four per cent of the site has been exca-
vated.195 J. Lepiskaar, the osteologist, has identified the remains of
twenty rats found in the site of a monastery in Gudhem in western
Sweden (specifically the southwestern region of Västergötland) dating
back to the fourteenth and fifteenth centuries. The same scholar found
bones from a rat in Uppsala north of Stockholm datable to the fifteenth
century and another from about 1470–1530 at a nunnery in Ny-Varberg,
a small town situated on the Sound (close to Varberg).196 A find of rat
bones in the site of a hostel for travellers in Ramundeboda in the dis-
trict of Tiveden, in a central region of Sweden (county of Örebro) is
dated to the fifteenth century197 (Ny-Varberg and Lund are situated in
regions that today are Swedish but in the Middle Ages belonged to the
Kingdom of Denmark).
Finds of rat bones in Sweden now date back to the early Viking
Period and throughout the whole medieval period; they have a wide
territorial distribution from Scania in the southwest to Hälsingland in
the northeast. These finds were made in both urban and rural ecologi-
cal environments. This corresponds to interesting linguistic evidence
190
Vretemark 1983: 294, 467.
191
Boessneck and von den Driesch 1979: 214–5.
192
Personal communications from G. Malmborg in e-mails dated 19 June, 20 June
and 21 June 2006.
193
Hälsingland is situated roughly 250 km north of Stockholm.
194
Faxeholm is situated not far from the present-day small town of Söderhamn that,
please note, was established at the beginning of the seventeenth century. Faxeholm was
quite a small and simple fortified place, not really a castle. Mogren 2000: 251–2.
195
Mogren 2000: 119–20, 249.
196
Lepiksaar 1965: 96–7; 1969: 38; 1975: 230–9.
197
Audoin-Rouzeau and Vigne 1994: 131.
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134 chapter three
which needs some general introductory comments. The major lan-

guage families do not contain a specific word for rat in their basic
vocabularies. In the past, people were not zoologists and had no schol-
arly or scientific education, and they used the same word to designate a
number of animals that looked quite alike to them such as mice, rats,
stoats and polecats. In languages of Indo-European origin, the basic
word is “mus,” e.g., in Latin, Norse and modern Scandinavian languages
“mus,” German “Maus,” English “mouse,” Russian “mysh.” Up to 1910,
the scientific name of the black rat was Mus rattus and of the brown rat
Mus decumanus. For this reason, it is often impossible to know which
animal a writer has in mind when the word “mus” or “mouse” is used.198
When a writer for some reason wished to be more accurate, additional
information was needed to identify the specific animal referred to.
Medieval authors writing in Latin might resort to the current vernacu-
lar word: a chronicler provides an account of an Irish bishop of the fifth
century whose library was destroyed by majores mures que vulgariter
rati vocantur, i.e., “big ‘mice’ that in the vernacular [by common peo-
ple] are called rats.” Thus, in fifth-century Ireland, ordinary people had
acquired a specific word in order to distinguish vermin in the form of
mice from vermin in the form of rats, probably from the Anglo-Saxon
invaders who appear to have had such a word.199
Also in the Norse language of the Vikings a specific term came into
use when people wished to identify the animal in question as a rat (long
before the word rat entered the Scandinavian languages), namely “vǫlsk
mus” which can be literally translated as “Frankish mouse.”200 In view
of what we know of the history of the brown rat, there can be no doubt
that this term refers to the black rat. The adoption of the term may
reflect either the fact that the black rat was a new animal in the early
Viking Period or that the Vikings learned a specific term abroad that
they found useful. The term “Frankish mouse” may contain some indi-
cation of the geographical origin and the time of frequent and wide-
spread introduction of black rats to the Nordic countries. It suggests
that the time was the Viking Age, quite likely in the first half of the
ninth century, when Viking fleets frequently sailed up the large French
rivers, landed hosts of armed men which ravished the countryside and
formed armies which besieged Paris. Since the black rat is not only the
198
Cf. for instance McCormick 2003: 4.
199
McArthur 1949: 170, fn. 2.
200
An Icelandic-English Dictionary 1975: 440, ‘mýss valkar’; Fritzner 1954: 755.
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rats 135
house rat but also the ship rat, this means that there must have been
many introductions of black rats into the Nordic countries as early as
the ninth century and also frequently later, also from other sources, for
instance, from Haithabu or England. This explains the frequent archae-
ological finds of rat bones from the early ninth century and later peri-
ods. These were rats which would have had centuries of adaptation to
the climates of northwestern France, England, and northern Germany.
Consequently, there would also be ample time for the evolutionary
development of an even more hardy and rough-coated breed of black
rats that would have been adapted to life under the prevailing climatic,
economic and social conditions of the Nordic countries. This process
would allow the development of a widespread and numerous popula-
tion of rats and the murine potential which could play a tragic part in
the spread of the Black Death and subsequent plague epidemics. The
early introduction of the specific term “vǫlsk mus” is probably the rea-
son that the word “rat” is not registered Scandinavian sources until the
Late Middle Ages.201
The numerous finds of medieval rat bones in the Nordic countries
present the proponents of alternative theories with great problems
which they handle in interesting ways. Davis discusses Scandinavia in
this regard under the pretence that there has been made only one find
of rat bones, namely in Lund, despite the fact that quite a number of the
finds of rat bones presented above had been published before he wrote
his paper. It is not true that Lund is a port, as Davis maintains:202 Lund
is situated on a fertile plain about eight km from the Sound without
pronounced commercial functions. In the Middle Ages, Lund’s growth
was mostly stimulated by its establishment as a national religious cen-
tre, a cathedral city, and as the site of the archdiocese of Denmark. It is
not readily comprehensible what Davis means in this context by stat-
ing that “none were found in Holland” which is a province in the
Netherlands. Perhaps, it is a garbled form of Halland which is a longish
region (at the time Danish) situated along the Sound (north of Lund),
in which case he is wrong, since Ny-Varberg was a small town in
Halland near present-day Varberg.
Relating to my discussion of the presence of rats in the medie-
val Nordic countries in my doctoral thesis,203 Cohn asserts in his
201
Bernström 1969: 578.
202
Davis 1986: 463.
203
Benedictow 1993/1996: 157–60.
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136 chapter three
monograph that in “these Nordic countries no skeletal remains of rats

has been found.”204 Clearly, this assertion is wrong. Most of the finds of
skeletal remains of rats mentioned above were published before I wrote
my thesis and they are all included in my presentation of this material
with a discussion of their epidemiological implications. At the time
Cohn was writing his monograph, he had the opportunity to avail him-
self of the overview of archaeological findings of black rats published
by Audoin-Rouzeau and Vigne in 1994 in which my information on
Nordic finds is included and greatly enlarged upon within a Europe-
wide perspective, and subsequent publications of finds up to 2002.
Instead, he denies the facts and makes disparaging comments on the
earnest efforts of colleagues to interpret the significance of these finds.
In my doctoral thesis I argue that the absence of finds of rat bones in
Norway so far was probably due to the incipient stage of development
of zoo-archaeology, and for this view I am ridiculed by Cohn.205
However, at the time Norwegian archaeologists had not begun search-
ing for and studying small bones in their excavations; such bone mate-
rial might be collected and stored but was not actively studied. In recent
years, the study of such bone material has begun, in the words of Ann
Kristin Hufthammer, the osteo-archaeologist who has taken the first
initiative in this field of study in Norway: “only recently have we begun
to sieve and systematically collect bones also of small species.”206 Up to
the time of writing, this has led to the following identifications of
skeletal remains of the black rat: in Trondheim (medieval name
Nidaros) skeletal remains of the black rat have been found in several
sites from the early High Middle ages, among them in the sites of
Folkebibliotekstomten and Televerkstomten; finds have also been
made in sites from the seventeenth century in the archiepiscopal man-
sion and in Televerkstomten. In Stavanger, rat bones archaeologically
dated to the early twelfth century have been found in strata at Skagen.
The oldest radiological dating of bone material of a black rat in
Bergen is 750 years before present time, calibrated to ad 1225–95. In
Tønsberg, archaeologists have succeeded in finding a rat nest contain-
ing several individuals. Skeletal remains of a rat found in it have
204
Cohn 2002: 53.
205
Ibid.
206
Personal communication from Ann Kristin Hufthammer by e-mail of 10 January
2006.
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rats 137
been radiologically dated to 700 years before present, calibrated to ad

1265–1375.207 It is tempting to consider this find a possible reflection of
the Black Death.
The finds of medieval rat bones in Norway are consonant with liter-
ary evidence. In Snorri Sturluson’s Saga of St Olav, the need for a spe-
cific designation of rats is resolved by using the description “mice as big
as cats” with obvious resemblance to the Latin wording of the Irish
chronicler mentioned above mures majores, “big mice” (in the vernacu-
lar called rats). This description is used for animals which are said to
have appeared when St Olav crushed a big wooden statue of the god
Thor to which food was sacrificed daily.208 This brief legend of St Olav
linked to his missionary work takes place in the principal inland valley
of Gudbrandsdalen, a completely rural region of central southern
Norway. This implies that at the time this saga was written, i.e. shortly
before 1230, the listeners or readers were comfortable with the notion
that rats were usual animals in central rural districts of southern
Norway and that this had been the case two centuries earlier. When
rats surface in this saga, it is in a context that demonstrates the ordi-
nary presence of rats in the middle of the high medieval Norwegian
countryside. Again, the crucial source-critical question is: why are rats
mentioned? Sagas are heroic tales of kings and warriors and serve the
ideological and political purposes of state-building and of confirming
the prestigious (and profitable) roles of kings and aristocratic elites.
Comments on rats have no useful practical or ideological place in this
literature and should not be expected to occur, particularly as they were
pests in human habitats. In this case rats are mentioned because they
serve a religious propagandistic function, demonstrating the stupidity
of serving food to heathen wooden gods. The great saga writer who
constantly seeks literary effects does not use the term “vǫlsk mus”
because he wishes to dramatize his story and enhance the impact of its
moral teaching by emphasizing the ludicrous point that the heathen
peasants had fed rats so lavishly that they had grown big as cats.
The question of evolutionary adaptation to northerly climates by rats
and the quantitative and distributive aspects of their presence in the
Nordic countries can be enlarged upon on the basis of written sources.
There are so many references to rats in literary works that a leading
207
Personal communications by e-mail 10 January 2006.
208
Snorri Sturluson 1899/2003: 295.
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138 chapter three
Swedish scholar in this field of study concludes: “During the late medi-
eval period, rats and mice are mentioned as generally known pests in
and around human buildings”; and “it appears likely that this animal
[the black rat] at the middle of the fourteenth century had a numerous
presence in Scandinavia’s and Denmark’s rural districts.”209 “Rats and
even mice must have been very troublesome pests for medieval man,”
as evidenced by both the great number of maledictions and curses and
also the extensive use of rat traps.210 For zoo-historical reasons, all of
these references must be to the black rat. This literary evidence and the
conclusions drawn by Nordic scholars with respect to the quantitative
aspects of the presence of black rats and their territorial distribution in
the Nordic countries accord with the material finds of rat bones, and
we may be certain that rats had a broad rural presence.
This presentation of skeletal remains of the black rat so far found in
Norway and Sweden puts in perspective Twigg’s assertion that Norway
and Sweden are countries “which provide especially poor conditions
for Rattus rattus,” and makes it clear that his view is based on precon-
ceived and arbitrary assumptions which are at variance with histori-
cal reality as reflected both in the form of rat bones and in literary
sources.211
This confirms O. Nybelin’s view which he formed long before archae-
ological finds of rat bones were made to the effect that the black rat was
spread all over medieval Sweden and the southern parts of Norrland.
To him it was important that this was still the case in large parts of
Sweden in the nineteenth century, but at the time the black rat was in
rapid decline because of the expansion of the brown rat and the mod-
ernization of housing. Nonetheless, the black rat was still observed in
inland rural regions with very cold winters such as Värmland and
Småland, and at the time it was still common in southern Norrland,
especially in Hälsingland. Actually, in Hälsingland the black rat was
still living in four rural parishes in the early 1920s as well as in seven
rural parishes in Halland, in northeastern and southwestern Sweden
respectively. In Finland, black rats were observed in about 20 localities,
mostly in rural regions, in the first decades of the twentieth century.212
For obvious reasons, the brown rat spread first to ports and urban
209
Bernström 1969: 577–83. My translation from Swedish. Törnblom 1993: 367.
210
Berg 1969: 576–7. My translation from Swedish.
211
Twigg 1984: 57.
212
Nybelin 1928: 852–5.
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rats 139
centres and from there to rural districts, thus, logically the last surviv-
ing “tribes” of the old black rat were found in peripheral rural districts.
However, this also constitutes evidence that the black rats in the Nordic
countries were spread all over these countries, and that they were usual
rural animals not at all confined to ports or urban centres. Sweden and
Finland have colder winters than large parts of Norway because they
are situated further way from the warming effects of the Gulf Stream.213
In this respect, there is complete compatibility and accordance between
the written sources and the material finds of skeletal remains of these
animals.
This point should be considered from wider chronological and geo-
graphical perspectives. Until the 1790s, the black rat was the only rat in
Sweden and Finland, the Nordic countries with the coldest winters.
The arrival of the brown rat meant that the black rat was gradually
driven from its habitats by the brown rats, and was prevented from
seeking alternative refuge or habitats by contemporaneous changes in
the construction of buildings and increasingly hostile countermeas-
ures implemented by the human inhabitants against rats in their
houses and immediate vicinities However, in the first decades of the
twentieth century black rats were still found in a number of urban and
rural areas in these countries; in Sweden the last colonies could still be
observed in the 1950s.214 In Norway, the black rat may possibly still live
in a few rural localities.215
In the Middle Ages, Finland had a tiny and territorially widely dis-
persed population numbering about 65,000 persons at the time of the
Black Death. There was only one small urban centre, namely Åbo
(Turku),216 consequently, rats would have to be animals living in con-
junction with rural human settlements. In fact, black rats were still
observed in the remote rural districts of the region of Tavastland in
Central Finland in the 1920s.217 Presumably, rats were introduced
into Finland by Swedish peasants who moved across the Baltic Sea and
213
Eldevik 2006: 48. Eldevik is researh leader at the G.C. Rieber Climate Institute at
the Nansen Environmental and Remote Sensing Center and Bjerknes Centre for
Climate Research. The average temperature in these parts of Norway is 10 °C higher
than other regions situated at the same northerly latitudes.
214
www.skansen-akvariet.se/vara_djur/html/svartratta.html
215
Personal communication from Rolf Lie, Zoological Museum, University of
Bergen, in 1991.
216
217
Vilkuna 1969: 584.
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140 chapter three
settled there in the Viking Period, but, of course, these rats might have
a much longer history. And these black rats were also burrowing and
living in the vicinity of human habitation,218 despite Twigg and Davis’s
assertions to the contrary.219 Davis actually consistently calls the black
rat a “roof rat.” As shown above, the black rat can, in fact, freely burrow,
in nature as peridomestic rodents and in beaten earth floors and walls
of human housing220 on the condition that they are not exposed to
brown rats which will hunt them down, kill them or drive them out of
their burrows, and that would not happen before the late eighteenth
century in Europe. As mentioned also above, in Macquarie Island
which is situated quite close to Antarctica (54° 30ʹ S, 158° 57ʹ E), in a
very inhospitable cold climate and subantarctic ecology, thriving colo-
nies of black rats have settled as burrowing rodents, temperatures in
the burrows ranging from 4.8 °C. to 9.2 °C.221
Largish specimens of the black rat have been found in England at
Faccombe Netherton on the Hampshire-Berkshire border,222 among
the Norwegian finds in Bergen and the Swedish finds in Visby,223 and
also in Corsica (see above). This can be taken as further evidence of the
adaptability of rats by selection, which also adapt by size to environ-
mental challenges by selection of larger animals with improved chance
of survival in competition with other small rodents and which would
make them less vulnerable to small predators like stoats or polecats.
Perhaps rounding off of body-shape could also increase resistance to
cold (which could not have been a selective factor in Corsica).224
Under the circumstances, the wide geographical spread and the sub-
stantial number of finds of medieval rat bones in the northerly parts of
Europe are quite remarkable. In the words of McCormick: “Judging
from 143 rat contexts of the ninth to the fifteenth centuries, medieval
Europe’s rat colonies were extensive and abundant […].” And these
218
Nybelin 1928: 850–7; Bernström 1969: 578–9, 584; Vilkuna 1969: 583–4.
219
Twigg 1984: 80; Davis 1986: 456–7.
220
See. for instance, IPRC 1907 g: 746; Lamb 1908: 9, 13.
221
McCormick 2003: 22–3.
222
James 2001: 12.
223
Malmborg, personal communication by e-mail 19 June 2006: “Even here we have
a morphological variant which appears a little larger than the black would be expected
to be.” My translation from Swedish.
224
I have noted with interest that the IPRC found that black rats in Belgaum 400 km
southeast of Mumbai were much larger than in Pune (Poona) about 120 km southeast
of Mumbai. IPRC 1910c: 456.
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rats were not far and few between at the time: in sixty-six cases the
archaeologists estimated the minimum number of individual rats,
which proved to be 601 rats or an average of 9.1 per site, and twelve of
the most-infested sites were from the thirteenth century or later.
“Overall, the raw rat counts hint at hugely expanding rat populations
around the fourteenth-century plague.”225 Clearly, the arguments of
the advocates of alternative theories against a numerous and broad
presence of the black rat in medieval Europe, including in the north-
erly parts and in the Nordic countries, are not tenable and represent
serious underestimation of “rats’ adaptability” by evolutionary selec-
tion and the development of regionally adapted variants or biovars.226
As pointed out above, this is also the case with rat fleas, X. cheopis:
“As shown by its wide geographical distribution, X. cheopis is able to
adapt itself to a considerable range of climatic conditions. It is, as has
been previously noted, the common rat-flea in Manchuria and is also
the prevalent species in the tropical section of Brazil.”227 This shows
that a full potential for epidemics of bubonic plague must have been
present in the Scandinavian countries at the latest from the High
Middle Ages.
This does not prove that epizootics among rats fuelled historical
plague epidemics, but does constitute crucial evidence which permits
solid assumptions to the effect that there was a sufficient murine basis
all over Europe, that the potential for epidemics of bubonic plague was
present. Whether or not this potential was realized must be demon-
strated through manifestations of the epidemiological processes that
are explicable only by a concomitant epizootic of plague among rats.
Central aspects of this question will be discussed in the next subchap-
ter on the sociology of rat-based plague, and in Part 4 on defining fea-
tures in chapters on epidemic latency periods and other temporal
aspects of the development of plague epidemics, the inverted correla-
tion between population density and morbidity and mortality rates in
modern as well as historical epidemics of plague, and on the seasonal-
ity of plague epidemics, and elsewhere. Assertions that historical plague
epidemics could not have been bubonic plague because there was not a
murine basis must be rejected.
225
McCormick 2003: 14.
226
McCormick 2003: 22; Wigh 2000: 125; Nybelin 1928: 855.
227
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142 chapter three
Sociology of Rat-based Plague
Social conditions can systematically affect the intensity of infective

processes in relation to particular social categories of persons accord-
ing to the distributive functions of relative risk of exposure. At the heart
of the matter is the fact that epidemiology is fundamentally a subdisci-
pline of sociology which aims to explain how various social conditions
and interrelated patterns of behaviour of human beings, animals and
insects affect the probability of contagion being transmitted to human
beings or between human beings. It is, therefore, important to note Wu
Lien-Teh’s general statement:
Most investigators are agreed that, on the whole, differences in the age,
sex, racial and also occupational incidence of bubonic plague are due to
differences in exposure to infection as brought about by varying modes
of life and not to intrinsic causes.228
Pollitzer supports this position unequivocally when he cites it quite
closely: “Most workers are agreed that differences in the race and sex
incidence of bubonic plague cases, as well as […] among certain occu-
pational groups […] are due merely to differences in the degree of
exposure of the various groups to the infection and not to intrinsic
causes.”229
Population density affects the intensity of social interaction and
therefore also the probability of being infected and also of being infected
repeatedly and, thus, by multiple infective doses, which produce differ-
ent morbidity and lethality rates according to social class and other
social categories. This explains the typical supermortality in epidemic
disease of indigent and destitute people who tend to live in overcrowded
rooms and in overcrowded quarters.
On the other hand, diseases spread by cross-infection may also neg-
atively affect the affluent classes who tend to have large households
with several or many servants and an active social life, producing a
high level of social interaction and a corresponding increase in expo-
sure to contagion by droplets. R. Schofield remarks in his study of the
plague epidemic in Colyton on the sociological dimension of epidemi-
ology that “men and women living in isolated farmsteads may be less
228
Wu Lien-Teh 1936c: 399.
229
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likely to meet infected people than would those living in a village street.
Also the chance of catching a disease may […] vary systematically with
the social and economic status of the household.”230 R. Engelsen found
that affluent or well-to-do farmers in Norway at the end of the eight-
eenth century had a slightly higher risk of contracting infectious dis-
eases than the poor rural classes who tended to live more isolated on
their sub-tenancies (“undersettles”) or small holdings.231 This pattern
of social variation in the incidence of epidemic disease is basically
associated with risk of exposure. This demonstrates the important
point that risk of exposure in relation to diseases spread by cross-
infection, by droplets or inter-personal physical contact should be
expected to produce clearly different social manifestations from the
pattern of epidemic bubonic plague disseminated and transmitted
from rats by rat fleas to human beings.
Sticker, summarizing in his big two-volume work of almost thou-
sand pages an almost incomprehensibly wide reading of sources and
studies written in classical and modern European languages, pointed
out the great variation in the incidence of plague among people of dif-
ferent occupations. Persons working with food stuffs and in environ-
ments where food is stored, bakers, millers and butchers, were
particularly at risk of contracting the disease and dying from it.232 In
E. Woehlkens’s outstanding study of plague in Uelzen (northern
Germany), six of seven bakers, ten of twelve linen weavers, and five of
six butchers died in the plague epidemic of 1597 but only two of nine
smiths, and only four of the town’s fifteen carpenters, wheelwrights and
coopers.233 This is clear evidence of the workings of the rat epizootic
associated with an epidemic of bubonic plague, because the activities of
some occupations attract rats while the activities of other occupations
drive them away. Bakers, linen weavers and butchers are very vulnera-
ble to plague disease because their work material is highly attractive
food for rats (flax seeds in the case of linen weavers), while the shops of
smiths, coopers and wheelwrights do not contain significant amounts
of edible material attractive to rats, and rats avoid high sharp sounds
produced by their work, so these occupations are little exposed to rats.
Thus, the human sociology of a plague epidemic reflects the sociology
230
231
Engelsen 1983: 161–202.
232
Sticker 1910: 266–8. Cf. Mate 1984: 351–2.
233
Woehlkens 1954: 72–5.
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144 chapter three
of rats which is influenced by human activities which are attractive or

repellent to rats.
Woehlkens who could follow the spread of the epidemic house by house
concluded that
the direction of spread of the epidemic, the formation of new centres in
the specific phases and the progress from block to block were determined
by the localization of these houses: the topographic course of plague was
governed by the places with the highest accumulation of food stuffs for rats
(bakers, linen weavers, butchers). A comparison of average numbers of
deaths shows that the probability of being killed by plague in such a place
was more than five times higher than in the case of occupations working
with wood or iron.234
The crucial sociological point is that this differential pattern of mortal-
ity among various occupations and types of artisans or craftsmen can
be easily explained as reflections of rat-borne plague transmitted by rat
fleas, and is inexplicable as reflections of a disease spread by cross-
infection. This pattern constitutes therefore sociological evidence of
bubonic plague. Woehlkens makes also quite a number of other obser-
vations that reflect the workings of rat-based plague, for instance that
the affluent citizens who lived in housing of stone or bricks with tile-
covered roofs were largely spared by the epidemic while poor people
living in housing suitable for nesting of rats were violently attacked, a
pattern that also took the form of strongly differential mortality accord-
ing to social-class divisions by side of street.235 Notable is also the for-
mation of new centres of spread, demonstrating metastatic spread of
plague by transportation of rat fleas.
Cohn has not noted this important aspect of supermortality among
occupations working with food stuffs attractive to rats and submortal-
ity among occupations repellent to rats. In his discussion of differen-
tial mortality among occupational categories, he is only able to mention
supermortality among professions like notaries, attorneys, and parish
priests on the one hand, and of gravediggers according to two chroni-
clers and of wax chandlers of London according to an “apocryphal”
personal communication, on the other. Wax chandlers are supposed
to suffer supermortality because they did not only supply candles
for funerals but also quite remarkably are asserted to have embalmed
234
Woehlkens 1954: 74. My translation from German, and my italics.
235
Woehlkens 1954: 70–1.
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bodies,236 which may be the reason that such assertions have not been
accepted for publication. The point is that supermortality among these
professions does not obviously imply the role of rats and their fleas
but can be associated with diseases spread by cross-infection and pro-
fessional exposure; in the case of gravediggers and wax chandlers they
are surprisingly supposed to contract the disease from dead bodies.
However, Cohn must ignore the fact that these professionals would
tend to enter houses with persons dying or dead from plague and that
this behaviour would produce high exposure to infective rat fleas. If we
take seriously the assertions with respect to gravediggers and to wax
chandlers in the purported role of embalmers, one must also take into
account the possibility that they could be infected by rat fleas hidden in
the clothing of dead plague victims. On page 122, Cohn maintains that
gravediggers according to two chroniclers suffered great supermortal-
ity in plague because this seemingly serves his case for cross-infection.
However, on page 138 he cites another chronicler to the effect that he
“marvelled at the gravediggers, who he said were rarely struck by plague
or died from it by his day (the mid-fifteenth century),” because this dia-
metrically opposite view now seemingly serves his argument for immu-
nity among survivors. This is just one of many instances of weak
consistency and high tolerance of cognitive dissonance in Cohn’s work,
since his selection of material is governed by his ambition to establish
a pre-conceived revolutionary theory of historical plague. He only cites
occupations or professions with supermortality or a pattern of death
which seem at least superficially to suggest cross-infection; why butch-
ers, bakers, millers, linen weavers, and so on, should suffer supermor-
tality from cross-infection and smiths, carpenters, wheelwrights and
coopers should on the contrary suffer submortality is not readily
understandable. In fact, only bubonic plague can provide a cogent
explanation for these patterns of occupational supermortality and
submortality.
In his study of the plague epidemic in Colyton 1645–6, Schofield
puts forward a working hypothesis which predicts that, among other
things, “diseases like bubonic plague and typhus [transmitted by insect
vectors] are likely to be associated with geographically clustered pat-
terns of death, while airborne infections, such as influenza, will show
much less clustering.” As shown in quite some detail above, Schofield
236
Cohn 2002: 121–3.
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146 chapter three
succeeded in uncovering the typical pattern of clustering in families

characteristic of rat-born plague transmitted by rat fleas.237 Dijkstra
carried out a study of the pattern of spread of plague in the Jordan
quarter of Amsterdam during the epidemics of 1617 and 1624. The
clustering of plague cases, the contiguity of spread, and the type of pro-
gression showed that “plague in the seventeenth century has been
dependent on rat plague.” As the Jordan quarter had changed little
physically between the seventeenth century and the first decades of the
twentieth century, he is able to elaborate further on the topic of epi-
demic spread. With a number of maps he illustrates the strongly con-
trasting patterns of epidemic spread in Jordan during the plague
epidemics of the seventeenth century on one hand, and the influenza
epidemic in 1918 on the other. The latter represents the pattern pre-
dicted by the interhuman model of transmission and dissemination.238
As a part of her dissertation on epidemic diseases in early Renaissance
Florence, Carmichael conducted a study of the spread of plague in the
quarter of Santo Spirito during the minor epidemic of 1430. In my
opinion, the pattern agrees closely with the findings of Dijkstra,
Woehlkens, Slack (see immediately below) and Schofield. The extreme
local character of dissemination, the initial clustering of deaths in one
part of this traditional working class district and even along certain
streets within this small area, the clustering of plague deaths within
some families even as the immediate neighbours escaped unharmed,
the slow progression of the epidemic, and the impression that many
streets seemed to begin to function as local plague foci as the epidemic
spread through the summer months, all point to the same explanation.
The maps showing the spatio-temporal progression resemble quite
closely the maps of Dijkstra and Woehlkens.
Slack’s analysis of plague in Bristol in 1540–60 also provides acute
observations of rat-borne plague and the relative risk of exposure of
various social classes. He could identify the typical slow spread of
plague which reflected its movement through contiguous rat colonies:
“The disease was carried relatively slowly through the town by rats,”
and it “moved haphazardly, sometimes missing out two or three house-
holds in its progress along a street.” He registered sudden leaps to a
house surrounded by uninfected houses,239 which then might or might
237
Schofield 1977: 102–8. Above: 62–9.
238
Dijkstra 1921: 64–74. My translation from Dutch. Cf. above: 67.
239
Slack 1977: 53–7.
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not start to function as new infective centres of spread. The conspicu-

ous outcome of his study is “the variations which emerge between par-
ishes and their apparent coincidence in many cases with social class
differences. For plague mortality was not spread evenly over the town.”
Christ Church parish comprised broad, fine streets inhabited by afflu-
ent citizens and also the poor and the overcrowded back street of the
Pithay:
The Pithay lost a higher proportion of its inhabitants in both epidemics
than any other part of the parish […]. Bubonic plague was concentrated
in the back street of this otherwise prosperous parish.
Slack concludes in this way: “Plague thus had a socially selective impact
on Bristol in these years, and this is important for any understanding of
its demographic and economic effects.” His sociological explanation of
the social variation in plague mortality is clear:
The vital determinants behind this association were of course variations
in standards of housing and hygiene which might attract or repel the rats
and fleas which carried plague.240
This view accords with the fact that there exists much evidence show-
ing that ecclesiastics, aristocrats, well-off urban residents and other
persons living in houses built of stone or brick in relative terms con-
tracted plague far less frequently than social categories living in other
types of housing, e.g., the poor in Milan’s “stalli” or in London’s out-
parishes.241 Mortality among the English baronage was much lower
than among the peasantry.242 A.E. Nash is quite probably correct in
assuming that many of them escaped infection because they lived in
“stone-built accommodation.”243
Cazelles concludes his study of the differential social impact of the
Black Death by stating that “the nobility apparently lived through the
mortality without significant losses.”244 In the Black Death, monasteries,
churches and hospitals in Avignon were left unscathed whilst the city
in general was cruelly ravaged. This cannot be explained by acquired
240
Slack 1977: 54–7.
241
Cipolla 1974: 283; Cipolla and Zanetti 1972: 201; Bell 1951: Chapters 4, 6, and
pp. 158a, 329; Hirst 1953: 128; Dyer 1978: 309.
242
Benedictow 2004: 343, 360–77. See also below: 383–92.
243
In the epidemics of 1369 and 1374, the “lords of the manor” appear to have been
left almost unscathed. Nash 1980: 39.
244
Cazelles 1962 (165): 300: “la grande noblesse traverse apparement la mortalité
sans pertes sensibles.” My translation from French.
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148 chapter three
immunity, as it was the first plague epidemic in southern France for

about 700 hundred years. In the terrible epidemic of 1720–2, mental
hospitals and closed monasteries remained untouched. The previous
epidemic, which killed about 8,000 persons, occurred in 1649.245 Only
a very few members of the resident regular clergy (living in a popula-
tion with an average life expectancy of c. twenty-five years246), could
possibly have acquired immunity to plague. Closing such institutions
to the outside world would not have provided protection against the
plague, if the stone buildings had not prevented rats from entering the
premises. In Moscow, the Imperial Orphanage which contained a thou-
sand children and a staff of 400 was similarly spared in the violent
plague epidemic which ravaged the city in 1770–1.247 At that time, there
had not been plague in Moscow since 1665,248 so neither children nor
adults could have been protected by immunity to plague.
The reason for this pattern is that houses built of stone or brick were
far less amenable to rats than houses built of wood or wattle and daub
and roofs covered by thatch. In fact, the increasing use of stone and
brick for house construction beginning in the seventeenth century was
for quite some time the favourite explanation with historians for the
disappearance of plague from Europe.249
In more recent times, the IPRC concluded that the extensive use of
stone and brick for house construction constituted an important expla-
nation of why East Bengal and Assam were only lightly hit by plague.250
This fact is flatly rejected by Cohn. Encouraged, perhaps, by his being
in the favour with the editors of The New England Journal of Medicine
Cohn apparently does not fear that his scholarly reputation will be
affected by the following assertion in his review of my monograph on
the Black Death:251
Benedictow maintains that people in well-built stone housing were pro-
tected against plague because rats could not enter these dwellings. The
plague commissioners [IPRC: my insertion] again discovered the oppo-
site: that rats penetrated stone and brick houses, even those with cement
245
Colonna d’Istria 1968: 18–9.
246
Fourastié 1972: 30.
247
Sticker 1910: 264; Alexander 1980: 263–4.
248
Biraben 1975: 429.
249
See e.g., Clark and Slack 1976: 142–9; Liston 1924: 902–3; Appleby 1980: 166–7;
Slack 1981: 472.
250
IPRC 1911c: 187–92.
251
Cohn 2005: 1354.
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rats 149
floors, inflicting some of the highest rates of death in these residences,

whereas often some of the poorest people, living in bamboo huts, fared
much better.
The IPRC comments on these matters in Report No. XLVI of 1911,
“Observations On Plague in Eastern Bengal and Assam,” in Chapter H.
“The Causes for the Comparative Scarcity of Rats in the Houses.” In the
second sub-chapter titled “The Structure of Their Houses,” the follow-
ing statements can be found:
the Bengali seems to have adopted a method of house construction which
succeeds in practically eliminating rats from his house, be the house a
pucca or kutcha one.
“Pucca” houses, being built of stone or brick or mortar, often with con-
crete roof, from the very nature of the materials used in their construc-
tion afford little harbourage for rats. These animals may however effect
an entrance from outside either through the floor or by the door. Many
Bengali houses however have been so constructed as to prevent rats gain-
ing an entrance in these ways, being built on raised plinths of special
construction. These plinths are erected with a brick or masonry facing,
along the upper border of which runs a bead of varying depth which
projects for from four to six inches or more over the base. The floor is
made of a layer of concrete faced with hard polished cement, below which
is a layer a foot or more deep of dry sand. These devices are said to have
been adopted for a number of reasons: […] (3) to prevent the access of
rats which cannot make their burrows in the sand or climb the overhang-
ing plinth […].
The “kutcha” houses, too, afford little shelter for rats. For, being con-
structed of thin bamboo matting or wattle covered with a thin layer of
mud, the walls afford no shelter for these rodents. The roofs too, being
made of corrugated iron, split bamboo, or thin grass thatch, fail to shelter
these animals. Perhaps one of the most noteworthy features of the build-
ings in this province is the almost complete absence of tiled roofs which
are so commonly seen in many other parts of India.252
The Commission summarized their findings in its “General
Conclusions”:
(3) The freedom of the province from plague can chiefly be attributed to
the scarcity of rats in the houses as compared with other parts of India
[…].
(5) The structure and design of the Bengali homes, whether it be of the
solid masonry type on the one hand or of the flimsy matting or grass type
on the other, afford little shelter for rats.253
252
IPRC 1911c: 190–1.
253
IPRC 1911c: 192.
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150 chapter three
Thus, Cohn’s assertion on this point is contrary to fact. It is a clear mis-

representation of the findings of the IPRC and their unequivocal con-
clusion which indisputably supports the notion that stone, concrete
and masonry protects against rat invasion and the establishment of rat
colonies in human habitation. Nothing is said to the effect that the
small incidence of plague cases in this region was higher in the “pucca”
houses than in the “kutcha” houses, as Cohn’s maintains.
Thus the sociology of historical plague epidemics exhibits the char-
acteristic reflections of rat-based bubonic plague and constitutes evi-
dence of the presence of black rats.
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CHAPTER FOUR
THE SPREAD OF BUBONIC PLAGUE OVER DISTANCES
Contiguous Spread and Metastatic Spread
The advocates of alternative theories, particularly Twigg,1 Scott and

Duncan,2 and Cohn,3 deny that bubonic plague spreads by leaps (per
saltum) by the movement of people or goods, technically often also
called metastatic spread. Although they must have seen Shrewsbury’s
presentation of the principle and mechanisms of metastatic spread of
plague by transportation of rats and rat fleas,4 they insist that bubonic
plague spreads only by contact between adjacent rat colonies, techni-
cally called contiguous spread. In the words of Twigg:
An important aspect of plague spread is the continuity across a rat popu-
lation. The more isolated the rat units the slower will be the movement of
plague amongst rats, and ultimately, to people.5
Among the specific examples he cites in accordance with his view that
this factor alone has the power of invalidating or undermining the rat-
and-flea-based bubonic-plague theory is the following:
The disease would be expected to have spread northwards from the coun-
ties of East Anglia, which it had reached in May 1349, spreading through
the rat population and causing local epizootics. Yet throughout this
large area the high mortality occurred only one month later over the
whole diocese. Plague is said to have reached York on 21 May but accord-
ing to Thompson (1914)6 the deaths of clergy over the whole of this vast
1
Twigg 1984: 57, 100, 185. However, Twigg acknowledges that plague can be spread
by fleas over various distances on pages 128–9, see below.
2
Scott and Duncan 2001: 79–80; Scott and Duncan 2004: 177.
3
In his monograph, Cohn accepts that bubonic plague can be spread by shipments
of grain, but denies all other types of spread by goods, textiles or clothing: see Cohn
2002: 29, 31–2. However, later, in a review of my monograph on the Black Death, he
denies flatly the relevance of the concept of metastatic spread and the fact of spread by
leaps, see Cohn 2005: 1354–5. Cohn repeats this view in a recent paper, Cohn and
Alfani 2007: 178.
4
Shrewsbury 1971: 29–34.
5
Twigg 1984: 100.
6
A.H. Thompson has written two valuable papers on the mortality of the beneficed
clergy in the Black Death which will be discussed at some length below in the chapter
on seasonality. See also the bibliography.
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152 chapter four
northern diocese were on the increase soon afterwards. As we have seen,

bubonic plague can be excluded from the reckoning if these facts are cor-
rect, and there is no reason to doubt them.7
Objections against this account of the spatio-temporal pattern of spread
are not important at this point; I cite the passage to illustrate the implied
unconditional view that plague spreads according to a territorially
contiguous epizootic process, by direct contact between adjacent rat
colonies, and, consequently, that the Black Death could not have been
bubonic plague.
Presumably the advocates of alternative theories all adhere to this
view of the very slow territorial spread by contact between rat colonies
because it is obviously incompatible with the real spread rates of his-
torical plague epidemics. Since this can be seen as a sufficient condition
for rejecting the conclusion that historical plague epidemics were
bubonic plague, they can therefore triumphantly conclude that histori-
cal plague epidemics must have been a different disease, which justifies
their endeavours to identify an alternative disease. This erroneous view
is misleading other serious scholars in the field, derailing potentially
good research.8 The time is ripe for taking the advocates of these asser-
tions to task.
The metastatic mode of spread has long been empirically established
as a characteristic feature of the epidemiology of bubonic plague (as of
most other epidemic diseases). Since the advocates of alternative theo-
ries deny or ignore the facts on this crucial point in order to save their
theories, I will now not just paraphrase or summarise the scholarly lit-
erature on the mechanisms of spread of bubonic plague, but will supply
a broad collection of citations from the primary studies and standard
works on plague which should settle the matter definitively. However,
Cohn’s assertions on the matter in particular are so extraordinary that
they warrant some concluding remarks on the background of the evi-
dence presented.
In this chapter, the citations constituting the heart of the subject will
be presented chronologically to demonstrate the history and develop-
ment of this insight, how conspicuous this feature of plague epidemio-
logically was, how early plague researchers identified these mechanisms
7
Twigg 1984: 185.
8
Wood, Ferrel, DeWitte-Aviña 2003: 444; Drancourt, Houhamdi, and Raoult 2006:
234–41; below: 193–4, 461.
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the spread of bubonic plague over distances 153
of spread and the consistency and firm tenability of these findings over
time. Observations of these features were first made several years before
the IPRC began its work.
The first standard work on bubonic plague based on modern medi-
cal studies in India, China and elsewhere was published by Simpson in
1905. Twigg cites and refers to it twice9 and must be presumed to know
it. Nonetheless, Twigg passes over in silence Simpson’s information on
the great importance of metastatic spread, for example, that
in Canton, many persons, especially the well-to-do, removed to the coun-
try, thus forming fresh foci for its dissemination; and in the same way the
outbreak in Hongkong no doubt arose from persons having migrated
from Canton to Hongkong.10
He notes that in China, “the infection on land has followed chiefly the
routes of busiest intercourse.”11 Simpson also provides much informa-
tion on spread by leaps in India in connection with the mass exodus
out of Mumbai, for instance, when the plague epidemic suddenly
blazed up: “Fugitives from Bombay and the Bombay Presidency were
not long in carrying infection to the other provinces of India.”12 W.G.
Liston, who joined the IPRC in 1905 as the Commission’s entomologi-
cal specialist, stated in a paper published earlier the same year that
infection could be conveyed from one place to another, either by infected
rats and fleas transported by ships and trains conveying merchandise or
by infected fleas carried on the clothing of man.13
In 1906, W.B. Bannerman, the director of the modern medical labora-
tory that had been built outside Mumbai at Parel and was placed at the
disposal of the IPRC,14 published a paper in The Journal of Hygiene
where he summarized plague-related research in India:
Spread of Infection by Means of Clothes
[…] Major Collie, I.M.S. (1898), relates the following striking instance
from his experience. “A man lost his wife from plague in Bombay, and ten
days later he brought her clothing and ornaments to his house in a village
near Harnai in the Ratnagiri Collectorate. In about a week dead rats were
found in this man’s house and neighbourhood, then one relative after
9
Twigg 1984: 135, 212.
10
Simpson 1905: 62.
11
Simpson 1905: 65.
12
Simpson 1905: 71.
13
IPRC 1907f: 713.
14
IPRC 1907g: 725; Lamb 1908: ii–iii.
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154 chapter four
another sickened and died from plague, and ultimately the man himself
became the sixth victim. None of his relatives had been out of their vil-
lage. Eventually, this village and others suffered severely, and many lives
were lost. No plague cases had occurred up to the direct infection.”
Captain W. Ronaldson Clark, I.M.S. (James, 1899, p. 152) brings for-
ward several instances in which conveyance of infection by clothes seems
the most likely means of introduction in some villages in the Punjab
[…].
In the report of the fifth season of plague in the Punjab (Wilkinson
1904, a, p. 29) it is recorded: “That infection could be carried by clothes
was however recognised by the people of Ambala district fairly soon, and
in all towns the practice of burning the clothes of persons who died of
plague was introduced and acquiesced in by sweepers who had previ-
ously suffered severely from taking the abandoned clothes of the dead.”
In Patiala State it was noticed that infection was also conveyed by cloth-
ing and bedding of persons who had died from plague, and this was so
borne in upon the sweepers of Patiala that they refused to touch these
articles, which often had to be burnt where they lay in consequence
[…].
In the report in the Punjab for 1902 the following information is given
on what is regarded as “fairly definite” evidence. The mode of communi-
cation from one place to another was considered to be: “Human
communication in 88 instances. Probably human communication in
7 instances. Clothes in 25 instances. Probably clothes in 7 instances.” The
Government review in commenting on these results says (Wilkinson,
1902, p. 15), “It is therefore clearly established now that plague is spread
from infected to uninfected places almost entirely by personal communi-
cation on the part of persons who have resided in, or visited the infected
places during the existence of plague there.”
It serves to explain the infectivity of clothes so often noticed. It is prob-
ably the fleas in the clothes that are the danger, not the clothes
themselves.
We may sum up the above evidence as follows: —As regards introduc-
tion into a new area remote from a focus of disease, it seems certain that
human beings are the carriers of infection.15
Persuasive cases of spread of plague over considerable distances in
clothing were among the early observations made by British medical
personnel in India. Cohn and Twigg refer to Bannerman’s paper, which
they therefore presumably have read, but completely ignore these find-
ings, which are here presented in the form of a number of extracts that
easily could have been multiplied.
15
Bannerman 1906: 189–95, 208.
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Similar observations were made during the plague epidemics in

Australia which occurred more or less simultaneously with these early
Indian epidemics. These observations were presented in a paper pub-
lished by the distinguished leader of the combat of plague in Australia,
Ashburton Thompson, in The Journal of Hygiene immediately after the
publication of the first reports released by the IPRC. His observations
pre-date shortly the establishment of the rat-flea theory of spread over
distances by the IPRC:
Extension of local infection by contiguity
The infection always first made its appearance at some one spot; never at
more than one. From that spot it extended continuously. […] this way of
spreading I distinguish as “extension by contiguity.”
Extension of local infection per saltum
While infection was apparently present only at the point of invasion or
central focus, it often made appearance quite suddenly at some distant
point, and there created a new focus […].
It appeared that the infection could be transported safely, be planted
afar, and could there take effect. In that there is nothing novel, for the
same happens with several communicable diseases. It becomes remark-
able and important when it is remembered that, in accordance with our
fundamental observation, the infection of plague is not maintained or
diffused by communication with the sick. This way of spreading I distin-
guish as “extension per saltum.”
For convenience of description outbreaks which result from extension
per saltum may be called “sub-epidemics.” In reality they have their own
independent status. […]. The numerous secondary outbreaks which we
have witnessed were not the less independent that they were isolated by
but a mile-wide ring of plague-free houses, nor the more independent
had they occurred (as we have seen) 70 or 2300 miles away from the
point of primary invasion.16
Ashburton Thompson introduced the concepts and terms of spread or
extension by contiguity and spread or extension per saltum, in English
“spread by leaps.” These concepts and terms were, as we shall see,
accepted and used by members of the IPRC, although they often relied
on accurate descriptions rather than on specific terms and concepts,
writing that infection was transported, imported, carried, transferred
or conveyed, or with other similar words and corresponding nouns,
from one place to another. As their studies progressed, they tended to
16
Ashburton Thompson 1906: 542–3, 546, 561.
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156 chapter four
develop supplementary terminology and write for example of the,

“implantation” of infection and of infections which are “implanted.”17
Thus observations of these modes of spread of bubonic plague belong
to the initial phase of scientific plague research, before the IPRC had
set to work, as a consequence of their being very obvious features of the
characteristic modes of spread of this disease.
Ashburton Thompson’s paper can either be ignored and passed over
in silence, which is the strategy adopted by Twigg and Scott and
Duncan, or it can be viciously attacked without mentioning these
observations, which is the course chosen by Cohn (see above), in both
cases presumably because they recognized its disastrous consequences
for their own alternative theories which are based on the denial of
spread by leaps of bubonic plague.
The IPRC’s first observations on the spread of plague by the agency
of rat fleas were presented in a study of rat fleas’ willingness and ability
to use man as a host. Some central findings were:
We have made many observations which show that P. cheopis [= Xenopsylla
cheopis] will make use of man as a host, and may be captured in large
numbers on men in houses infested with rat fleas […]. We have on many
occasions caught rat fleas on our own persons, as well as on those of the
attendants […]. From the above experiments it is seen that we were able
to keep rat fleas alive for nearly four weeks by feeding them on human
blood […] (a) that they fed readily on man, and (b) that some of them
were still alive after 25 days.18
The willingness of rat fleas to attack men and the great number of fleas
involved were underlined by the outcome of another experiment.
A (vaccinated) person went inside a house in Mumbai which had been
evacuated after finds of dead rats and human cases of plague, and stayed
in one room only briefly. After he came out, a flea count was made,
with the following result: April 18, 51 rat fleas, April 19, 34 rat fleas,
April 20, 60 rat fleas.19 As Liston, a former member of the IPRC, later
commented:
It is quite possible that, had we not examined this man’s legs and removed
the fleas from them, he might have carried some of these fleas to his
home […].20
17
IPRC 1910d: 528, 534.
18
IPRC 1907e: 472–3.
19
IPRC 1907e: 474–5.
20
Liston 1924: 997. Cf. below: 164–5.
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Scott and Duncan refer to this paper, but apparently did not see these
central statements.21
Summing up their findings, IPRC also stated that this study “shows
how readily and in what large numbers rat fleas may under certain cir-
cumstances come on to man.” They also concluded that the experi-
ments “indicate that rat fleas may often be transported in this way from
place to place, especially from plague-infected houses.”22
The next step was to study the arrival of plague in isolated villages on
the outskirts of Mumbai, specifically the villages of Sion, Wadhala,
Parel and Worli. A useful illustration of the IPRC’s work and method-
ology and the observations they made in these villages is provided by
the following example from Worli village:
Jankibai was a woman close on 70 years of age who lived in Worli. She left
the village in perfect health on the 14th February to attend the funeral of
her nephew, Laxuman Narayan, who lived at 94–6 Sonapur Street in
Bombay City. Motiram Ramji, another relative of the old woman, was ill
with plague in the same house in which Laxuman had died. After the
funeral Jankibai remained on at Sonapur Street nursing this latter patient.
Dead rats had been found in the house at Sonapur Street, and many dead
rats, found in the neighbourhood at this time, were proved by us to be
plague infected. Motiram died on the 18th February. Jankibai in the
meanwhile had developed fever. She came back to Worli on the 19th suf-
fering from plague, as evidenced by high fever and a well-marked bubo
in the groin. She went to a house in Block I, building No. 54, where we
saw her on the 21st February.
Two days after Jankibai came to the village, we placed two guinea-pigs
in her house […]. One of the two guinea-pigs which had been placed in
Jankibai’s house after isolation in the laboratory died of plague on the 9th
March […].
Taking all the facts into consideration it seems to us that the guinea-
pig which contracted plague in Jankibai’s house probably derived its
infection from infected fleas imported by Jankibai from Sonapur Street
in Bombay City. This case closely resembles one recorded in Parel village.
In this instance, it will be remembered, another such woman, coming
from the city, appeared to have brought infected fleas to that village (Case
1; Parel village).23
21
Above: 88, 90.
22
IPRC 1907i: 888.
23
IPRC 1907h: 869–70.
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158 chapter four
The IPRC concluded their study of Worli village thus:

Three cases of plague which occurred in the village were investigated. It
is probable that these three cases all contracted the infection outside the
village.
In two instances there is evidence which points to infection having
been introduced in the clothing or persons of people [sic! my insertion],
and of this spreading in one instance to a guinea-pig, and in the other
instance to rats.24
Thus, at the very beginning of their studies of the mechanisms and pat-
terns of spread of bubonic plague the IPRC ascertained that plague
spread over distances, in this case from “Bombay City” into villages on
the outskirts of the city. They were also able to establish empirically at
a substantial level of tenability that in two of these cases the infection
had been imported in the clothing of a person and in a form that caused
spread of plague to a guinea-pig or rats, which strongly incriminates rat
fleas as the agent of transportation of the infection, riding in clothing
from the city into houses of the village, attacking their preferred hosts,
namely the black rat or alternatively other available rodents. This
explains also that “the carrier of the infection may not contract the
disease, as the Sion and Wadhala cases show.”25
Clearly this material exposes some central flaws of Scott and Duncan’s
work, since they repeatedly refer to this report for their views on the
role of rats in plague epidemiology,26 while maintaining throughout
their monographs that plague spreads only by contiguous contacts
between rat colonies, not by leaps. If they had really read the report,
they should have known better and ought to have eagerly acquired
more knowledge of the Commission’s work or at least have read Lamb’s
ninety-three page summary. However, as will be shown below, they
apparently had not read the IPRC’s reports, although it is a overriding
motive of their work to show that the results of the Commission’s work
is not compatible with the manifestations of historical plague epidem-
ics. Instead, they think it is adequate to build on Hankin’s pre-IPRC
paper of 1905 for their assertions regarding the epidemiology of plague
in India.27
24
IPRC 1907h: 873. The word “persons” could conceivably by a slip of the pen for
luggage.
25
IPRC 1907i: 891.
26
Scott and Duncan 2001: 72–3, 112, 357.
27
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Inspired by their early observations, the IPRC moved briskly to

expand and deepen their knowledge on the spread of bubonic plague.
First, they did so by extending their studies of the spread of plague in
“Bombay City and Island.” In their next Report (no. XXIV), Section III
is called “The Transportation of Infection to a Distance,” which all
advocates of alternative theories have avoided or evaded, whilst it
should have been of great interest and of obvious crucial importance to
their projects. The IPRC begin by stating their principal explanatory
theory:
If we can exclude modes of spread of the infection of plague other than
the rat flea, we must conclude that the transportation of infection to a
distance is attributable solely to the conveyance of the infection in the rat
flea. A little reflection suffices to show that transportation of infection in
this medium is not only conceivable, but that under certain circum-
stances it may be a very likely contingency.
They go on to discuss “Transportation in Merchandise, Grain etc.” and
“Transportation of Rat Fleas in Clothing.” The last subtitle is too brief,
since it does not reflect an important experiment described in this sec-
tion which took into account an expanded concept of implicated
textiles:
Bundles of clothing, bedding, etc, were sent to the laboratory from houses
in the City in which plague cases had occurred. The bundles after being
opened out were kept in a flea proof godown28 for several days […].
Along with the clothing guinea-pigs were placed in the godown. In some
instances the animals were allowed to run free, in other cases they were
placed in pairs in cages, the control animal being protected from fleas
either by means of a layer of tanglefoot or by a curtain of wire gauze
[…].
The result of the experiment was that two rat fleas were caught on the
animals, that one of the free-roaming guinea-pigs died from plague,
and that one of the three rat fleas caught on the tanglefoot of one of the
cages was shown to contain plague bacteria in its stomach contents.
This permitted the IRPC to conclude:
(1) that rat fleas may be transported to a distance in bedding and cloth-
ing removed from plague houses; and
28
“So convinced were Colonel Bannerman and Captain Liston of the tenability of
the flea-transmission theory that they had designed and built at the Plague Research
Laboratory, Parel, special godowns or cabins, in which it was proposed to carry out
large series of experiments to test and prove this theory.” Lamb 1908: 2, 38.
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160 chapter four
(2) that such rat fleas may prove infective if transferred to a susceptible
animal in the place to which they are carried.
We would point out that in whatever way rat fleas are transported,
whether in clothing or merchandise, they will select, when carried to
their new surroundings, either their true host, i.e., the rat, or the next
best available animal. If then infected fleas are imported into a house they
will by preference attack the rat rather than the human occupants of the
house. It is apparent from the account we have given of the rat infestation
of houses in Bombay, that under such circumstances opportunities for
transference of infected rat fleas to rats in houses are abundant. It would
appear, then, that the introduction of infected rat fleas into a hitherto
uninfected locality may lead to serious consequences by giving rise to an
epizootic amongst the rats.
It has been shown that infection may be transported to a distance by
means of rat fleas in clothing or merchandise and that such infection,
when imported into a hitherto uninfected locality, may give rise to an
epizootic in the rats.29
We may in effect complete this statement by mentioning that an epiz-
ootic among commensal rats is the point of departure of plague among
human beings in their proximity.
The following year, 1908, the IPRC published another study on fleas
containing specific subchapters on rat fleas and “The Mode of Dispersal
of Fleas.” Among their findings were:
That rat fleas may be attracted to man, jump on him but take some time
to feed on him. Plague infected fleas might in this way be carried from
one place to another without infecting the man, but would, when brought
near a rat, attack it in preference to man.
We would, however, like to draw attention to the ease with which rats
with their fleas can be transported in certain kinds of merchandise. We
have seen rats dive, as it were, into bags containing bran and disappear, so
that the bags could be moved without any evidence of the presence of the
rats within. M. rattus [= Rattus rattus, the black rat] from its habits is
particularly liable to be transported in this way […].
From what has been said above it will be apparent that merchandise
and grain, which have been visited by rats, may have fleas deposited on
them and these fleas may be transferred with these articles to distant
places […].
Fleas will be more readily carried on the clothes of a person, in that the
man who wears the clothes forms an attraction for the insects […] exper-
iments carried out in the godowns […] show how readily and in what
large numbers rat fleas may, under certain circumstances, come on to
29
IPRC 1907i: 886–90, 894.
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man, and leave us certain that rat fleas must frequently be transported in
this way from place to place, especially from plague infected houses,
where they are more likely to take to man because of the absence of their
true host.
In whatever way fleas are transported, whether in clothing or mer-
chandise, etc., they will select when carried to their new surroundings,
their true host or the next best available animal.30
Also in 1908, G. Lamb, the Director of the IPRC, published a summary
of the Commission’s studies in the period 1906–May 1907 as published
in The Journal of Hygiene, some of them in the second half of 1907. This
summary is a good alternative source of knowledge of the opinions of
the IPRC on various issues, particularly on the subject of mechanisms
and types of spread discussed here. There is no excuse for the advocates
of alternative theories not having used at least this easy way to obtain
basic knowledge of their results, but none of them availed themselves
of this opportunity. Part VII is called “The Importation of Infection
from an Infected to an Uninfected Locality.” In this part, the main
points are presented in three easily readable pages.
In conclusion, then, we may state that all evidence points to the usual
method of the importation of plague from an infected to an uninfected
locality being by means of infected rat fleas and to the fleas being brought
in by human agency, namely, by healthy men, by plague cases or in their
belongings.31
In the following years, the IPRC continued to deepen and enlarge on
these findings. In their study of plague in Belgaum, a small town situ-
ated roughly 400 km south-east of Mumbai, in 1908–9, the Commis-
sion noted that plague probably was introduced into the urban centre
from an outside village and that there arose three effective centres of
spread in the town and that, in addition, plague was transferred in a
bag of bran over a distance of about two km from the centre to the fort
on the outskirts of the town. The Commission also emphasizes that
Given an epizootic such as we have seen raging in the Market it would be
difficult to imagine more favourable conditions for the dissemination
and spread of infection than this weekly gathering afford, a spread not
only to other parts of Belgaum but to surrounding villages. The commis-
sion agents, such as those whose stores, as we have seen above, were har-
bouring plague infected rats, import and export grain etc. by road and
rail and sell it to retail and other wholesale dealers. The grain is contained
30
IPRC 1908b: 253–5.
31
Lamb 1908: 81–3, cf. 91, 93. See also IPRC 1911b: 76.
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162 chapter four
in gunny bags which are capable of harbouring not only rat fleas but rats
as well. It requires little imagination to picture what a serious danger a
market such that of Belgaum is, in times of plague, not only to itself but
to all places with which it has trade intercourse […]. There is always a
danger of importation of plague infected rats or fleas or both in the sacks
of grain and other stores that are continually being imported into these
godowns and when once introduced with the large rat population that
these buildings shelter there is nothing in he plague season to prevent the
disease spreading and an epizootic and epidemic resulting.32
As can be clearly seen, the fact of metastatic spread or spread by leaps
over small and intermediate distances is very obvious to the IPRC as is
the importance of grain and grain trade in the spread of infected rats
and rat fleas.
At about the same time, a similar study was carried out in Pune
(Poona), a city situated about 120 km south of Mumbai, with similar
results which however deepened the Commission’s understanding of
some aspects of the mechanisms of spread. As in the study of how
infection was introduced into villages outside Mumbai, special empha-
sis was put on the introduction of infection into the city. The pressure
of infection on the city was obvious; since the earliest cases of plague
were imported from Mumbai by the railway, people were either sick on
arrival and were taken to hospital directly from the train or fell sick
soon after their arrival. The IPRC suspected that the first indigenous
plague cases would be associated with the railway station. This hypoth-
esis was borne out: rats dead from plague were first found in the goods
sheds of the railway close to the station. Thus, the early history of the
epidemic and epizootic “started in the neighbourhood of the station,
the rats acquiring the disease from infection probably imported by the
railway.” The first indigenous plague case occurred in the sweeper’s
chawl, the railway servants’ quarters at the station and soon nearby
hotels and restaurants where people contracted plague and could act as
carriers of infected rat fleas to other parts of the city.33 The IPRC also
observed that a number of infective centres arose in the city that could
not be linked directly to persons coming from Mumbai or elsewhere, a
development with which they were familiar and which reflected the
fact that infected rat fleas carried in luggage or clothing would often
first seek out rats at their place of arrival and trigger an epizootic which
32
IPRC 1910c: 466–7, 470–1.
33
IPRC 1910d: 506–07.
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would run its imperceptible course and in due time manifest itself in
human cases. This pattern was particularly likely in this case because it
took only four hours by train from Mumbai to Pune. At the same time,
the IPRC were closely monitoring the situation in the part of the city
called the “Poona Cantonment.” As the epidemic situation in the region
unfolded,
large numbers of people meanwhile were flocking into the city from the
surrounding infected areas to live there with friends […] one would
expect to find therefore, first a number of imported cases of the disease,
occurring in widely scattered localities: then later a large number of
indigenous cases, also widely scattered, arising from numerous infected
centres […] especially when we bear in mind the fact that rat fleas are
readily carried by man, almost unknown to himself, from one place to
another, and that the fleas by choice select rats for their hosts rather than
man. Centres of epizootic infection arise in this way in areas where a his-
tory of the importation of the infection could only be obtained with the
greatest difficulty. The history of the epidemic in the city will be seen to
bear out this latter hypothesis.
Next there follows a detailed description of the early appearance of
plague cases which corresponds closely to this outline of the epidemic
process and to the IPRC’s notions of plague epidemiology as developed
in their research projects in the field and in the laboratory.34
Other aspects of spread over distances were studied in especially
designed research projects. Greenwood’s major epidemiological study
“On the Spread of Epidemic Plague Through Districts with Scattered
Villages,” namely villages in three districts situated in the northern
provinces of the Punjab and the United Provinces (corresponding
roughly to the present-day province of Uttar Pradesh) is of particular
interest. He was able to conclude that the origin of the great majority of
village outbreaks was the importation of the disease from elsewhere,
and the corollary that recurrence of plague could in the main be attrib-
uted to re-importation of the disease, and that the chance that a village
would be attacked increases with increasing population.35 The implica-
tion was that plague was spread by leaps between scattered villages by
human agency by old-fashioned means of transportation. It was
also shown in another study that certain regions were conspic-
uously exposed and that the proximity to habitual lines of travel and
34
IPRC 1910d: 510–18, 527–9, 534–5.
35
IPRC 1910b: 361, 363, 368, 371, 374, 377–9, 443.
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164 chapter four
transportation, especially railways, was a factor in this result; this study

also emphasized the importance of metastatic spread, this time by
modern means of communication.36
Shortly afterwards, Greenwood published yet another report on the
epidemiological structures of plague in the Punjab and pointed out,
among other things, that “effective centres of spread” arose in three
ways:
(1) By the introduction of an infected human being.
(2) By the human importation, on the person or in the clothing, of infec-
tive fleas.
(3) By the importation of infective fleas or infected rats in merchandise.
All the methods by which a centre is established ab extra, will still apply
for the establishment of secondary centres within the community, and in
addition we have to reckon with chances of spreading through the rat
population by the transference of infective fleas from individual to indi-
vidual. […] What is material, however, seems to be the apparent fact that
the extent of an epidemic must largely depend upon the number of “effec-
tive” centres established early in the epidemic. The diffusive power of
plague is evidently not so great that one “effective” centre is sufficient to
develop a wide-spread outbreak […] many conflagrations will be
required.37
Indisputably, the IPRC showed that bubonic plague was spread by
human agency both between communities and within communities
and that the central means were importation and spread by infective
rat fleas in clothing or merchandise, and that spread between contigu-
ous rat colonies was only of minor importance, the epidemic process
being mainly dependent on an increasing incidence of new “effective
centres” where each new “conflagration” tended to increase the dynam-
ics of spread by multiplicative powers. This shows how completely
erroneous Twigg’s, Scott and Duncan’s and Cohn’s assertions are with
respect to the IPRC’s views on the mechanisms and dynamics of the
spread of bubonic plague.
In 1924, Liston, formerly a member of the IPRC, published a short
outline of bubonic plague. In the part on epidemiology of plague he
takes as his point of departure the study in which a vaccinated person
on three successive days went inside a house in Bombay which had
been evacuated after finds of dead rats and human cases of plague,
36
IPRC 1911a: 47–61.
37
IPRC 1911b: 76, 78.
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stayed in one room only briefly, and attracted 144 rat fleas that were
picked off his legs (see above). He writes: “It is quite possible that, had
we not examined this man’s legs and removed the fleas from them, he
might have carried some of these fleas to his home, and there they
might have transferred their attraction to their natural hosts,” unleash-
ing a rat epizootic among the rats that would translate into plague cases
among the persons in the house. He continues:
These observations show that infected rat fleas do not generally travel
far from the spot where they left their host; they generally lie in wait
for the passing of another host. If this new host is a rat, the fleas are
readily attracted to it and may then be carried to a distance limited by
the extent of the rat’s wanderings. If the new host is a man, then the
distance over which the fleas can be carried may be considerably greater,
and will be limited by the distance and by the speed at which the man
travels.
Plague thus progresses in two very distinct ways: first, to contiguous
areas—here infection is carried chiefly by rats; secondly, to more distant
centres per saltum—in this case infection is transported by men. Men
may carry rat fleas either on their person or in their clothing, or they may
transport rats and their fleas with merchandise, in which case railways
and ships materially assist the dissemination of the disease.38
This may be considered a final summary of the IPRC’s findings. As can
be seen, Liston underscores the fact that plague spreads in two main
ways, by contiguous spread between rats and per saltum, that is by
leaps. However, in the last case, Liston clearly distinguishes between
spread by rat fleas over short or intermediate distances by human
beings in clothing or luggage, and spread over long distances in mer-
chandise by ship, railway or lorry; in a pre-modern perspective one
could also add by horse and cart or pack horse. In this way he distin-
guishes between more or less local spread in short-range leaps estab-
lishing new centres of spread in a locality in a more or less multiplicative
way and, thus, constituting an important and even crucial element
in the dynamics of the development of plague epidemics in urban cen-
tres, localities or districts; and longer distance disseminations. This
view is clearly completely compatible with the presentation of IPRC’s
work above.
The IPRC’s findings are not unique, they do not differ from the
results of epidemiological studies of the modes and mechanisms of
38
Liston 1924: 997, 999, 1001.
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166 chapter four
spread of plague elsewhere. Plague researchers working on plague epi-

demics in Egypt stated that they were of the opinion
that the creation of apparently independent foci of rat and human plague
in a town like Qûs is attributable to the transportation of infective rat-
fleas by persons who inhabit or visit infected areas in the town; these
persons may or may not suffer from plague in consequence.
The possibility of the carriage from one hamlet to another of infected
fleas by human beings is strengthened by the results of examining the
clothes of four plague patients from Atmour Mistigid. Only two P. irri-
tans [human fleas] were found in the four lots of clothes, and the num-
bers of X. cheopis were 4, 4, 4, and 1 […]. And, further, 185 X. cheopis
were taken from the clothes of three of our rat-catchers after they had
dug out [rat] nests in houses in Atmour Mistigid.39
The highly localized character of the work of these plague researchers
and its consequent short-range perspective is reflected in these conclu-
sions, which emphasize that in local towns or villages the spread of
plague is engendered by the movement of rat fleas in the clothing of
human beings.
In a manual for medical and health workers working in China writ-
ten by several leading plague specialists, C.Y. Wu agrees completely
with the IPRC and subsequent researchers’ findings that plague is
spread by infected rat fleas in clothing and goods, the central state-
ments here being enumerated from 1 to 5:
(1) “All the evidence available goes to prove rather […] that infected
fleas imported into a locality through human agency first cause
plague among the rats, than that human beings are directly
attacked.”
(2) It is accepted that “X. cheopis may be carried great distances on
human beings or in their baggage,”
(3) It is also accepted that in this part of Asia the “medium of trans-
portation of infected rat-fleas over long distances [was] by ship
transporting rice and grain,” and it is specifically mentioned that
Rangoon had acquired a “sinister reputation” as a source of impor-
tation of plague in these commodities.
(4) Wu notes that “Cotton is another effective vehicle for the transpor-
tation of X. cheopis,” and that Hirst had come to the conclusion that
39
Petrie, Todd, Skander et al. 1924: 128, 131.
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“raw cotton, weight for weight, is an even more dangerous vehicle

of X. cheopis than grain or any other kind of merchandise.”
(5) He also underlines the “ever-present menace of dissemination by
infected rats hidden in cargo or by infected fleas secreted in grain
and cotton shipments.”40
Obviously C.Y. Wu here describes spread of plague over various
distances by transportation of rat fleas in clothing, luggage or
commodities.
The term spread per saltum is used by Wu Lien-Teh in this compos-
ite standard work on plague written by several specialists and, in his
monograph on primary pneumonic plague, he distinguishes between
contiguous spread and spread per saltum for this type of plague.41 He
also cites J.D. Long’s observation in a report on plague on the
West Coast of South America, that under favourable climatic conditions,
such as low temperatures and relatively high humidities, “fleas can act as
reservoirs of plague infection, carry it over long distances and later under
favourable conditions transmit the disease.”42
In 1914, J.J. van Loghem and N.H. Swellengrebel, two Dutch research-
ers, published a study on the epidemiology of plague in Java (Indonesia)
titled “Contiguous and Metastatic Spread of Plague.” For reasons that
will become clear below, the gist of this paper will be presented in more
detail than would be necessary under normal circumstances. At the
heart of the matter is a discussion of the pace and pattern of spread as
defining features that can distinguish between modern bubonic plague
and historical plague epidemics. Van Loghem and Swellengrebel note
that
at the start of an epidemic of human plague it seems often as if the plague
has moved by leaps: the neighbouring localities of a plague infected vil-
lage remain often untouched while villages situated farther away become
involved in the sufferings […]. There can hardly be any doubt that rat-
borne plague can be introduced from far away by human agency. The
epidemic in Java is no exception in this respect. The question is how this
rapid transfer over longer distances (metastatic spread, as we will call it)
comes about.43
40
C.Y. Wu 1936a: 285–90, and 1936b: 485.
41
Wu Lien-Teh 1936b: 204; Wu Lien-Teh 1926: 182–3.
42
C.Y. Wu 1936a: 286–7.
43
“Kontinuerliche und metastatische Pestverbreitung” = “Contiguous and Metastatic
Spread of Plague.” My translation from German. See also below: 176–7, 179, 182–3.
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168 chapter four
They point out that the IPRC explained “metastatic spread over land by
the assumption that human beings transport rat fleas in their clothing
or luggage,” but also that the conditions in Java were fundamentally
different for two main reasons:
(1) because there were far fewer cases of human plague in Java than
in India, “which indicates a lower intensity of plague among
rats” and
(2) because the number of fleas on the rats was far smaller.
For these reasons “the likelihood that rat fleas would ride with human
beings and that human beings would assume a significant role in the
transfer of plague, seemed therefore at the outset smaller than in British
India,” although the occurrence of metastatic spread of plague between
distant villages had been noted and discussed with interest.
In this context, they point out that a leading Dutch medical scholar
(Dr de Vogel) had shown that in the city of Malang the centres of infec-
tion were in places where large quantities of rice were stored and then
distributed to the surrounding districts. He had also shown that the
beginning of plague epizootics in Java occurred shortly after the impor-
tation of large quantities of rice from plague infected areas abroad
(Rangoon and Singapore). Plague was first introduced into the harbour
of the city of Surabaya, and subsequently several smaller urban centres
connected with Surabaya by railway were attacked almost simultane-
ously and large numbers of dead rats were found in goods wagons of
the railway:
This indicates the predominant significance of transportation of com-
modities for the metastatic spread of plague.
This view was corroborated by a study of the clothing and luggage of
inhabitants of Malang that wished to leave the city because of the epi-
demic there. Only very few rat fleas were found, and the case was much
the same in the plague hospitals, evidence that supported
the view that it was transportation of commodities and not transporta-
tion by human agency that played a predominant role in the metastatic
spread of the epizootic. [….]
Furthermore, it has been shown that the epizootic was spread along
the lines of communication and that, in this connection, we have also
been able to ascertain the transportation of house rats and their fleas
in public means of transportation (railways, ships). We would also like
to mention that the different conditions in British India are at least
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partly due to the fact that there the flea numbers are much higher than
in Java.44
As the reader will have noted, the concept of metastatic spread appears
not only in the paper’s title, but also six times in the passages just cited
from van Loghem and Swellengrebel’s paper (other instances could
have been quoted). This suffices to show and to prove that this concept
is real and represents the same notion of the mode of spread by plague
over considerable distances that the IPRC and other plague researchers
call spread per saltum45 or spread by leaps.
This clarification is necessary to a discussion of Cohn’s misleading
assertions in his “review” of my monograph on the Black Death in The
New England Journal of Medicine:
Benedictow casts aside any rate of disease spread that was faster than he
likes: at these junctures, the Black Death made “metastatic leaps.” But
even with his various stratagems, his results still show the medieval
plague travelling 30 times as fast as the modern one—a discrepancy he
does not explain or even admit to.46
The meaning of the word ‘stratagem’ should be explained, in this case
according to Oxford Advanced Learner’s Dictionary of Current English:
“trick, plan or scheme to deceive sby [= somebody] (esp an enemy).”
This means that Cohn accuses me of doing my best to deceive col-
leagues, students and other readers who are interested in the Black
Death, and that at the heart of this alleged stratagem is the concept of
metastatic leaps. According to Cohn, then, this concept is not based on
scholarly studies and facts but is fabricated,47 in order to preserve by
dishonest means my conventional theory of the microbiological nature
of the Black Death as bubonic plague. Clearly, Cohn’s assertion is com-
pletely unfounded and untrue in every respect.
Cohn maintains that medieval plague spread thirty times faster than
modern bubonic plague. This assertion is obviously based on his false
assertion that bubonic plague does not spread by metastatic leaps. He
also asserts that
44
Van Loghem and Swellengrebel 1914: 460–1, 468, 470–80. My translation from
German.
45
See also Wu Lien-Teh 1926: 182, and 1936b: 204.
46
Cohn 2005: 1354–5.
47
See also above: 151 and fn. 3.
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170 chapter four
Historians have realized since the work of Graham Twigg, in 1984, that
the Black Death and the subtropical Y. pestis traveled at vastly different
speeds. Even with the railway and the steamship, the 20th-century plague,
because of its dependence on the homebound rat, spread overland at
about 8 miles per year, whereas the contagious Black Death almost
equaled that speed per day.48
The only correct assertion in this citation is that Twigg also claims that
bubonic plague spreads only contiguously between adjacent rat colo-
nies. However, Twigg does not assert that the modern spread rate
according to this mechanism of dissemination was “about 8 miles per
year,” since he correctly refers to IPRC’s observation on the spread rate
of contiguous rat plague (see below),49 so the spread rate of 8 miles per
year is falsely attributed to Twigg by Cohn. The assertion that the yearly
spread rate of 20th-century plague was about eight miles or 12.9 km
per year is at variance with the studies of the IPRC and subsequent
researchers on plague epidemiology broadly presented above and also
with all standard works on plague: it is simply a fictitious figure. One
could also wonder how it might be possible that so many excellent
plague researchers, many of them with strong interests in the history of
plague, should collectively have overlooked the fact that the Black
Death and modern plague “travelled at vastly different speeds.”
Accurate information on the pace of contiguous spread of plague
among colonies of black rats was obtained in one instance by the IPRC,
namely 300 feet or 91.4 m in six weeks, corresponding to 792 m in a
year. The IPRC organized some large-scale projects in order to study
the mechanisms and process of the spread of plague over considerable
distances, what they called spread per saltum50 (which Dutch scholars
called metastatic spread). The observation of the territorial spread rate
between conterminous rat colonies was made in one of several quite
remote and isolated villages on the outskirts of “Bombay Presidency”
selected by the IPRC in order to study how plague arrived.51 It was
observed in Sion Koliwada, Sion village’s northerly part (see above)
after it had been evacuated by inhabitants following the discovery of a
dead rat and the occurrence of a case of human plague.52 Thus in
48
Cohn 2005: 1354–5.
49
Twigg 1984: 131–2.
50
IPRC 1907h, 1907i, 1907j.
51
IPRC 1907h: 799–873.
52
IPRC 1907h: 805–28.
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Sion Koliwada the plague could not be spread further by the dynamics
of human agency,53 by persons picking up rat fleas in their clothing at
home or elsewhere or in locally purchased grain and redistributing
them among neighbours in a process that would establish new effective
centres of spread at a multiplicative rate, as would be the case in histori-
cal plague epidemics. The observation of spread between rat colonies
was an unplanned result of the experiment and occurred under highly
artificial circumstances.
The study corroborated (again) the by then well-established obser-
vation that plague is spread over short and intermediate distances by
persons carrying rat fleas in their clothing or luggage or to a distance
especially by transportation of certain types of merchandise by ship or
railway. The crucial part of the study of this specific case in Sion
Koliwada is that the IPRC investigated the origin of the infection there,
identified the person who had arrived with it and whence she had
arrived: “the infection of Koliwada was not of indigenous origin but
was imported, as it were by mere chance, from “Bombay City,” having
been brought by a woman who resided in an infected quarter of the
city.” In other words, plague arrived in Koliwada by a metastatic leap
trough the agency of a person coming from an infected locality. One
could also take interest in the relationship between the first find of a
dead rat in Koliwada and the subsequent first human death there in
plague, which shows that the woman had brought with her an infected
rat flea which had first sought out its natural host, a black rat, unleash-
ing an epizootic and soon the release of a swarm of increasingly hungry
rat fleas.54
Conspicuously, Cohn does not mention that the central objective of
the IPRC’s studies on the mechanisms of spread of plague around
Mumbai (and in the Punjab) was specifically to study metastatic spread
of plague, the type of plague spread which Cohn denies that the
Commission observed or found to be crucial in the epidemiology of
bubonic plague. Cohn can only make such a highly misleading and
unfair assertion as a basis for his attack on my monograph exactly
because he denies established fact, that bubonic plague spreads meta-
statically and that the usual vehicle of this mode of spread is infected
rat fleas.
53
IPRC 1907h: 827; Lamb 1908: 19.
54
IPRC 1907h: 805–7, 835.
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172 chapter four
To my knowledge, none of the scholars who has studied plague epi-

demiology in the last hundred years has suggested that bubonic plague
spreads over land by movement of black rats between rat colonies, as
maintained by Twigg, Scott and Duncan and Cohn. The fact is that the
black “homebound” rat is exactly that, and the technical names for the
animal are the Latin-derived terms “commensal rats,” meaning rats
which are associated with the table, or “domestic rats,” meaning rats
which are attached to or associated with human housing. Rats do not,
or are loath, to move “over land” but are sedentary animals seeking
shelter in burrows and nests near their source of food. If possible, they
avoid the dangers from birds and beasts of prey inherent in crossing
open land, and for the same reason they are nocturnal animals, leaving
their nests or burrows for foraging at night.55 Scholars generally deny
that bubonic plague is spread by black rats by movement over land. The
IPRC never found infected black rats at any great distance from human
habitation. Only in Java has it been reported that black rats “may be
trapped almost a kilometre along the side of roads between villages.”56
Rats are inadvertently spread in goods by human agency, by ship,
railway, cart, or packhorse, or other means of transportation.
Cohn maintains that
He [Benedictow: my insertion] speeds up the 20th-century plague by
reporting infection times only for California, where the disease is carried
by the prairie dog, not the homebound rat, and has been known to move
as fast as 15 miles per year.57
The fact is that the geographical term California is never mentioned in
my monograph which can be easily ascertained in the “Index of
Geographical Names and Peoples,” and I have never stated anything to
this effect. In order to produce this spurious assertion, Cohn must con-
fuse the pace of expansion of plague foci by wild rodents in nature58
with the spread rates of rat-plague epizootics and plague epidemics
among human beings in their human social contexts, which makes his
disparaging comment obviously fallacious and unfounded. To my
55
Pollitzer 1954: 285–6; Wu Lien-The 1936b: 213–5. In the countryside, black rats
may move from their nests and burrows associated with farm houses and into the fields
when crops are harvested, later to return to their home base. This is, then, a highly
localized cyclical occurrence.
56
Hirst 1953: 305–6.
57
Cohn 2005: 1355.
58
See Benedictow 2004: 46–8.
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knowledge, conterminous colonies of black rats which cover contigu-

ous large areas outside urban structures are not found anywhere in the
world, presumably for the reasons mentioned above.
In contrast to Cohn, and in contrast to what Cohn maintains, in all
my monographs I have endeavoured to gather all information on
spread rates of plague epidemics. In my monograph on the Black Death,
all available information on the spread of the Black Death across
Europe is presented in 180 detailed pages with an accompanying map;
the factual circumstances on the ground can be scrutinized, tested and
pondered59 (six years after its publication, no one has pointed out rel-
evant material that I missed). This material is easily accessible for all
readers interested in the material facts. Adequate information on the
findings of the IPRC on the mechanisms and patterns of spread of
bubonic plague is also presented.60 In this comprehensive work, which
takes into account contemporary means of transportation, I have found
nothing in data about the Black Death that is at variance with the spread
rates and pattern of spread of modern bubonic plague, and my findings
are broadly similar to the small material gathered by Biraben on this
topic. In general terms, the Black Death can be seen to spread over land
by an average pace of 0.5–2.5 km per day, and along main roads usually
on average by 1–2 km per day.61
It must therefore again be emphasized, now with the ample back-
ground of the facts just presented, that the observations of the IPRC on
the pace of spread of plague between rat colonies in Sion Koliwada in
the absence of human beings constituted only a tiny part of their obser-
vations on the spread of plague. The IPRC emphasize that, taking into
account spread by leaps in a normal epidemiological plague process,
many other centres of spread would arise and the spread rate of the
epidemic as a whole would be very much higher and would tend to
increase multiplicatively in the first half of the epidemic. As shown
above, the IPRC also established comprehensive evidence to the effect
that bubonic plague is spread by rat fleas in clothing, luggage and mer-
chandise by human agency, and that the spread rates of bubonic plague
under similar climatic circumstances are decided by two main factors,
59
Benedictow 2004: 44–224, Map 1 opposite page xvi.
60
61
Biraben 1975: 85–92; Benedictow 1993/1996: 78–80; Benedictow 2002: 33–8, 50;
and Benedictow 2004: 227–33, where the material is summarized and generalized. See
also the index under Plague, Pace of spread, and p. 418 for local data according to
country and region.
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174 chapter four
by the underlying rates at which human beings or commodities travel

or are transported, on foot, on horseback, by horse and cart, by railway
or by ship,62 and by the time needed for plague disease to develop at
each place of arrival. Modern bubonic plague tends to spread faster
than medieval plague because modern means of travel are much faster
and more efficient, but the type of spread is metastatic. Cohn’s assertion
flies in the face of the obvious outcome of elementary analyses and
comparison of the means of transportation in the Middle Ages with
modern means of communication and transportation. The discrepancy
that he presents as scientific “truth” is therefore merely something
invented by him.
Cohn unconditionally denies all of these facts, asserting that
against earlier speculation [fn. 14], the commissioners [of the IPRC: my
insertion] found that plague was not transmitted through clothing or
baggage of travellers, or other effects of infected persons.
In footnote 14, Cohn cites The Journal of Hygiene, Vol. 7, 1907, page
541, as corroborating evidence where, according to Cohn, the IPRC
state:
We have no ground for suspecting that the infection of plague can be
spread by clothing, bedding or other articles of household use.63
In fact the citation comes from The Journal of Hygiene 1906, p. 541, in
the paper by J. Ashburton Thompson which Cohn used to level the
accusation of racism discussed above and found to be groundless
(above: 46–50). This means that Cohn’s line of argument is doubly false
and misleading: the citation is not taken from a publication by the
IPRC and it does not represent the Commission’s opinion, in fact, it
does not relate to any Indian experience at all. Ashburton Thompson’s
paper presents and discusses the findings of Australian scholars under
his leadership who studied a number of small plague outbreaks in
Australia in the period 1900–5. These plague epidemics occurred in a
population overwhelmingly of British extraction and culture and living
in a modern social system with modern medical education and facili-
ties and level of hygiene. In these circumstances, it is not surprising
that transportation of rat fleas in “clothing, bedding or articles of house-
hold use” was of no significance. However, as shown above, “Ashburton
62
Cf. Wu Lien-Teh 1926: 182–3.
63
Cohn 2002: 28.
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Thompson introduced in relation to plague epidemiology the concepts

and terms of spread by contiguity and spread per saltum,” thus, he made
it clear that plague did not only spread contiguously but also, and very
importantly, spread by leaps (metastatically) and in this way established
new and independent epicentres of epidemic spread which greatly con-
tributed to the pace and dynamics of spread. In the quite comprehen-
sive citations from Ashburton Thompson’s paper above, which easily
could be multiplied, this is made abundantly clear. Ashburton
Thompson explains that in Australian society plague was spread per
saltum by transportation of “produce-trade in hay, straw, chaff in bags,
maize and potatoes.” He emphasizes the difference between the mecha-
nisms and dynamics of spread of plague and suitable measures for the
combat of plague in modern Australian society and in traditional
un(der)developed Indian society, which is the basis for Cohn’s mali-
cious attack on him for racism. This means that Ashburton Thompson’s
findings and conclusions cannot be taken in support of Cohn’s position
and that Cohn unavoidably must know this fact. Thus, in flagrant con-
tradiction of both Ashburton Thompson’s and the IPRC’s clearly stated
views, Cohn takes Ashburton Thompson’s paper falsely in support of
his own position after having transformed it from the work of the “rac-
ist” Asburton Thompson on plague in Australia into a study by the
IPRC’s on the pattern of spread of plague in India.
Since the IPRC’s results on the mechanisms of spread by leaps by
human transportation of infected rat fleas represent a dire threat to
Cohn’s alternative theory, their work cannot be presented correctly. He
endeavours to convey the impression, by reiteration as it may seem,
that their findings support his view. He makes, for instance, a similarly
misleading reference to the IPRC in his paper in The American
Historical Review 2002 in order to be able to defend his repeated asser-
tions that the IPRC found that plague can only spread contiguously
between conterminous rat colonies and therefore exceedingly slowly,
only 300 feet in six weeks.64 In footnote 51, he purportedly refers for
support to the “Indian Plague Commissions,” but none of the refer-
ences is to any member of the the preliminary fact-finding Indian
Plague Commission or of the Indian Plague Research Commission
which replaced it in 1905. The reference to IPRC 1907h: 839, pertains
64
See Cohn 2002b: 712, and fns. 51–2 where he misrepresents IPRC 1907 e,g,h,i.
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176 chapter four
to the end of a small preliminary survey of the findings in Sion

Koliwada but he avoids the substance of the study of this village and
also the early part of the survey where it is stated, for instance, on page
735, that “the available evidence inclines strongly that the infection in
Koliwada was not of indigenous origin but was imported, as it were by
a mere chance, from Bombay City, having been brought by a woman
who resided in an infected quarter of the city.” He also avoids the final
summary of this report on page 873 where it is stated that positive
evidence had been adduced that contagion was introduced into these
villages by transportation of rat fleas in the clothing of persons. Cohn’s
assertion that studies of other villages had shown the same slow spread
as evidenced by the special study in Sion Koliwada is not correct and
the implication that this should also be corroborated by the same refer-
ence to IPRC 1907h: 839, is therefore also not correct. As emphasized
above, the study of these peripheral villages outside Mumbai was
designed to find out exactly how plague was transported from the city
to the villages, it was designed to study spread of plague by leaps, exactly
the opposite of what Cohn claims. In reality, nothing supports Cohn’s
statement that “Without the assistance of the railway or the steamship,
the fourteenth-century disease spread almost as fast per day over land
as modern plague does per annum.”
In his “review” of my monograph in The New England Journal of
Medicine, Cohn attributes to the IPRC that the assertion that
from studies of the clothing and luggage of tens of thousands of people
migrating from plague-stricken regions, the plague commissioners con-
cluded overwhelmingly that Y. pestis was not transmitted by these
means.65
As so often, Cohn presents this assertion without a supporting foot-
note. However, the IPRC have made no such study and drawn no con-
clusion to this effect. Possibly, Cohn has attributed to the IPRC the
study in Java by van Loghem and Swellengrebel presented above where
such a research project is described and the results are cited and
explained,66 at least this is the only study I know that fits the descrip-
tion. If this is the case, it would be remarkable that Cohn pretends not
to know the term ‘metastatic spread’ which is the central subject of the
paper and which is included in the title, and that he does not discuss
65
Cohn 2005: 1354.
66
Above: 167–9; below: 182–3.
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the Dutch researchers’ explanation which incorporates this finding

within the conceptual framework of the theory of plague epidemiology
constructed and established by the IPRC. The true epidemiological
findings of IPRC are presented above and document the completely
misleading character of Cohn’s assertions. In fact, Twigg also mentions
the terms contiguous and metastatic spread of plague in a brief com-
ment on these observations in Java.67 Thus Cohn, who repeatedly refers
to Twigg’s monograph, certainly had the opportunity to acquaint him-
self with this term there. I note that Cohn repeats this false assertion in
his “review” of my monograph on the Black Death as evidence that my
epidemiological analysis is unfounded and deliberately misleading.68
In support of his assertions on these crucial points of plague epide-
miology Cohn refers also to a paper by Pollitzer and Meyer from 1961,
page 435. On this page, nothing in support of Cohn’s assertion is men-
tioned, but on the contrary, it is stated that plague “is primarily an
insect-borne, especially a flea-borne, disease.” Thus, this is also a false
reference. Twenty pages later Pollitzer and Meyer comment directly on
the means, modes and mechanisms of spread and their true views on
the matter can be ascertained beyond doubt or dispute from this
quotation:
A distinction has to be made between what Gill adequately called the
“intramural” spread of the disease from one house, block or part of a set-
tlement to adjacent houses, blocks, or precincts or, as observers in Java
have called it, “metastatic” spread.
It is easy to understand how plague, conveyed either by the rats them-
selves or by their fleas, may creep from one house or group of houses to
others […]. Such a spread of the infection may be extremely slow. One
instance has been reported in which a rat epizootic in India took six
weeks to travel 300 feet (approximately 91 m.) [….]
The question of whether active movements of the rats are responsible
for the long-distance spread of plague, and if so to what extent, has been
the subject of considerable debate. In the opinion of the Plague Research
Commission, this factor was of no importance because the spread of
infection per saltum was effected by the passive transportation of rats or
their fleas by goods or human traffic. This opinion has been shared by
most subsequent observers.69
67
Twigg 1984: 131; see below: 181–3, Twigg explains away the Dutch researchers’
findings with respect to metastatic spread and provides no reason for why they needed
this concept.
68
Cohn 2005: 1354.
69
Pollitzer and Meyer 1961: 454.
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178 chapter four
Here it is unequivocally stated by two of the Grand Old Men of plague

research that the IPRC rejected the theory that long-distance spread of
plague takes place through dissemination between rat colonies. Instead,
the IPRC concluded on the basis of great research efforts that contigu-
ous spread was not important for the spread of bubonic plague but that
saltatory or metastatic spread was of pre-eminent importance, and this
view has later come to be shared by most scholars observing plague
epidemics in the field. This is why this view is emphasized in all stand-
ard works on plague. This is what Twigg, Scott and Duncan, Cohn and
other advocates of alternative theories purportedly have collectively
failed to notice. They maintain that they have only noticed the tiny
remark on contiguous spread in Sion Koliwada on page 827 in a paper
of seventy-five pages, also that this is the main topic of the Report con-
taining the study of plague in Sion. The great mass of research on salta-
tory spread has been overlooked by the advocates of alternative theories.
Also this citation of Pollitzer and Meyer confirms that Cohn’s denials of
the reality and concepts of metastatic spread or spread per saltum are
made against his better knowledge.
Furthermore, Pollitzer and Meyer return to the question of spread
per saltum. In a sub-chapter titled “Role of Flea Transport in the Spread
of Plague,” they first state:
Fleas can be passively transported by (1) their specific hosts or temporary
hosts […]; (2) transport vehicles; (3) the persons or the baggage of travel-
ers; and (4) the movement of goods.
While it is generally admitted that plague-infected fleas may be carried
on the persons or in the baggage of travelers, in the opinion of most
observers this means of spreading plague is of comparatively limited
importance, and, in particular, is never responsible for a carriage of the
disease to far distance localities.
Most observers agree that the transport of infected fleas in goods, par-
ticularly in grain, raw cotton, gunny bags, rags, and hides is of great
importance in the spread of plague.70
This shows that Pollitzer and Meyer support the view that bubonic
plague spreads by metastatic leaps or per saltum, but that they, like
Hirst, place less emphasis on the importance of transportation of rat
fleas over great distances in clothing or luggage, and more on the
importance of transportation in commodities by railway or ship. This
70
Pollitzer and Meyer 1961: 469–70. Cf. Pollitzer 1954: 335.
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should be compared with the continuation of Cohn’s assertion cited

above:
Instead, adult fleas outside their normal host, the rat, rarely live more
than five days and do not travel in passengers’ baggage, in wool packs, or
cotton bales as recent historians such as Le Roy Ladurie, John Aberth,
and Norman Cantor for medieval Europe, [fn. 15] Paul Slack for Tudor
and Stuart England, [fn. 16] Ole Jørgen Benedictow for late-medieval
Scandinavia, [fn. 17] and Klein for twentieth-century India, [fn. 18] con-
tinue to report as solid epidemiological facts of modern plague.71
As can be readily seen, Cohn’s assertion that all these serious historians
have fabricated similar erroneous and misleading assertions to the
effect that rat fleas were transported over long(er) distances in various
types of goods, but also in the luggage of travellers, is without founda-
tion. On the contrary, as shown above, the IPRC, van Loghem and
Schwellengrebel, Pollitzer72 and Meyer,73 Hirst,74 and C.Y. Wu,75 all
strongly support this view. Much eminent scholarly work has produced
a truly impressive corpus of evidence to the effect that bubonic plague
is mainly spread over short-range and medium-range distances by rat
fleas in clothing or luggage and over longer distances in grain, rice, raw
cotton, textiles and other commodities, and all leading plague research-
ers agree on the importance of these means of spread. This view is also
comprehensively presented in all standard works on bubonic plague.
Cohn’s assertions to the contrary are unfounded, and his disparaging
characterisations of plague historians groundless.
Cohn argues that spread of plague over distances cannot occur
because “fleas outside76 their normal host, the rat, rarely live more than
five days.” This assertion is based on obsolete research from the very
infancy of rat-flea studies, research that was soon corrected. In the
words of Hirst:
The contention that rat fleas, when separated from their host, have too
short a life to survive long journeys in the midst of merchandise and then
transmit the plague bacillus, has substance when the climatic conditions
en route are exceptionally unfavourable and not otherwise […]. In the
light of recent research it is evident that rat fleas are much hardier than
71
Cohn 2002: 28–9.
72
Pollitzer 1954: 385–7, 389–90.
73
See Pollitzer and Meyer 1961, and the preceding pages here.
74
Hirst 1953: 306–13, 316–23.
75
C.Y. Wu 1936a: 285–90; 1936b: 485.
76
Presumably he means away from their hosts.
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180 chapter four
was formerly imagined. Earlier ideas on this question were based mainly
on the results of experiments on the viability of starved fleas isolated in
test tubes. We now know that experiments on the bionomics of fleas in a
highly unnatural environment are very apt to be misleading. In this
respect the observations of Estrade [fn. 8577] on the prolonged survival of
X. cheopis in cereal dust in Madagascar are especially relevant […] long
after the rats have died of plague […] Not infrequently such infected fleas
are transported considerable distance by human agency and give rise to
sporadic outbreaks of plague at destination […].
At temperatures below 15° C. the chief vector of bubonic plague
[X. cheopis] can certainly survive in a very heavily infected state for at
least fifty days […]. Macchiavello has found X. cheopis still alive after six
months unfed in a protected rat burrow (personal communication).78
[.…] It is highly improbable, however, that the maximum longevity of
unfed, infected rodent fleas is known.79
Since ships appear to have sailed, on average, around 40 km per day in
the Middle Ages,80 a voyage of fifty days would correspond to a distance
of 2000 km; in natural conditions of 27° C X. cheopis transmitted plague
after 29 days of starvation,81 corresponding to transportation over a
distance of 1160 km.
Clearly, Cohn’s assertion flies in the face of basic facts and misrepre-
sents Pollitzer’s and Meyer’s view on the matter, and also the view of all
other serious scholars who have studied the epidemiology of plague.
His disparaging remarks on historians are unwarranted.
Twigg was the first advocate of an alternative theory of plague who
denied the reality and importance of metastatic spread of plague by rat
fleas, a denial of which all later advocates of alternative theories have
availed themselves. Twigg’s point of departure is a double assertion:
(1) there were hardly black rats in medieval Europe, thus, there could
not have been bubonic plague.
(2) “An important aspect of plague spread is the continuity across a rat
population.” Since bubonic plague spreads contiguously only
between conterminous rat colonies, contiguous distribution of this
animal must be a necessary condition for spread over distances, it
is impossible that the Black Death or medieval plague epidemics
77
Hirst refers to Estrade 1935.
78
This piece of information can be found in a paper by Machiavello published in
1917, see Pollitzer and Meyer 468, fn. 74, p. 586.
79
IPRC 1914a: 437; Hirst 1953: 322–4.
80
Benedictow 2004: 102–3, fn. 20.
81
Hirst 1953: 330–1; Pollitzer and Meyer 1961: 468.
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could have been bubonic plague: “If it is assumed that rat popula-
tions were contiguous throughout the region—and they would
need to have been—then the rate of spread across France is as fol-
lows […].”82
These assertions are presented as objective facts. The comprehensive
empirical material documenting the reality of the broad presence of
the black rat all over medieval Europe, also in the northerly parts of the
Continent, has been presented above, and Twigg’s denial is untenable.
No plague researcher has ever asserted that colonies of black rats are
distributed contiguously over the landscape and as such could provide
the basis for contiguous territorial spread over districts, areas, regions
or countries.
About seventy pages later,83 Twigg’s line of argument takes a different
turn. He states, seemingly on the basis of an independent reading of the
works of IPRC, that:
From their experiments the Plague Research Commission concluded
that the spread of infection at a distance was effected by infected fleas
carried either on a person or in the bedding of travellers who had either
lived in plague houses or had visited them.
Although this is not incorrect, it is, as shown above, highly unrepre-
sentative since the IPRC rapidly reached the conclusion that infected
rat fleas in various types of goods also played a major role in the spread
of plague over distance and with increasing importance with the dis-
tance (see also below). Twigg does not refer to the works of the IPRC in
a footnote; the reason is that he has in fact based his discussion on a
chapter in Pollitzer’s monograph of 1954 titled “Role of Flea Transport
in Spread of Plague,” but only discusses it very selectively in a small
sub-chapter called “Transport by Travellers and their Baggage.”84 Twigg
goes on to state that such persons would not be bitten and infected
themselves, which is not correct: it is quite a usual occurrence.85
82
Twigg 1984: 57–9, 100.
83
Twigg 1984: 128.
84
Pollitzer 1954: 386–7.
85
This may or may not occur depending on the duration of starvation of the rat flea
from the time it leaves a dead rat and the time of the person’s arrival at the destination,
since rat fleas of this type normally endure about three days of starvation before they
attack human beings. Apparently, Twigg insouciantly cites Pollitzer’s statement that
“such fleas [that were carried on persons or in bedding] were not directly responsible
for the causation of human plague (even the travellers carrying flea-infested baggage
were able to escape infection) […]”: Pollitzer 1954: 386.
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182 chapter four
However, the main point is made, namely that the IPRC were of the
opinion, based on their empirical studies, that rat fleas in the clothing
or luggage of persons moving from a plague infected place to an unin-
fected place would on arrival at the destination preferably seek out rats
in the immediate proximity, and thus could trigger a rat epizootic and
spread plague over a distance. Next, Twigg continues to follow Pollitzer’s
text (without acknowledgement) and mentions that Petrie and Todd
[and Skander et al.] reached the same conclusion in Egypt. Then, Twigg
sets out to refute the tenability and significance of these opinions.
He does this by paraphrasing in a highly selective fashion Pollitzer’s
presentation which is a tertiary source based on van Loghem’s and
Swellengrebel’s brief presentation of the results of Dr de Vogel’s large-
scale study of the clothing of plague refugees from Malang and
of patients in plague hospitals there which produced insignificant
evidence of rat fleas.86 This study has been quite thoroughly discussed
above and the reason for this finding and de Vogel’s conclusions pre-
sented. Twigg omits the title of van Loghem’s and Swellengrebel’s paper
which contains the terms contiguous and metastatic spread which are
at the centre of the paper’s contents and restricts his discussion to con-
tiguous spread87 in accordance with his need to make bubonic plague
theory incompatible with the epidemiology of historical plague.
However, on methodological grounds it is impossible to reject the
validity of the empirical findings of the IPRC in India or of the research-
ers in Egypt of rat fleas in clothing or bedding on the basis of different
results in Java. These findings in India and Egypt remain tenable and
valid, as do similar findings in Madagascar and South America men-
tioned on the same page by Pollitzer, and results from China could
have been added. In order to refute these findings, Twigg would have to
show that they were untenable and based on invalid studies, or else he
would have to search for an empirical explanation of why the case
should be different in Java. However, the strong limitations of this
approach, which leaves unaddressed the great mass of evidence to the
contrary elsewhere, would not provide the general refutation which his
theory requires.
Like Cohn, Twigg fails to cite or consider the Dutch researchers’
explanation of the outcome of Dr de Vogel’s study, which explanation
underscores the special conditions underlying this finding in Java,
86
This study is cited and discussed at some length above: 168–9.
87
“Kontinuerliche und metastatische Pestverbreitung” = “Contiguous and Metastatic
Spread of Plague.”
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namely that both the intensity of plague was much lower and the num-
ber of fleas on rats was much lower than in India. Consequently, the
incidence of rats dying from plague was much smaller and also the
number of fleas leaving each rat dead from plague was much smaller,
facts that epidemiologically relate multiplicatively to each other and as
such produce a corresponding order of reduction of the number of
infected rat fleas which could attack human beings in Java compared to
the situation in India. In short, the chance that plague-infected rat fleas
would attach to clothing or bedding was much smaller in Java than in
India or Egypt. As shown above, the two Dutch scholars incorporate
their findings on plague in Java within the conceptual framework of the
theory of plague epidemiology established by the IPRC. Dr de Vogel’s
findings in Java do not falsify the findings in India or Egypt or else-
where, but serve only to describe a special case that can be adequately
explained and understood within the framework of the established rat-
flea theory of the spread of bubonic plague. Twigg’s attempt to refute the
rat-flea theory of the spread of plague in clothing, bedding or luggage is
methodologically and empirically invalid and dependent on a flawed
and selective presentation of van Loghem’s and Swellengrebel’s paper.
However, the rat-flea theory of the spread of bubonic plague also has
another dimension, namely spread over considerable or long distances
in merchandise. Again the discussion will be based on a citation from
Twigg’s monograph which will shed light on his way of arguing his case
on this crucial point:
Pollitzer (1954) says that one ought to agree with the opinion of Hirst
that, in general, a spread of flea-borne plague through travellers is of
comparatively limited importance.
The transport of infected fleas in goods, especially in raw cotton, gunny
bags, rags and hides is generally agreed to be of great importance in the
spread of plague. There has, however, been plenty of debate on just how
far the infection can be carried by such fleas. Hirst (1931) said that the
available evidence pointed to the fact that when an overseas source of
infection was only a few days away, an infected flea might be readily
transferred directly in grain from the port of origin to the port of entry
but otherwise it would be inferred that a plague epizootic had occurred
among the rats aboard ship […].
After examining various evidence of plague transport, Pollitzer (1954)
concluded that it was unlikely that long-distance transportation of infected
fleas played a generally important role in plague dissemination.88
88
Twigg 1984: 129.
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184 chapter four
Twigg unfortunately omits a crucial word in his citation of Pollitzer’s

1954 text on the types of goods that are especially important for the
transport of infected rat fleas, namely “grain,” which can be seen from
the verbatim citation of this point in Pollitzer and Meyer 1961 cited
above on page 178. The meaning or conclusion Twigg here endeavours
to achieve and convey to his readers is obviously at variance with the
citations above from Pollitzer and Meyer, which gives grounds for
scepticism. In the first passage, the central point is associated with the
words “travellers” and “comparatively little importance.” The word
“travellers” should be seen in light of the problem of transportation of
plague over considerable or great distances. It is in this connection that
Pollitzer and Hirst opine that transportation in the clothing or luggage
of travellers is of comparatively little importance, that is in relation to
other means of transportation of plague. This passage should be seen in
immediate connection with the following passage. Here the crucial
words are “generally agreed,” i.e. Twigg suggests that it is the general
opinion of plague researchers who have studied the mechanisms of
spread of bubonic plague that transportation of infected fleas in goods,
in raw cotton, gunny bags, rags and hides, is of “great importance” in
the spread of plague over considerable or great distances (a fact flatly
denied by Cohn, as we have seen). As can be seen from the citations
above, the IPRC and the research team in Egypt maintained that they
had succeeded in showing that plague was distributed locally or at rela-
tively short distances by rat fleas in clothing, bedding or luggage, and
that this process by engendering new centres of spread fuelled the pow-
ers of spread of local epidemics.
The heart of the matter according to Pollitzer’s text is very different
from the meaning Twigg attributes to him in his presentation, because
he has omitted the crucial passage. This passage addresses the question
of whether metastatic leaps of plague are mainly effected by the trans-
portation of rat fleas in goods or by transportation of infected rat fleas
on rats in goods. On this issue, Pollitzer takes a clear stance that Twigg
does not mention, namely:
There can be no doubt, therefore, that infected rats, rather than infected
fleas, carried in consignments of goods are responsible for this dissemi-
nation of the infection.89
89
Pollitzer 1954: 389–90.
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Based on the passages cited above it is clear that among serious schol-
ars of plague research there is no disagreement that bubonic plague
spreads by metastatic leaps or per saltum. And clearly Pollitzer is of the
same opinion as other plague researchers on this point, that metastatic
spread is of great importance. There is, however, a debate on the rela-
tive importance of the various mechanisms which effect spread over
considerable or great distances. To be more precise, at the centre of this
discussion is the question of whether this transportation to a distance
is dependent on the presence of rats with which rat fleas can travel for
a substantial part of the voyage, or whether rat fleas can make a long(ish)
voyage on their own. Twigg misrepresents Pollitzer’s view on the mat-
ter by using an incomplete citation which omits Pollitzer’s central
opinion.
Pollitzer’s opinion is also of great interest in relation to Twigg’s view
that the Black Death could not have been transported all the way from
Constantinople to Italy on board the big Italian galleys that sailed this
route, which ships certainly could accommodate more than one rat
colony. One must take into consideration the fact that from the infec-
tion of a rat colony on board it would be about twenty-one days before
the first death among the people on the ship, providing that the rat fleas
did not find new rat hosts in another colony which expanded into the
area of the decimated rat colony in order to take advantage of their
food resources, and the whole process would have to be repeated.90
A few other clarifying comments are warranted in relation to Hirst’s
opinions, since Twigg attributes to Hirst the view that plague could not
be transported over long distances by ships, for instance the 1985 km
from Rangoon in Burma/Myanmar to Colombo in Ceylon/Sri Lanka
even by steam ship,91 which makes it surprising that plague could have
been transported the much longer distance from Hong Kong to Kolkata
(Calcutta) in 1896. Since it is well known that around 1900 plague was
transported repeatedly by steam ships all the way from India to England,
obviously with infected rat fleas which triggered outbreaks of plague
on arrival, Twigg’s opinion would appear to go against observed fact.
Surprisingly, eighteen pages later in a chapter called “Twentieth-
Century Plague in Britain […]” Twigg mentions a number of these
outbreaks, for instance in Glasgow, Liverpool, Cardiff, Hull, Bristol,
90
Below: 582–3.
91
Twigg 1984: 129.
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186 chapter four
London, and Freston (Suffolk), and he could also have mentioned other
instances of long-distance transportation of plague to Australia, the
Americas, and so on. Unexpectedly, Twigg refers to Hirst’s monograph
of 1953 for support,92 and he could therefore also have cited Hirst to the
effect that “the disease broke out in Hong Kong in 1894 and com-
menced to spread overseas to the ports of several continents,”93 which
seems to indicate that Hirst considered spread over much longer dis-
tances than from Rangoon to Colombo as fully possible. Twigg’s state-
ment of Hirst’s purported view to the contrary eighteen pages earlier is
supported by a reference to a rather peripheral work by Hirst published
in Sri Lanka (Ceylon) in 193194 that is very difficult to get hold of, at
least my efforts have not succeeded, although the librarians at the
University Library of Oslo are excellent. One could suspect that Twigg
has taken the reference from Pollitzer’s monograph.95 However, Hirst’s
excellent 1953 monograph on plague provides easy access to his views
on all matters of importance, and moreover gives his final views after
he had had the opportunity to bring together and structure his vast
knowledge of the scholarly literature on plague and his unique per-
sonal experience in the laboratory and in the field and in the combat of
this epidemic evil. This is, of course, the work that Twigg should have
used, and Hirst’s opinion is clear. His opinion on the matter is cited at
length above in my discussion of Cohn’s assertions; Hirst emphasizes
that rat fleas are much hardier than formerly assumed and that such
fleas in moderately warm and humid circumstances can survive unfed
and in heavily infected conditions under transportation for at least fifty
days.96 Seen against the background of the usual situation on board
ships which commonly contain several rat colonies, this fifty-day inter-
val could be activated after a considerable time at sea, producing a
much longer total duration of journey for infected fleas as they succes-
sively found new hosts on rats invading the territories of rat colonies
decimated by plague which could not any longer defend their food
92
Twigg 1984: 147–8.
93
Hirst 1953: 332.
94
L.F. Hirst, The protection of the interior of Ceylon from plague with special reference
to the fumigation of plague-suspect imports. Municipal Printing Office: Colombo,
Ceylon 1931.
95
See, for instance, Pollitzer 1954: 387or 404; Pollitzer and Meyer 1961: 467–71,
585.
96
Above: 179–80.
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resources. In this context, a brief supplementary citation from Hirst’s

monograph removes any doubt about his opinion on the subject:
In view of the observations on flea longevity shown on pages 330–1, there
seems no reason to doubt the theoretical possibility that infection might
be carried in the bodies of live, unfed fleas half-way around the globe.97
If we consider these diverse materials together, it might seem that
Pollitzer and Hirst tend to underrate the great importance that the
IPRC attribute to transportation of merchandise for the spread of
plague over considerable or long distances. In the case of spread over
short or intermediate distances, the commissioners seem to put some-
what more weight on the significance of rat fleas in clothing, bedding
or luggage. In general there is great continuity in the views on the
mechanisms and modes of spread of bubonic plague, but it is also clear
that there are regional variations due to differences in climatic and
social conditions and customs, traditions of clothing, communication
technology and social structures.
Spread per saltum or metastatic spread explains the ability of bubonic
plague to spread quickly over long distances, particularly by ship, but
also to some extent by land with transportation of goods, or over
shorter distances in the luggage of travellers or in people’s clothing.
This must also have been the case under medieval conditions when
ships sailed at an average pace of forty km a day, so that infected rat
fleas surviving for fifty days could have travelled 2000 km, and as we
have seen, there are good reasons to assume that the duration of their
survival at sea and the distance they travelled could easily have been
considerably longer. Much evidence to this effect is presented in my
monograph on the Black Death.98 The findings of the IPRC and other
modern researchers in frontline combat of plague during the first half
of the previous century in this respect are contrary to what is loudly
asserted on their behalf by the advocates of alternative theories.
Scott and Duncan insist repeatedly that bubonic plague spreads only
contiguously between rat colonies,99 and despite the abundant docu-
mention that the disease has spread spread per saltum, they repeatedly
97
Hirst 1953: 327.
98
Benedictow 2004: map by p. 1, 20, 227–3, for general discussion, and Index under
Metastatic spread p. 418 for accounts of concrete events. See also the comprehensive
discussion below.
99
See for instance Scott and Duncan 2001: 45–6, 57, 79–80, 98–9, 280–1, 350, 358,
361, 383, 394.
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188 chapter four
deny that bubonic plague can spread by “saltatory”100 movement or

“transmission,” for instance:
these stories of a blocked flea carrying bubonic plague over very long
distances through the countryside and starting an epidemic are quite
impossible.101
They make this same denial in a passage which is so comprehensively
flawed that the constituent assertions must be enumerated for com-
ments following the quotation:
[1] Bubonic plague could not have spread in the saltatory fashion seen in
many of the epidemics in England and, particularly, in France when it
jumped more than 30 miles in a few days with no intermediate outbreaks.
In the outbreak at Malpas [Cheshire] (section 9.3) it travelled nearly 200
miles in this way. The speed of this transmission is completely inconsist-
ent with bubonic plague: [2] the Plague Research Commission (1907a,b)
gave an example where the epidemic [sic!] in rats took 6 weeks to travel
300 feet; [3] this slow diffusion is one of the most common characteris-
tics of bubonic plague and [4] we see this pattern in the hinterland of
Marseilles in 1722 (Chapter 12). [5] Bubonic plague in South Africa in
1899–1925, moved about 8–12 miles per year and this spread may have
been aided by steamtrains (Twigg, 1984). [6] The Black Death, in stark
contrast, spread from the toe of Italy to northern Europe in 3 years
[…].102
(2) Scott and Duncan contend that “The speed of this transmission is
completely inconsistent with bubonic plague: the Plague Research
Commission (1907a,b)103 gave an example where the epidemic [sic] in
rats took 6 weeks to travel 300 feet.” The first of these reports does not
relate to questions of spread rates but to other aspects of the role of rats
and rat epizootics in Mumbai and is not relevant for the subject in
question. The second report is relevant and is a careful and detailed
study how plague spread from Mumbai to villages on the outskirts of
100
Scott and Duncan 2001: 317, 347, 358, 361, 372.
101
Scott and Duncan 2001: 262–3. This assertion should be seen in relation to their
great efforts to prove that the famous epidemic at Eyam (Derbyshire) could not have
been bubonic plague.
102
103
The two reports are: (1) Indian Plague Research Commission. 1907g. Reports on
Plague Investigations in India, XXII. “The Epidemiological Observations made by the
Commission in Bombay City.” The Journal of Hygiene. 7: 724–98; and (2) Indian Plague
Research Commission. 1907h. Reports on Plague Investigations in India, XXIII.
“Observations made in four villages in the Neigbourhood of Bombay.” The Journal of
Hygiene. 7: 799–873.
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the city. In other words the report is a study of metastatic spread or

spread per saltum, also called saltatory spread by Scott and Duncan,
exactly the opposite of what Scott and Duncan maintain is the typical
or normal pattern of spread of bubonic plague. Within this large-scale
study, the IPRC also made some incidental observations which have
been referred also above, and will now be repeated since all advocates
of alternative theory cite this account of slow spread rate but all are in
denial regarding the contextual facts. Sion was one of the villages stud-
ied, and the observation area in question was in a part of this village
called Koliwada after it had been evacuated by the inhabitants after the
find of a dead rat and the occurrence of a case of human plague. Thus,
the plague could not be spread further by the dynamics of human
agency, and for this reason this case is not directly comparable to epiz-
ootic spread in populated environments; rather it is a study of spread
under artificial conditions.104 The IPRC succeeded in identifying the
person who had brought with her an infective rat flea from a contami-
nated part of Mumbai. This case history provides a corroboration of
the rat-flea-based theory of saltatory spread. The fact remains that
Report XXIII by the IPRC provides a comprehensive collection of
material on and analysis of saltatory spread by bubonic plague—this is
the purpose of the Report, and strong empirical confirmation of the
process was observed and reported. If Scott and Duncan had read the
report, it is a serious matter that they pretend not to know this; if they
have not read it, it is also a serious matter, because it would demon-
strate unsatisfactory attitudes to scholarly research and the responsibil-
ity of honesty to readers. They have these serious issues in common
with all other advocates of alternative theories.
(2 + 3) It has been shown above in this chapter that the IPRC did not
think that slow diffusion is the characteristic pattern of spread of
bubonic plague. The Commission maintain that plague is spread
according to at least two main patterns, by contiguous spread and by
metastatic spread.
(1 + 4) These assertions deny central epidemiological facts relating
to the pattern of spread of historical and modern bubonic plague. It has
been documented above that bubonic plague spreads at rates and in a
pattern corresponding to the ways and means of movement, travel and
104
IPRC 1907h: 807–28, the oft-mentioned finding on the spread rate under these
conditions is found on page 827.
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190 chapter four
transportation of persons and goods. The fact that many times there
are not intermediate outbreaks between an established plague centre
and an outbreak some distance away is characteristic of the metastatic
spread of bubonic plague; neither of the two examples or illustrations
mentioned provides any proof that it was not bubonic plague, but are
compatible with the pattern of metastatic spread of bubonic plague.
(4) Here Scott and Duncan misrepresent the realities of the epidemic
in southern France in 1720–2 and indeed their own knowledge of it. A
few pages earlier, in their discussion of this epidemic which Scott and
Duncan in the face of overwhelming evidence, must admit was bubonic
plague, they also have to concede that there “were examples of saltatory
behaviour.”105 This is a minimized admission of the facts. Instead of
addressing the evidence for saltatory behaviour, they endeavour to
convey a picture of an epidemic spreading slowly and contiguously,106
and claim that:
The epidemic continued to spread slowly from these foci to the east of the
Rhône, affecting neighbouring villages […] the movement was gradual,
travelling to nearby localities, but there were examples of apparently sal-
tatory behaviour.107
However, metastatic spread was the ordinary, dominant way this great
epidemic of bubonic plague spread in Provence, the Comtat and the
Languedoc, at short distances or over hundreds of km. This can be eas-
ily ascertained from Biraben’s lengthy discussion of it in the first vol-
ume of his plague history to which Scott and Duncan also refer. It can
be easily ascertained also by studying Biraben’s chronological table
of the attacked localities which shows the beginning and end of
the epidemics. The point can be illustrated by a small excerpt from the
first page relating to the year 1720: 1 August – Aix; 1 August – Apt;
2 August – Vitrolle; 7 August – Sainte-Tulle; 8 August – Riez; 15
August –Aubagne; 15 August – Mayrargue; 15 August – Mirabeau and
Les Pennes-les-Septèmes; 15 August – Gignac; and so on. As can be
readily seen, the plague appeared simultaneously or almost simultane-
ously over considerable distances with no intermediate outbreaks, and
this occurred all over these large regions.108 Biraben himself is
very clear on this point and directly contradicts Scott and Duncan’s
105
106
Scott & Duncan 2001: 346–51.
107
108
Biraben1975: 240–87.
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endeavours to minimize the prevailing saltatory pattern of spread to a

distance when he states:
If one marks on a map all the localities touched by the epidemic, it is
remarkable to ascertain that, far from spreading between neighbour-
hoods, it is compartmentalized in small centres [“foyers”], almost all iso-
lated from each other by parishes that remained healthy […]. This
extension did not, by the way, come into being by chance, but mainly
along the roads […] the chronological order is not the same as the geo-
graphical succession [of localities] out of […] a result of transportation
by human beings.109
Thus, Scott and Duncan’s assertion that bubonic plague in Southern
France in 1720–2 predominantly and typically spread contiguously and
in accordance with the observation by the IPRC that plague in an
instance used six weeks to move 300 feet [91.4 m) is not correct.
(5) “Bubonic plague in South Africa in 1899–1925, moved about
8–12 miles per year and this spread may have been aided by steam
trains (Twigg, 1984).” As will be clear from the discussion of Scott and
Duncan’s presentation of purported South African evidence on the epi-
demiology of bubonic plague above,110 their assertion on this point is
misleading. This observation does not relate to contiguous spread
between rat colonies, but relates to the spread and development of a
plague focus among wild rodents, predominantly gerbilles. This devel-
opment was reflected in a highly sporadic incidence of cases of bubonic
plague among human beings with an average of 2.2 cases per incidence
and 1.4 deaths. This is not an epidemic of bubonic plague, but an epi-
sodic endemic manifestation of enzootic plague among rural rodents,
and consequently there is no case of spread of a bubonic plague epi-
demic based on black rats in South Africa and no evidence of spread
rate.
(6) Scott and Duncan’s assertion that the Black Death spread from
the toe of Italy to northern Europe in three years is erroneous: the Black
Death did not spread contiguously from Italy’s toe, it arrived by long-
distance ships in Genoa and Venice whence it spread into parts of
France and Central Europe; it spread from the original epicentre of
Marseilles to the northerly parts of Europe in a process that comprised
a number of metastatic leaps, as I show in my monograph on the
109
Biraben 1975: 285–6. My translation from French.
110
Above: 87–90.
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192 chapter four
Black Death and as can easily be ascertained by a glance at the map in

that book.111
After having rejected the microbiological evidence produced by M.
Drancourt and D. Raoult in two papers of 1998 and 2000 to the effect
that the identity both of modern and historical plague contagion was
Yersinia pestis on the basis of speculative arguments about laboratory
contamination, which arguments are shown to be groundless below in
Chapter 10 (and having apparently overlooked two other studies
(namely nos. 3–4 in Table 6), J.W. Wood, R.J. Ferrel, and S.N. DeWitte-
Aviña had cleared the ground for arguing against the bubonic-plague
theory. Firstly, they have maintained that a difference in the temporal
progression of the Black Death as reflected in institutions of (new) par-
ish priests (after the incumbents’ death) in the diocese of Coventry and
Lichfield in 1349 and general mortality of bubonic plague in Kolkata
(Calcutta) (1903) constitutes evidence that the Black Death could not
have been bubonic plague. According to the principles of comparative
methodology, I cannot accept that a comparison can be valid and ten-
able when performed without active interest in the significance of
spatial-territorial, urban-rural, housing-related, religious, cultural,
political-organizational, public sanitary, medical, and climatic differ-
ences.112 These are all societal dimensions that make for vast differences
in the interrelationship of behavioural patterns and physical structures
with epidemic disease, even the same epidemic disease. The territorial
and demographic comparability of modern Hong Kong, Kolkata or
Mumbai around 1900 with archdeaconries in the diocese of Coventry
and Lichfield at the time of the Black Death seem unconvincing, a point
that the authors appear eventually to realize but not really to under-
stand.113 The central methodological question must be asked: is it not
similarity of historical circumstances that make phenomena in pari
materia and comparable, and must not historical, cultural and societal
structures therefore be made part of the study? Should not differences
of circumstances be carefully taken into account in order to explain
differences of manifestation in different countries and different histori-
cal periods? Is it not only when intensive study of the differences of
circumstances and their significance has failed to provide explanatory
grounds and culture-specific and period-specific factors of causation
111
Benedictow 2004: 50–224, map xviii–xix.
112
Wood, Ferrel, and DeWitte-Aviña 2003: 429. Ibid.: 436–7, 441.
113
Wood, Ferrel, and DeWitte-Aviña 2003: 436–7, 441.
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have been eliminated that the comparison can be taken further and
resemblances determined, because this analytical and methodological
process has established elements that are in pari materia? Finally, they
admit that the inference from the comparison of such diverse materials
from so different cultural and organizational settings so many centu-
ries apart “can be challenged on both statistical and substantive
grounds,” however, the main objections are methodological. When
such methodological weaknesses are linked with erroneous assertions
which limit the spread of plague to contiguous spread between rat col-
onies,114 the outcome will be invalid.
Metastatic spread of bubonic plague was observed in the last large-
scale epidemics of this disease, although none of the advocates of alter-
native theories has taken notice. The observations of American
physicians during the Vietnam War are summarized by Butler who
present “three factors responsible for the spread of plague,” of which
the second factor is of interest to us:
2. Transportation network. Vehicles carried goods from remote villages
to cities, junks and boats transported goods between coastal cities, planes
shared in the transportation of passengers, and highways were
built. Thus, plague spread from provinces, which were considered as foci,
to neighboring provinces along the ways of communication and
highways.115
The importance of grain transports was also noted, since plague often
arrived in an uninfected locality or town with shipments of rice,116 as
was observed also by plague researchers working in Asia half a century
earlier.117
Summing up, all advocates of alternative theories misrepresent the
work, research and opinions on the mechanisms and modes of spread
of plague published by leading plague researchers, from the IPRC to
Hirst and Pollitzer. Spread of bubonic plague by leaps over short or
long distances is at the heart of their work and their understanding of
the disease’s powers of spread.
114
Wood, Ferrel, and DeWitte-Aviña 2003: 444.
115
Butler 1983: 37.
116
Marshall, Joy, Ai et al. 1967: 604–5, 610.
117
Above: 166, 168, 179. Cf. Benedictow 2004: 20–1.
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CHAPTER FIVE
MORTALITY IN INDIA
Effects of the Anti-epidemic Efforts by British Colonial Authorities
In the previous chapter, the subject was introduced of the great efforts
made by the British colonial authorities in India to combat plague
immediately after its outbreak in Mumbai in 1896. This provides a
background for discussions of the assertions first made by Twigg and
after him by Karlsson, Cohn, and Scott and Duncan to the effect that
the consistently relatively small human mortality rates in India, in
sharp contrast to the mortality rates caused by the Black Death, show
that the late medieval and early modern plague epidemics must have
been different diseases.1 Some of these scholars correctly point out a
clear difference in the distribution of mortality, specifically that multi-
ple plague cases in the same household were rather “uncommon” in
India,2 but usual in historical plague epidemics, a fact they argue con-
stitutes an independent argument to the same effect.3 Recently, related
assertions have been presented by other scholars with respect to the
dissimilarity of the temporal progression of mortality in Kolkata
(Calcutta) in 1903 and in the Black Death. It may seem that this misun-
derstanding or misconception is taking hold.4
At the heart of the matter is the fact that all of these advocates of
alternative theories have overlooked or ignored important differences
between India around 1900 and historical Europe of the plague era
which make their use of comparative methodology fallacious. Firstly,
they appear to have overlooked the fact that when, in the decades
around 1500, it was more widely recognized in Europe that plague was
a communicable disease, this brought about great and decisive change.
In their monograph, Scott and Duncan mention related subjects on
1
Twigg 1984: 187–9, 195–9; Karlsson 1996: 283; Cohn 2002: 2; Cohn 2005: 1355;
2
IPRC 1907i: 878–81; IPRC 1907j: 922, 956.
3
Cohn 2002: 102, 119–21; Cohn 2005: 1354; Cohn and Alfani 2007: 179, 194–6,
202–3; Scott and Duncan 2001: 361.
4
Wood, Ferrel, and DeWitte-Aviña 2003: 429.
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mortality in india 195
pages 118, 204, 278, 283, 358, 366, 379, but without taking them into
consideration or understanding the implications, as it seems. Although
this early epidemiological theory was distorted by many misconcep-
tions and an incomplete understanding of the epidemiological proc-
esses, it nonetheless gave rise to important notions to the effect that it
was important to avoid contaminated houses or areas and clothing or
goods coming from contaminated persons or areas, and that plague,
consequently, could be effectively combated by administrative counter-
measures like quarantines of ships, isolation of infected communities
and diseased persons, trade embargoes, and so on. On this basis,
European governments and municipal authorities soon drove plague
back to such an extent as to allow vigorous population growth and
recuperation of pre-plague population levels.5 This means that mortal-
ity from plague at a generalized demographic level of analysis was
reduced to about the average annual level of mortality found in India
around 1900 and in the following couple of decades, that is, to a level
compatible with population growth. Around the middle of the seven-
teenth century, European authorities succeeded in stamping out the
plague from most of Europe, namely the modernized parts (and, thus,
with the exception of Russia, parts of Eastern Europe and Turkish
Balkan), rearing its ugly head only on a few occasions when it suc-
ceeded in slipping through the anti-epidemic barriers.
Against this background, I find it entirely reasonable that the British
colonial authorities in India, by using the same countermeasures from
the very beginning of the outbreak of plague, including at the outset
some of the misguided ones, made substantial and comparable success
in the combat of the disease. Lamb, the Director the Indian Plague
Research Commission, begins the preface to his summary of the
Commission’s research up to May 1907 with the following statement:
In the early days of plague in India most strenuous efforts were made to
stamp it out by the means adopted in European countries in dealing with
epidemic disease.6
5
England’s population started to grow some time in the second quarter of the 1500s
(about the same time as in Norway). It is well known that England’s population did not
reach pre-plague levels until hundred years after plague disappeared. However, the rea-
son that England’s population recuperated later than most other populations must
therefore be unrelated to plague and appears primarily to be associated with the early
and strong transition to the so-called western European marriage pattern character-
ized by relatively late age at marriage and relatively high percentage of permanently
celibate persons and consequent relatively low fertility.
6
Lamb 1908: i.
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196 chapter five
Thus, from the very beginning of plague in India the British colonial
authorities made enormous efforts to combat the disease, and although
mistakes were made, especially with respect to the cultural differences
between Europeans and Indians in the face of epidemic diseases, these
mistakes were soon corrected and the measures adapted to Indian soci-
ety (see above). This puts into perspective Cohn’s assertion that “the
British medical corps in India faced the plague’s mounting annual
death tolls from plague with fatalistic resignation.”7
It is true that the British colonial authorities were confronted with the
very unmedieval problems of mass transportation of people and goods
by railway and steam ships. On the other hand, they enjoyed important
advantages over their European predecessors: the new sciences of bac-
teriology and epidemiology provided a far better framework for inte-
gration of empirical observations into a rapidly developing factual
understanding of the processes of transmission and dissemination of
plague. Of particular importance was the fact that they had at their
disposal a vastly superior and larger organization which permitted
comprehensive control of travellers and of the transportation of goods.
They could also almost immediately implement mass vaccination, and
millions of doses of Haffkine’s anti-plague vaccine were administered.8
The truly gigantic scale of the measures implemented from the very
beginning can be indicated by mentioning that in February 1897, six
months after the appearance of plague, the Municipal Council of
Mumbai employed a staff of 30,699 persons in anti-plague work. All
travellers leaving infected localities by road or rail were medically
inspected, and systematic medical inspection of fugitives from Mumbai
by rail was initiated as early as October 1896. When Kolkata (Calcutta)
was believed to be threatened, 1,800,000 travellers were medically
inspected, 40,000 detained as suspects, and so on. Mass flight out of
these cities when plague broke out was partly a solution, and partly a
problem to be confronted.9
Importantly, the climate allowed the widespread use of mass evacu-
ation of populations of infected villages into nearby camps. In this
7
Cohn 2002: 240, repeated verbatim in Cohn 2002b: 738. He refers for support to
Hirst 1953: 451, where the perspective is very different but not to the relevant pages
that would demonstrate that his assertion is contrary to fact and Hirst’s real opinion,
Hirst 1953: 115–8, 416–7.
8
Sticker 1910: 438–61. Cf. Simpson 1905: 402–9.
9
Hirst 1953: 115–8, 416–7.
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early phase, the best measures to restrict mortality from plague proved
to be
evacuation of infected areas and so-called “health camping,” the effects
of which were reported to be “almost magical”. When the population
of an infected area could be deported in bulk into the country, leaving
the rats behind them, plague returns fell with striking rapidity to zero.
Such measures were practicable and were carried out in the case of small
towns and villages, but were impracticable in large towns such as
Bombay.10
The early conviction among British medical personnel and British
authorities that house rats played an essential part in plague epidemics
and the early observation that immediate evacuation of the popula-
tions of infected local towns and villages into camps in nearby fields
until the plague season was over functioned perfectly in the sense that
not a single certain instance of a person infected with plague in any of
these camps was ever recorded:
it is well known that the evacuation of an infected village by its inhabit-
ants and their removal into a temporary camp, if only a short distance
away, is one of the best measures for checking an outbreak of plague.11
This gave the anti-plague campaign organized by the British authorities
a great and effective strategy which was implemented on a grand
scale.
In 1907, the British colonial Government appointed a committee of
influential Indian gentlemen and placed in their hands funds to be used
for measures against plague. This enlightened committee carried out an
extensive scheme of operations which resolved itself in instructing the
people by holding public meetings and circulating popular pamphlets on
the most recent views of the manner in which plague is spread, and urg-
ing and encouraging the people by pecuniary assistance and otherwise
(a) to resort to evacuation of their houses as soon as rats were observed
to be dying, and before cases of the disease occurred among the house-
hold, (b) to be inoculated with anti-plague vaccine if evacuation was not
possible, (c) to destroy rats.12
Soon, the Indian population recognized the dangers when a person
suddenly died from plague or they came across a rat fall in the plague
10
Brownlee 1917–8: 130; the quotation is taken from a comment by a physician who
took part in the anti-epidemic work in India at the time.
11
IPRC 1907i: 882.
12
IPRC 1910d: 497.
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198 chapter five
season, and it became usual that they immediately and on their own
initiative emptied their villages and moved into temporary camps in
the fields. For instance in the case of Sion Koliwada:13
On 28th January the occupants of [building] A14 according to their own
admission found a dead rat in their house and threw it away. On the same
day these people and their neighbours in the other house of the building
vacated it and went to live in a building a short distance away, namely
building C […].
By the 11th February the Koliwada inhabitants with a few exceptions
had removed to a temporary camp in the neighbouring fields a few hun-
dred yards from the village. This action on the part of the villagers was
undoubtedly the outcome of severe lessons learnt during the earlier years
of plague in Bombay. For the past four or five years [1901–2] they have
been accustomed, acting on their own initiative, to leave the village and
to go into camp whenever human deaths associated with dead rats begin
to occur.15
Similarly, the inhabitants of Belgaum evacuated their dwellings and
went to live outside the city, also in huts especially constructed for the
purpose, either when there was a plague case in their vicinity or in their
family, and also when dead rats were found in their houses—this
“caused householders to suddenly vacate their houses.”16
Much of this can be summarized and illustrated by the case of Pune
(Poona), a city situated roughly 120 km south-east of Mumbai.17
According to the Government’s guidelines, the chief measures that
were adopted until 1907 had been disinfection of infected houses with
perchloride of mercury, evacuation of infected houses (when they were
not disinfected), isolation of the sick in hospital and inoculation with
anti-plague vaccine: there were both a General Plague Hospital and
hospitals in the administrative divisions of the city called cantonments
to which plague patients were admitted. Also, a campaign against rats
had been in force in the city for some years, a rat catching staff had
been established consisting of a “Rat Inspector” and ten “coolies” work-
ing under the supervision of the Health Officer of the Municipality.
13
Koliwada is Sion village’s northerly part. Map I on Sion village, IPRC 1907h: by
page 800.
14
Building A refers to Map II–III on Koliwada, Map II–III, IPRC 1907h: by page
802.
15
IPRC 1907h: 806, 808.
16
IPRC 1910c: 452–3.
17
See also above: 162–3.
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The Health Officer was responsible for registering all plague cases and
to implement suitable anti-plague measures. According to the munici-
pal authorities, during the epidemic of 1908–9 4,900 persons occupied
municipal huts in the plague camps, and 5,000 persons lived in private
huts in the fields; they also estimate that 15,000–20,000 persons left the
city for the surrounding towns and villages. This indicates that around
one-fourth of the city’s population evacuated their houses during the
epidemic. Furthermore, 16,998 persons had been inoculated with anti-
plague vaccine.18
Thus, there was in operation a comprehensive anti-epidemic organi-
zation which worked efficiently in accordance with modern epidemio-
logical and bacteriological principles and with considerable means at
its disposal in order to reduce the impact of plague on the population.
The IPRC characterized these anti-plague measures as “elaborate
arrangements for the suppression of plague,” emphasizing particularly
the importance of the large-scale implementation of preventive vacci-
nation and “the enormous extent” of evacuation, and concluded that
“these measures had a marked effect in checking the epidemic.”19
Compared with the epidemiological understanding and the adminis-
trative counter-epidemic methods at the disposal of early modern
European municipal and government organizations there can be no
doubt that the Indian anti-plague organization which operated in Pune
was greatly superior. Nonetheless, the historical European authorities
succeeded in driving back and eventually in defeating plague and keep-
ing the scourge out of their countries with only a few unfortunate epi-
sodes. Why should British colonial authorities in India have not had
even greater success?
Evacuation of infected local societies as an integral part of the strat-
egy for combating plague is the reason why multiple cases of plague in
Indian households were quite rare, in contrast to the situation in medi-
eval and early modern Europe. As the IPRC stated in connection with
local studies of plague: “evacuation of houses soon after the finding of
plague rats in them appreciably reduces the incidence of plague among
the occupants.”20 I have also pointed this out in a paper published in
Population Studies in 198721 which was known to Scott and Duncan,
18
IPRC 1910d: 497–9.
19
IPRC 1910d: 534.
20
IPRC 1907j: 959.
21
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200 chapter five
who refer to it twice but failed to take into account its central points,
which go directly against their theory (see below).22 Since the extent and
effects of evacuation in India appear to be poorly understood or known,
I here provide a footnote with several references for further reading.23
When Cohn and Alfani in 2007 repeat that the usual incidence and
pattern of clustering of multiple cases in the early modern Italian urban
centres of Milan and Nonantola is very different from the pattern in
India, this does not, as Cohn and Alfani assert, prove that the epidem-
ics were different diseases, since they have not taken into account the
effects of the gargantuan anti-epidemic measures implemented in India
on the basis of rational modern medicine and epidemiology and the
significance of differences with respect to climate and other factors.24
Further, the observation that household members tended to fall ill and
die in close succession does not, as Cohn and Alfani assert, prove that
historical plague was a viral disease spread by cross-infection: the IPRC
commission observed in village studies of bubonic plague in the Punjab
that “when multiple cases did occur in a house they were attacked prac-
tically simultaneously, as if from a common source of infection.”25 The
explanation is associated with the process of the rat epizootic. As rats of
a plague-infected rat colony die off, their fleas leave their dead hosts’
bodies and gather on the remaining living rats. When a colony of house
rats is severely decimated, over a hundred rat fleas are usually released
from each dead rat and they have great difficulties of finding a new rat
host. At this point of the rat epizootic suddenly over a hundred and
very soon hundreds of rat fleas, many of them infective, swarm in the
immediate proximity of the household members, which means that
they will be infected closely in time and exhibit the epidemic pattern of
falling ill almost “simultaneously, as if from a common source of
infection.” Thus, there is nothing pertaining to the Indian plague
epidemics with respect to pattern of spread, household clustering of
cases or mortality that can be used as evidence against the notion that
historical plague epidemics were bubonic plague.
22
Scott&Duncan 2001: 315, 377.
23
Bannerman 1906: 186; IPRC 1906a: 468, 480–1; IPRC 1907f: 711; IPRC 1907h:
806, 808, 812, 828, 830, 833, 840, 842, 870–1; IPRC 1907i: 882; IPRC 1907j: 958–9;
IPRC 1908c: 294; IPRC 1912: 210–2; Lamb 1908: 18, 25; Liston 1924: 998. Hirst 1953:
416–7.
24
Cohn and Alfani 2007: 177–205. See also Cohn 2002: 119–21; Cohn 2005: 1354.
25
Lamb 1908: 65.
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For climatic reasons, European populations could not so readily

evacuate their houses, but I have noted some examples from fifteenth
and sixteenth-century Europe of mass exodus from plague-infected
towns into the immediate surroundings, in Alessandria in the Pied-
mont and in Poitiers in western France, respectively.26 The affluent
classes which could afford to leave and stay away for the duration of the
epidemic may, to some extent, have practised evacuation from the very
beginning, as is suggested, for instance, by Boccaccio in his introduc-
tory description of the Black Death in Florence in the Decameron.27 In
sixteenth-century Scotland, evacuation of infected houses was imple-
mented on a more systematic basis.28 This behaviour can only be
explained on the basis of concrete observation of the plague’s attach-
ment to houses and locality and that moving out was a good way to
avoid the disease. Of course, in the case of diseases spread by interper-
sonal cross-infection, by droplets or otherwise, such action would be
useless and quickly revealed as such by the epidemic’s immediate con-
tinuation among the evacuees. Analytically, this type of action must be
distinguished from another behavioural strategy for evading plague:
“When the plague hit an urban center, most of those who could afford
it left the town for the countryside.”29
With this background in mind, it would in fact be difficult to under-
stand how high mortality rates, rapid succession of multiple cases, or
household clustering of cases could become usual in India, in other
words, how the manifestations of plague in India could be similar to
the manifestations of plague in late medieval and early modern Europe.
The advocates of alternative theories have ignored important research
bearing on the matter, excepting Cohn who, as shown above, makes
misleading assertions instead.30 Since they have not taken into account
important differences between the two parts of the historical compari-
son, their use of comparative methodology is fallacious. Clearly, the
underlying observations are explicable in terms of the effects of anti-
epidemic organization and epidemiological knowledge of plague.
It is not correct that modern bubonic plague did not retain its inher-
ent ability to cause great mortality. Where traditional administrative
26
Roccatagliata 1976: 210; Favreau 1967: 354–5.
27
Boccaccio 1982: 11–6.
28
Simpson 1905: 348.
29
Cipolla 1981: 102.
30
Above: 26–69.
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202 chapter five
structures more or less broke down and countermeasures of European

origin were weakly or reluctantly applied for cultural reasons, as in the
case of the Mandarin authorities, bubonic plague showed its old epi-
demic might. In 1894, probably 70,000 and perhaps as many as 100,000
persons died from plague in Canton. In sharp contrast, when plague
reached Hong Kong later the same year, the British authorities managed
to keep the mortality down to about 3,000 persons, demonstrating the
great efficiency of European epidemic countermeasures.31 To this day,
no one has doubted that this was the same disease and contagion that
reached India in 1896 in a long-distance metastatic leap by ship. There,
the British authorities immediately implemented the same epidemic
countermeasures as in Hong Kong, only on a much larger scale, demon-
strating their excellent administrative skills and putting to good use the
rapidly improving knowledge of the nature and epidemiology of plague
disease and recently developed vaccines,32 all to very good effect.
One of the previous century’s leading historical demographers,
R. Schofield, asked some acute questions in the analysis of the data
resulting from a family-reconstitution of the population of Colyton
which was ravaged by the plague epidemic of 1645–6. The town con-
tained a population of 1513 inhabitants of whom 298 or about 20 per
cent died. He pointed out the crucial distinction that strong clustering
by household would indicate a disease spread by the rat flea, while a
strong association with household size would indicate a disease spread
by cross-infection, because if the disease was spread by cross-infection,
infection rates should increase with increasing family size and the con-
sequent increasing household density and intensity of interaction. If
this was not the case, the disease would have to be transmitted accord-
ing to a different mechanism, as for instance in the case of bubonic
plague from rats to human beings by the agency of rat fleas. He there-
fore organized his material on deaths also according to the size of
families. The conclusion of the analysis was that “person-to-person
transmission of the disease in close physical proximity was not an
important element in the Colyton epidemic.” This analysis was followed
by another in which the number of persons dying in families was cor-
related with size of family. It appeared that
the number of families with extreme experiences (no-one dying; every-
one or almost everyone dying) was greater than would be statistically
31
Hirst 1953: 103; Wu Lien-Teh 1936a: 20–1.
32
Simpson 1905: 402.
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expected by chance, and the number of families with some people dying
and others surviving was correspondingly far fewer than would be statis-
tically expected by chance. There was therefore a marked tendency for
deaths to cluster in some families, and for other families to escape the
epidemic altogether.
The outcome indicated that a person’s chance of dying “had little, if
anything, to do with the size of household in which he lived”. Schofield
concluded therefore that “it points to a disease whose distribution is
largely determined by ecological factors, and the most promising can-
didate would seem to be bubonic plague with the rat flea as the signifi-
cant vector.”33
Thus, clustering of deaths in families is not a one-dimensional,
mechanical manifestation of an epidemic process. It contains impor-
tant epidemiological and sociological information which can be
revealed by the acute and creative mind of a dedicated scholar and can
provide important evidence that historical plague was bubonic plague.
For two main reasons, it should not come as a surprise that the
British authorities did not succeed completely in their endeavours to
stamp out plague:
(1) As mentioned above, the Indian population in accordance with

ancient traditions and beliefs in relation to epidemic disease
resisted some of the effective countermeasures based on modern
scientific medicine or European experience. As pointed out by
Lamb,34 this resistance caused “the extension of the disease”;
(2) Plague in India found an extra-urban murine basis for continuous
enzootic existence, which functioned as a murine plague reservoir
(plague focus) from which new outbreaks could easily spring.35
In practice, it was impossible to root out murine plague in the large
cities like Mumbai where the rat populations were so immense that
33
34
Lamb 1908: i.
35
For the period before the Indian Plague Research Commission, see for instance
Simpson 1905: 333–456; Indian Plague Commission. Minutes of Evidence: 1998–9;
Hankin 1905: 75–6, 78–9; Bannerman 1906: 186, 197–9; Lamb 1908: 25. I would like to
underscore the importance of Simpson’s work, the first standard work on plague
written on the basis of the early development of modern scientific medicine and on
the basis of observations of plague epidemics and plague cases on a large scale. It
surprises me that it is possible to read this work and the works of the IPRC and not
note the comprehensive anti-epidemic measures that were implemented by the British
authorities in India, and see their efforts as a great success story of early modern
European governments. See also Hirst 1953: 115, 117, 131–2, 416–7.
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204 chapter five
they could bear the continuous circulation of plague for many

years, causing a number of cases between large-scale outbreaks,
much as in London in the period 1550–1670.
Some of the anti-epidemic measures applied by the British colonial

authorities in India from 1896 were undoubtedly misguided and pos-
sibly to some extent counterproductive, especially in the early years,
much like the measures applied by early modern authorities. However,
they made tremendous achievements, as did early modern European
authorities in their combat of plague, by relying on the notion of con-
tagiousness, although they were otherwise dependent on misconceived
theories of epidemic disease. For these reasons, it is an error to think
that the quite small mortality rates in the Indian plague epidemics con-
stitute evidence that late medieval and early modern plague epidemics
were two different diseases. It is also an error to assume that differences
in clustering constitute evidence that these waves of epidemics were
two different diseases.
It is completely untrue that the British colonial authorities made
these huge efforts to save lives from plague for any other reasons or
motives than European authorities would try to protect their own pop-
ulations, as Cohn falsely asserts, making groundless accusations of
Imperialistic callousness (see above).
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CHAPTER SIX
WAS HISTORICAL PLAGUE A VIRAL OR BACTERIAL DISEASE?

THE QUESTION OF IMMUNITY
Introduction
Cohn and Scott and Duncan advocate alternative theories to the effect
that historical plague was a viral disease and maintain, in accordance
with this view, that survival of plague infection provided persistent and
strong immunity. As a rule, bacterial diseases confer only modest and
transient immunity in survivors who therefore may repeatedly fall ill
from the same bacterial diseases; it is viral diseases such as small pox,
chicken pox, measles and mumps that produce persistent and strong
immunity in survivors. Most medical authorities on plague who had
the opportunity of observing large plague epidemics in the first dec-
ades of the twentieth century agree that survival of plague infection
conferred only weak and transient immunity (see below).1 If the obser-
vation or assertion were correct that survivors of historical plague dis-
ease acquired strong and persistent immunity, it would constitute
substantial evidence that historical plague epidemics could not have
been bubonic plague or indeed any other bacterial disease, and proba-
bly was a viral disease instead. Since this type of assertion, like the
assertions on the manifestations of plague discussed above, tend to fal-
sify the bubonic plague theory and to justify the search for a tenable
alternative, this subject of immunity must also be examined sufficiently
thoroughly to decide the matter. Twigg, who advocates a bacterial
alternative, has not recognized that there is such a problem and does
not discuss it, which in itself can be taken as an indication of the weak-
ness of this case.
Theoretically, a dangerous epidemic disease producing high mor-
bidity and lethality rates can produce a violent reduction of a popula-
tion, but some essential distinctions must be made. Diseases producing
strong and persistent immunity in survivors are characterized by strong
1
Benedictow 1993/1996: 126–30.
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206 chapter six
limitations with respect to possible long-term demographic effects. In

naïve populations (i.e. populations without prior experience with the
disease) exceeding 500,000 to one million persons, after a first onslaught
which may be dramatic, such diseases will recur in the constituent local
societies normally in a five to ten year cycle, in the meantime circulat-
ing elsewhere. This is the period needed to bring into existence suffi-
cient numbers of interacting persons without previous infectious
experience with these pathogens to allow rise of epidemic spread
among them (as distinct from endemic spread). In other words, in
ordinary populations there must have come into being a sufficient
number of susceptible children to assure that each case of an epidemic
disease will be transmitted to at least one other child or susceptible
person,2 otherwise no epidemic will arise and the disease’s presence
will take on an endemic (sporadic) pattern or disappear. The older
populace will contain too large proportions of resistant survivors to be
much involved in the epidemic. In the typical mortality pattern of, e.g.,
smallpox, the rate of mortality in no age group older than 5–10 years
amounts to even one-fifth the rate in the age group 0–5 years.3 Even
smallpox, which is characterized by high virulence and extraordinary
powers of spread, will therefore normally produce modest general
mortality rates in populations where adult generations have previous
infectious experience with the disease. Scott and Duncan correctly
point out that recovered “persons were immune to the smallpox virus
for a long time so that each new epidemic swept with high infectivity
through only the children who had been born in the interim, of whom
about 20% died […].”4 This corresponds to a rate of population mortal-
ity of a few per cent, which does not prevent local or regional societies
from rapidly recuperating their demographic strength and producing
population growth between epidemic outbreaks, so that this epidemic
pattern is compatible with long-term population growth.
This is a specific reflection of a general pattern which ensures that,
in substantial populations, recurrence of acute infectious diseases
which produce strong and persistent immunity in survivors will nor-
mally have quite limited demographic effects over quite short periods.
In order to cause a large-scale and protracted diminution of the
2
Cf. Scott and Duncan 2001: 37–8.
3
Greenwood 1935: 240.
4
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was historical plague a viral or bacterial disease? 207
population like those witnessed in Europe in the late medieval period,

a disease must display a pattern of dramatic recurrence, sparing no
substantial sections of the populations. Obviously, epidemic diseases
which do not produce good persistent immunity in survivors will have
much larger powers of spread, recurrence and mortality than diseases
conferring persistent immunity. Consequently, other factors being
equal, they will also tend to produce much higher mortality rates over
time, since the whole population will be at risk every time they recur.
This is therefore a question of considerable epidemiological and demo-
graphic importance which will have to be sufficiently discussed to reach
a certain conclusion. The analysis above reveals that failure to produce
strong and persistent immunity in survivors is an essential property for
a disease if it is to function as a causal explanation for the type of demo-
graphic developments which took place in the Late Middle Ages. Thus,
epidemiological theory militates against the notion that the Black
Death and subsequent plague epidemics could have been a viral dis-
ease but is compatible with a bacterial disease.
Nonetheless, Cohn argues that historical plague epidemics after the
Black Death assumed the character of a child disease, and that this
shows that historical plague was a viral disease conferring persistent
immunity on survivors, a position that will be discussed below.
Scott and Duncan, who also maintain that historical plague was a
viral disease that should, accordingly, produce immunity in survivors,
conspicuously refrain from addressing this question in a focused or
systematic way, since children are strongly underrepresented in regis-
tered cases of filoviridal diseases, represented by Ebola disease and
Marburg disease.5 At various places in their monograph they present a
number of purported instances of possibly increased resistance or
immunity in persons or populations which have in common that they
do not constitute valid material for tenable inference—what they
present is speculation without a firm evidential basis.6
Although Scott and Duncan combine the professions of demogra-
pher and biologist, they do not discern between incidence as related to
degree of risk of exposure to infection and susceptibility. They assert
that Pollitzer should have maintained that “adolescents and adults aged
5
Khan 2003: 1167.
6
Scott and Duncan 2001: (104), 121, 139, 145, 155, 205, 232, 281–2, 329, 355–6,
377–8, cf. Index under immunity.
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208 chapter six
up to 45 years displayed the greater susceptibility.”7 However, Pollitzer

states that “according to most observers” “the incidence of bubonic
plague was highest in adolescents and in adults up to the age of about
45 years” which is certainly a very different opinion.8 It is, therefore,
important to note Wu Lien-Teh’s general statement on the matter:
“Most investigators are agreed that, on the whole, differences in the
age, sex, racial and also occupational incidence of bubonic plague are
due to differences in exposure to infection as brought about by varying
modes of life and not to intrinsic causes.”9 Pollitzer supports this posi-
tion unequivocally when he paraphrases it quite closely: “Most workers
are agreed that differences in the race and sex incidence of bubonic
plague cases, as well as […] among certain occupational groups […]
are due merely to differences in the degree of exposure of the various
groups to the infection and not to intrinsic causes.”10
“Differences in the degree of exposure of the various groups to the
infection” is a key phrase. Too often it is forgotten that epidemic appear-
ances can be deceptive, because social conditions can systematically
affect the intensity of the infective process in relation to particular
social groups according to the distributive functions of relative risk of
exposure. In this context it must be emphasized that this occurs in ways
that mimic the workings of acquired differences in immunity. As
explained above,11 at the heart of the matter is the fact that epidemiol-
ogy is fundamentally a subdiscipline of sociology, and attempts to
explain how various social conditions and patterns of behaviour affect
the probability of contagion being transmitted to human beings or
between human beings in a population of susceptible people. In short,
age-specific role-patterns may produce particular risks of exposure and
age-specific patterns of morbidity and lethality. This is the essence of
Wu Lien-Teh’s and Pollitzer’s statements on the matter.
Likewise, changes in mortality rates cannot be taken as evidence of
increasing immunity or resistance in a population as Cohn and Scott
and Duncan argue. It is important to take into account the fact that
human understanding of the contagious nature of epidemic disease
may lead to changes in individual behaviour and the implementation
7
8
9
Wu Lien-Teh 1936c: 399.
10
11
Above: 142–9.
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of more or less efficient countermeasures which will tend to reduce

mortality at national, regional and local levels and may affect the social
distribution of the intensity of exposure and the relative social inci-
dence of cases. Thus, epidemic case histories can only have evidential
value for a particular (type of) disease if there is no alternative inde-
pendent sufficient explanation. On the basis of the fact that “plagues in
Florence after 1424 killed many fewer people than they did in the 14th
century,” it is fallacious to infer, as Scott and Duncan do, that this “sug-
gests a greater resistance in the population or a decrease in the viru-
lence of the causative agent,”12 when alternative explanations are not
considered. The two main points are that (1) a dramatic fall in the
numbers of dead persons can reflect a drastic fall in the population as
was the case in Florence,13 and that (2) decreasing rates of mortality are
independently fully explicable by cultural and social factors, by increas-
ing recognition and understanding of the contagious nature of epi-
demic disease which translate into increasingly rational social behaviour
and efficient administrative countermeasures in the face of epidemics.
In fact, northern Italy is the part of Europe where the Renaissance
originated and where effective anti-epidemic organizations were for
the first time established, as described by Cipolla in several fine stud-
ies.14 This point is also underlined by L. Del Panta in his fine overview
of Italian epidemic history,15 and by Ciano in his general study of the
development of sanitary precautions for shipping by Italian commer-
cial city states in the period c. 1300–1700.16 Scott and Duncan note the
anti-contagious and anti-epidemic actions of populations and authori-
ties in England several times in their monograph, but only incidentally.
They do not consider the fundamental significance and explanatory
potential of these developments, and the likelihood that along the time
axis of this historical process mortality rates would tend to decline
independently of their discussion of immunity and resistance.17 This
implies also that they have not understood the central aspects or core
of Slack’s monograph which they refer to several times, in which he
shows how increasing understanding of the nature of epidemics
12
13
Herlihy and Klapisch-Zuber 1978: 165–88.
14
Cipolla 1973, 1976a, 1976b, 1977, 1978, 1979, 1981, 1986.
15
Del Panta 1980: 187–91.
16
Ciano 1976.
17
Scott and Duncan 2001: 118, 204, 356, 358, 366, 379.
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210 chapter six
induced people to change behaviour and authorities to implement

measures for protection of the population, leading to the disappear-
ance of plague from England after the last Great Plague of 1665–6.18
When plague disappeared from the British Isles after 1666, is the rea-
son that immunity or resistance had become total or that plague bacte-
ria had completely lost their virulence?
It appears that Scott and Duncan do not recognize that at the heart
of their line of reasoning is the concept of lethality, also called case
fatality or case mortality: increasing resistance and/or decreasing viru-
lence will be reflected in reduced case mortality rates and can only be
tenably studied in this perspective. I have done my best to collect and
present all historical and modern information on lethality in plague
epidemics, covering the period from the mid-fifteenth century in Italy
to modern studies in developing countries, and in the past eighteen
years I have not come across additional material. The conclusion of this
study of lethality is that lethality in plague epidemics appears to have
been quite constant throughout the whole period and at the same level
in historical epidemics and in developing countries (before the advent
of efficient medication), namely about 80 per cent.19 This represents a
strong indication of stable level of virulence and that historical and
modern plague epidemics were the same disease.
This strong indication of stability of plague virulence is strengthened
further by the establishment of an empirically well-founded explana-
tion. The reason for this stability of virulence over such a long period is
the close relationship between the virulence of plague bacteria and
their ability to cause blockage in fleas on which they are dependent for
securing transmission to new hosts and their survival as a strain of a
species with particular genetic properties for this process. Milder
strains are often observed in laboratories, but these cannot satisfy the
relentless demands of natural selection for the survival of the fittest,
thus, only the highly virulent strains remain in operation. These find-
ings, which were originally made by Soviet scholars,20 have been sup-
plemented and supported by later Western research.21 Some of this
18
See my review of Slack’s monograph in Benedictow 1989: 655–9.
19
Benedictow 1993/1996: 146–9. 155. The only piece of information on this subject
I have found later is IPRC 1910c: 468.
20
Tiflov 1964: 181–98; Bibikova and Klassovskiy 1974: 115–23; Bibikova 1977: 28.
Cf. Benedictow 1993/1996: 241–2.
21
Hinnebusch, Perry and Schwan 1996: 367–70.
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Western research is known by Scott and Duncan who have recognized

a couple of points of importance, for instance, the general point that
“the evolution of the pathogen is highly dependent on this coupling
between transmissibility and virulence” and that “only those fleas that
were infected with normal [plague] bacteria developed blocking.”
However, they do not recognize the link to the high and constant level
of virulence of plague bacteria and the consequent high and stable
lethality rates characteristic of bubonic plague.22 They cannot, there-
fore, recognize the strong argument which these findings represent
against their opinion of increasing resistance and immunity and there-
fore against their alternative theory.
The constancy of a very high lethality rate reflecting an underlying
constancy of virulence, which is characteristic of plague, is at variance
with the typical historical tendency of reduction in the virulence of
diseases which are spread by cross-infection. This tendency of weaken-
ing virulence occurs because highly virulent strains tend to kill their
victims rapidly and will tend to have lower success rates of transmis-
sion and therefore fewer opportunities to reproduce their genetic prop-
erties. Weaker strains which cause milder and more protracted courses
of disease will more often succeed at being transmitted and will there-
fore increasingly establish genetic (pre)dominance.23 Scott and Duncan
touch rather casually upon this subject without showing recognition of
its significance.24
These aspects of plague disease and plague history are compatible
with Cipolla’s findings that the reduction in the importation and spread
of plague and the related diminution of population mortality from the
mid-fifteenth century to the mid-seventeenth century are due to
increasing human understanding of contagiousness and ability to
translate this understanding into anti-epidemic behaviour and rational
administrative anti-epidemic actions, which may serve to explain
Cohn’s disparaging attacks on him.25
This brief analytical and structural discussion paves the way for
identifying some decisive criteria which this viral-immunity theory
must satisfy in order to be viable or tenable:
22
23
See, for instance, Greenwood 1936: 240–3.
24
25
Above: 60–2; below: 226, 293–4, 352–3.
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212 chapter six
(1) absence of re-infection of survivors;

(2) after the first outbreak of an epidemic disease in a naïve or previ-
ously unaffected population, which may cause havoc in people of
any age, gender, or social class, recurrent epidemics will tend to
cause relatively small mortality rates because large proportions of
the adolescent and adult population are immune;
(3) corollary: recurrent historical plague epidemics take on the char-
acter of a child disease.
These questions will be discussed (further) in the subsequent
subchapters.
Re-infection or Immunity?
Neither Cohn nor Scott and Duncan take interest in the question of
re-infection which is so crucial to their theories, which are based on
alternative assumptions of viral contagion. If their theories were cor-
rect, re-infections should not occur or be exceedingly rare, and even
the single incidental mention in historical sources would be surprising.
As mentioned above, most medical authorities on plague who had the
opportunity to observe large epidemics of plague in the first decades of
the twentieth century and therefore to observe the potential for re-
infection agree that survival of bubonic-plague infection confers only
weak and transient immunity, as would be expected in the case of a
bacterial disease. Meyer states, for instance:
The immunity which follows a natural plague infection is probably tem-
porary and relative in nature. De Langen and Lichtenstein state, in their
Textbook of Tropical Medicine, that “reinfection with plague may occur
within a few months; surviving an attack gives but a very limited
immunity.”26
A decade later he reiterated his position in a standard work on micro-
biology.27 The other standard monographs on plague similarly state
tersely that survival from an attack of plague confers only a transient
and weak immunity.28 Pollitzer states in his central standard work that
26
Meyer 1946–7: 434. Meyer’s citation contains a number of small insubstantial
deviations from the original text. De Langen and Lichtenstein 1936: 195.
27
Meyer 1957: 414.
28
Sticker 1910: 265; Dieudonné and Otto 1928: 256.
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immunity to this disease, acquired under natural conditions, was evi-

dently relative in degree and limited in duration.29
This means that re-infections of survivors of bubonic plague should be
expected to occur and be recorded both in connection with modern
plague epidemics and historical plague epidemics. If this prediction
can be corroborated, the alternative theories of Scott and Duncan and
Cohn are ipso facto invalidated.
The views of the authors of the standard works on plague to the effect
that acquired immunity in survivors was weak and transient imply that
re-infections were observed. In fact, re-infections have been docu-
mented in modern epidemics, for instance in India by the Indian Plague
Commission and other medical observers: one case was a woman who
had first contracted plague in Hong Kong in 1894 and subsequently
contracted the disease in Mumbai in 1896; another person, a native
Indian, fell ill from plague 30 October 1896 and again 2 December. It
was also noted that subsequent attacks could be survived or end in
death.30 Wu Lien-Teh recorded the case of a patient who contracted
bubonic plague only four months after having recovered from primary
pneumonic plague.31
There are numerous other observations of re-infections in historical
plague epidemics which, because of the crucial importance of this topic
and its great evidentiary powers, will be discussed in detail in the pages
that follow. Beginning around 1700 medical science had developed to
a level where empirical observation and systematic study led to quite
detailed accounts of individual cases in epidemics, including cases
in plague epidemics, and this produced quite frequent and well-
documented observations of re-infections. For this reason, I will docu-
mentation will begin by describing these observations to provide a
background for earlier historical observations.
Historical observations of re-infections were first collected by
Sticker.32 G. Kirchoff, the physician, in 1714 published his observations
of the Austrian plague epidemic the preceding year,33 and he relates
that persons who had survived bubonic-plague disease in a previous
epidemic or had survived plague disease in the present epidemic
29
30
Simpson 1905: 294–6; Sticker 1910: 437–8.
31
Wu Lien-Teh 1927–8: 84, fn. 4.
32
Sticker 1910: 434–8.
33
See Sticker 1908: 449, bibliography.
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214 chapter six
contracted plague again. During the epidemic of 1720–2 in southern

France, J.B. Bertrand observed some persons who were attacked three
times.34 Bertrand’s work was published in English translation in 1973
and is used and cited by Scott and Duncan, who nonetheless do not
take note of these observations.35 In a contemporary study of the plague
epidemic in Aleppo in 1760–2, P. Russell recorded twenty-eight cases
of re-infection among 4400 plague cases, and several of the patients
contracted plague more than twice.36 G. von Orraeus, the Finnish phy-
sician, observed re-infections in the Moscow epidemic of 177137 as did
D. Samoilowitz, the Ukrainian epidemiologist, who himself contracted
plague three times.38 A. Chenot mentions several cases of re-infection
which he observed in the plague lazaretto at Kronstadt in 1755, among
them his own servant who contracted plague three times, at the end of
June, in mid-September, and in November when he died.39 In an
Egyptian plague epidemic in 1834–5, A.B. Clot-Bey observed so many
re-infections that he argued directly against the notion that survival of
plague conferred significant immunity according to the pattern of
small pox.40 Of course, at the time bacteriology was not established as a
medical or microbiological discipline and the vital differentiation
between bacteria and viruses and their immunity effects had not been
made, thus, the difference could not be understood or explained, only
observed.
By implication, re-infections in earlier historical plague epidemics
should be expected, and if documented, this would constitute strong
evidence that these plague epidemics could not be a viral disease
but could be bubonic plague. In fact the history of observation of re-
infections of plague is as old as the history of plague in Europe. Sticker
collected a considerable number of statements on this subject by physi-
cians of the past. He points out that Evagrius observed numerous cases
of re-infection in the Justinianic epidemic of the early 540s,41
34
Simpson 1905: 296.
35
36
P. Russell 1791: 190. See also Simpson 1905: 296.
37
Gustavus Orraeus, Descriptio pestis quae anno 1770 in Jassia et 1771 in Moscua
grassata est. Petrepoli [St Petersburg] 1784. Cit. Simpson 1905: 296. Sticker 1910: 436,
467.
38
Kowal 1972: 434–46.
39
Sticker 1910: 334. Cf. Sticker 1908: 433.
40
Clot-Bey 1851b: 89: “nous avons vu de fréquentes récidives.” Sticker 1910: 437.
41
Sticker 1910: 434–8. Cf. Meyer 1946–7: 434.
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a point that was first made by Clot-Bey in 1851.42 Surprisingly, there are
quite numerous observations of re-infections in the period 1480–1714,
most of them are registered by Sticker,43 and I have come across some
other instances. This material on historical cases of re-infections will be
presented in chronological order.
Marsilio Ficino [Marcilius Ficinus], the Florentine physician and
philosopher (1433–99),44 observed several cases of re-infections in the
epidemic of 1478:45
And say not that he who has survived from the disease once cannot
any more succumb, because one of our Florentines fell ill three times
in this year: the first two times he survived intact; the third time he
could not survive. Again, in this year, in September, I cured a woman
completely of plague, becoming as sound as any other person, then she
conversed with diseased and fell ill again eighteen days later and
perished.46
This is a work that Cohn knows well, as he refers to it at least eight
times, but he has apparently overlooked this piece of information that
is incompatible with his theory.47
Again one should note that a person could be attacked three times in
the same epidemic and also the brief time that elapsed between the
time a person had completely recovered and fell ill again, which explains
how the disease could be contracted three times in the course of the
same epidemic. W.P. MacArthur found information about a baker’s
wife who contracted plague three times in the London Epidemic of
1563, first around mid-summer, then in August, and then again at the
end of September, when she died.48
A. Massaria, the Venetian physician, relates in his two-volume work
on plague of 1579 that he observed numerous cases of re-infection in
42
Simpson 1905: 296.
43
Sticker 1910: 434–8.
44
See Bibliography in Sticker 1910: 502.
45
Del Panta 1980: 118, 128. See also fn. 49.
46
Ficino 1983(/c. 1481): 105. My translation from the original text which is written
in the vernacular. For dating see Cosmacini 1979: 22.
47
Cohn 2002: 62, 95, 133, 209, 214, 230, 231, 240, where he refers concretely to
pages 56, 57, 92, 109, 110, in Ficino’s work but has apparently not seen page 105. Cohn
states repeatedly inaccurately that Ficino related to the epidemic of 1480, but there was
not plague in Florence this year. Ficino makes it clear on page 109, to which Cohn
refers, that this epidemic occurred in 1478, the year identified also by Del Panta in his
history of Italian epidemics (see fn. 45).
48
MacArthur 1925–6: 358.
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216 chapter six
the Venetian epidemic of 1575–749 which swept away 46,752 of the

city’s c. 180,000 inhabitants.50 In the epidemic in Rotterdam in 1624–5
a woman contracted plague twice and survived both times.51 John
Woodall, physician at St Bartholomew Hospital in London, who pub-
lished a plague tractate in 1639, informs his readers that he contracted
plague twice and developed buboes both times. This case is mentioned
also by Creighton52 and on a page which Cohn asserts that he has read
and refers to in the accompanying footnote.53 I. Diemerbroeck, the
famous Dutch physician (1609–74), published a plague treatise in 1644
based on observations of the plague epidemic in Flanders in 1636–7. In
this work he set new standards of empirical approach and scientific
rigor and he introduced, among other things, the standard of providing
numerous case histories in which the disease was clinically described
in some detail. His treatise was rightly admired by contemporaries and
posterity and it was published posthumously in English in 1722. He
states that he had seen many persons who contracted plague twice,
among them a knight who after having recovered completely fell ill
from plague with a bubo a second time five weeks later. G.O. Giseler,
the physician, published his medical observations on the plague epi-
demic at Brunswick (northern Germany) in 1657:54 he noted, among
other things, that several children in a family contracted plague a sec-
ond time, when most of them died, while other persons died in the
third attack. W.G. Bell cites Dr Hodges who wrote after the plague in
London 1665: “I have known many infected who although all things
succeeded well the first and second time, and each cure was perfected,
yet the third seizure, upon the account of a new infection and not a
relapse, hath proved fatal to them.”55 A prominent Capuchin priest
contracted bubonic plague twice in the plague epidemic in Mainz in
1666. Ludwig von Hörnick, Dean of the Medical Faculty in Mainz, con-
tracted plague twice and survived both times.56
The Nordic experience agrees with this material. M.G. Block, the
Swedish physician who wrote an extraordinarily valuable account of
49
50
Del Panta 1980: 146.
51
Moquette 1925: 19.
52
See also Creighton 1891: 122.
53
Cohn 2002: 212 and fn. 73.
54
55
Bell 1951: 213, (244).
56
Sticker 1910: 436.
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his observations during the plague epidemic in Norrköping in 1710–1,

states: “I never imagined that a person who so recently had been to
bed with plague, should so soon be attacked again, as it happened.”57
Inspired by Diemerbroeck, Block provided detailed and acute observa-
tions of the epidemic process and numerous detailed clinical case his-
tories and descriptions which leave no doubt about the nature of the
disease: it was bubonic plague. This links Nordic plague history chron-
ologically with European plague history, where it continues with the
observations of Kirchoff and Bertrand, and so on.
As can now be seen, and without forgetting Evagrius’s observations,
there are numerous records of re-infections in historical plague epi-
demics, starting in 1478 and becoming quite frequent in the period
1563–1835. Records on observations of re-infections in plague epi-
demics begin as far back in time as one could reasonably expect that
the development of culture, mentality and sources would convey such
information to posterity, demonstrating that re-infections were a nor-
mal part of historical plague epidemics all over Europe. Also the conti-
nuity in time and European geography is interesting, particularly
because Scott and Duncan are willing to accept that the epidemic in
southern France 1720–2 was bubonic plague. These observations can,
as shown above, be readily linked with similar observations in India
from 1896.
I will submit that the material on case histories of re-infections pre-
sented above constitutes substantial evidence that historical plague epi-
demics cannot have been a viral disease, but could according to the
criterion of re-infection have been a bacterial disease, for instance,
bubonic plague. Since many of the physicians who provided these case
histories also specifically mention that these cases had plague buboes
or pestilential buboes, I submit that this combination of information
constitutes crucial evidence to the effect that historical plague epidem-
ics were bubonic plague. As is shown below, buboes as a normal clini-
cal manifestation of epidemic disease are an exclusive feature of bubonic
plague and constitute therefore a defining feature of this disease (see
below). This combination of information of buboes and re-infections
constitute a coherent pattern of clinical manifestations which consti-
tutes evidence of bubonic plague.
57
Block 1711: 104. My translation from Swedish.
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218 chapter six
Did Plague Become a Child Disease after the Black Death?
At the core of Cohn’s monograph is the alternative theory that histori-

cal plague was a viral disease, albeit with very different apparent prop-
erties from the viral agent of Scott’s and Duncan’s alternative theory,
almost as different as possible. At least one of them must for this reason
alone be incorrect, at least one of these theories must have been con-
structed from virtually nothing, at least one of them must be the out-
come of a great input of unscientific and unscholarly work. Since Cohn’s
alternative is a completely unknown disease which is presumed to have
disappeared long ago, the testability of this theory is problematic but
not impossible, since the compatibility of observed epidemic manifes-
tations with a viral disease can be studied. This can be a useful approach,
although the fact that no new disease has appeared in the significant
number of studies of microbiological DNA taken from the skeletal
remains of historical plague victims,58 whilst Yersinia pestis is system-
atically found, could justify the dismissal of Cohn’s theory as being
based on a phantom disease.
As the only advocate of an alternative theory, Cohn argues that
plague epidemics subsequent to the Black Death assumed the character
of a child disease which must reflect the fact that a large proportion of
adults had survived previous plagues and acquired good and persistent
immunity, the susceptible part of the population being to a large extent
children born later, a characteristic manifestation of viral diseases.
His view is based on an analysis of the Necrology of the Monastery of
San Domenico in Camporegio in Siena (see below) and statements
by some contemporary chroniclers who call the epidemic of 1360–3 a
child disease, pestilentia puerorum, pestis puerorum, “la mortalite des
enfauntz,” and the like, and the fact that a few plague epidemics up to
1400 were characterized in this way by some chroniclers.59 In his words:
“after several strikes, it became domesticated as a disease largely of
children,” and “by the end of the [fourteenth] century it had become
largely a disease of children.”60 This is obviously at variance with the
material on re-infections presented on the previous pages and also with
the constant and high levels of lethality documented above. It is also
very problematic for a number of other reasons, as will be seen below.
58
Below: chapter 10: 381–95.
59
Cohn 2002: 213.
60
Cohn 2002: 212, 238.
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In Cohn’s monograph, which purports to study the greatest demo-

graphic catastrophe ever caused by an epidemic disease, Cohn has no
chapter or section focusing on mortality rates in the Black Death or
subsequent plague epidemics. This is a reflection of his weak interest in
demography and consequent unfamiliarity with demographic science
and its emphasis on stringent concepts, intensive analysis and hard
facts. His monograph contains only a couple of attempts at producing
demographic data, and as we shall see below, his handling of demo-
graphic material is gravely flawed. My endeavours to collect Cohn’s
statements or views on mortality rates in order to form a general
impression of his opinion on the matter by use of the entry “mortality”
in his index led nowhere, and the subentry “statistics of ” does not con-
tain a single piece of statistics in any scholarly meaning of the term,
only untestable, subjective and arbitrary assertions of the chroniclers’
opinions. In a section on epidemiology within a chapter on “Chroniclers
and Doctors” Cohn insouciantly discusses mortality in the Black Death
over a few pages by citing various chroniclers’ more or less fanciful or
absurd assertions.61 Nearly 200 scientific demographic studies of mor-
tality in various localities caused by the Black Death are all ignored.62
Readers interested in this subject are referred to my monograph on the
Black Death. Cohn’s chronicle-based material on mortality in the Black
Death serves as a basis for his subtheory that plague developed into a
child disease in the subsequent epidemics. Cohn consistently ignores
the available demographic studies of mortality in the second plague;
this means that his subtheory that plague developed into a child dis-
ease is not based on hard demographic facts. Instead, he builds his case
on chroniclers and a minimalistic application of source-criticism. This
approach has the strangest consequences in the eyes of an historical
demographer (see below).
I have above made clear my reservations and cautiousness in relation
to medieval chroniclers and the need for unrelenting source-criticism
and independent testing of their assertions. Late medieval chroniclers
have a wide range of opinions, many of which all modern scholars
would reject as superstitious, prejudiced, ignorant or plainly wrong.
Most chroniclers believed in an other-worldly explanation of epidemic
disease, specifically that it was an expression of God’s wrath over man’s
61
Cohn 2002: 106–9.
62
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220 chapter six
sinfulness. No modern scholar would accept their alternative mias-

matic causal views on epidemic disease and the mechanisms of epi-
demic spread or those of contemporary physicians who were the chief
proponents of miasmatic theory.63
Chroniclers’ opinions on subjects related to demography or social
science and their notions of numbers tend to be demonstrations of
ignorance, subjectivity and rhetorical extravagance. Their assertions
with respect to mortality in plague epidemics vary enormously and are
quite often rhetorical exaggerations or phrases not intended to be
accepted at face value as factual. When they can be tested on independ-
ent material they quite regularly prove to be not just unrealistic but
outright fanciful, bizarre or absurd. According to one chronicler, 57,000
people died from the Black Death in one month alone in Marseilles,
which Twigg, for instance, accepts as credible information.64 However,
Baratier, the outstanding demographer of medieval and early modern
Provence, estimates the number of inhabitants before the catastrophe
at only 15,000,65 which makes it understandable but not credible that
another chronicler cited uncritically by Cohn asserts that the city
became “uninhabited.”66
Similarly, Cohn uncritically cites the fanciful figures of another
chronicler who maintains that in Avignon 62,000 persons died in the
three months following 25 January 1348 and that the epidemic peaked
on 14 March when 11,000 bodies were buried.67 There is no way that
Avignon could have had over 35,000 inhabitants on the eve of the Black
Death,68 and the only reason Cohn believes that the epidemic peaked
14 March is that he accepts the chronicler’s ludicrous fantasy figure.
The epidemic in Avignon lasted seven months, so if we accept the
chronicler’s figure, 62,000 persons died before half the epidemic period
was over. Assuming that the disease was bubonic plague with a normal
lethality rate of 80 per cent,69 this would mean that 77,500 persons had
63
Above: 78–84.
64
Below: M377–8.
65
Baratier 1960: 66–7.
66
Cohn 2002: 102.
67
Cohn 2002: 141.
68
Pounds 1974: 261 and 266. At the beginning of the fourteenth century, Avignon
was in the category of a large medieval city containing 10,000–25,000 inhabitants. The
arrival of the papal court in 1309 meant an influx of over 4000 court functionaries and
the city’s population may have increased by around 10,000 inhabitants.
69
All data on lethality rates in historical and modern plague epidemics are pre-
sented in Benedictow 1993/1996: 46–149.
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contracted plague, and a population far above 100,000 persons is indi-

cated. Cohn arbitrarily (but not consistently, as will be seen) implies a
much lower lethality figure for his unknown viral disease since he also
assumes that the survival rates were sufficient to turn the subsequent
plagues into a child disease, thus he implies in this case a correspond-
ingly very much higher population. This view is well adapted to the
chronicler’s assertion that 150,000 persons died in the Black Death in
Avignon.70 If half the population perished in the epidemic, this implies
that Avignon’s population was 300,000 persons, almost as many as the
whole population of Provence (350,000–400,000) at the time,71 twenty
times higher than Marseilles’ population, three times bigger than
Florence’s, and very much larger than Paris’s population, which was
probably twice as big (200,000) as any other city in Europe at the time.
Interestingly, Sticker cites a Dutch canon to the effect that 11,000 per-
sons were buried in Avignon in the six weeks after 13 March.72
This is only a small illustration of the nonsense that results from
placing any faith in chroniclers’ population figures or mortality figures
and the unrelenting need for merciless source-criticism and material
testability on the firm grounds of scientific historical demography.
Obviously, no person with elementary knowledge of demography and
source-criticism would land in such outlandish trouble. While reading
Cohn’s monograph the warning of John Hatcher, the leading scholar of
medieval demography in the world today, regularly comes to my mind:
“substantial advances in knowledge and technique have enabled us to
proceed far beyond the overwrought imaginings and hopelessly inac-
curate quantification of the chroniclers.”73 In short, chronicles are unus-
able sources for serious demographic research; all serious demographic
research is based on registrations of populations, manorial records, tax
lists, burial lists, censuses, and the like. It is the uncritical use of chroni-
cles by Twigg, Scott and Duncan, and to an incredible extent, Cohn,
which makes it necessary to emphasize this elementary point.
Cohn employs the “overwrought imaginings and hopelessly inaccu-
rate quantification of the chroniclers” in order to construct a basis for,
among other things, his immunity argument with its obviously impor-
tant implications for the possibility of developing an alternative theory
70
Sticker 1908: 57.
71
Baratier 1960: 67.
72
Sticker 1908: 57.
73
Hatcher 1977/1987: 21.
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222 chapter six
of plague. Cohn takes medieval chroniclers at their word, or more

accurately, some medieval chroniclers at their word, when they state
that plague epidemics took on the character of child disease. This
implies that he considers contemporary chroniclers’ use of the concept
of child disease reasonably equivalent to a modern medical scientific
concept of child disease, and to be useable in a modern monograph of
epidemic history without a significant input of source-criticism,
demography, epidemiology and social science.
Representativeness is a crucial tenet of the methodology of social
science and source-criticism. According to this tenet, presentation of
some chroniclers’ opinions to the effect that children suffered super-
mortality in plague can only be accepted as methodologically valid
material for inference, and therefore as material of scholarly value or
interest, if the following necessary condition is fulfilled: it must be
demonstrated that it is not possible to present a more or less similar
number of chroniclers’ opinions to the effect that plague had (an)other
marked specific social predilection(s) according to age, gender, social
class or occupation, for example that plague had a predilection for
women, or for men or for the poor or for noblemen or, conversely and
importantly, that many chroniclers did not observe any special social
predilections, and so on. There is a methodological and source-critical
condition or demand that Cohn demonstrates that his collection of
data is not a biased and unrepresentative sample resulting from a
single-minded quest for statements on child mortality, selected
and gathered to serve his alternative viral theory, but is, in fact, gener-
ally representative of chroniclers’ statements on plague’s social
predilections.
A discussion of this issue can only begin with the second Europe-
wide plague epidemic of 1360–5 on which Cohn focuses. It is easy to
illustrate the inherent methodological fallacy of Cohn’s approach.
Cohn states that “numerous chroniclers in Britain […] noted that it
[the second plague of 1361] struck down greater proportions of chil-
dren than the first, so much that they called it ‘the child plague,’ ” and
cites one chronicler and refers to some other chroniclers to this effect,
which he believes supports his view of the viral immunity effects among
survivors of the Black Death.74 Whether the word “numerous” is an apt
74
Cohn 2002: 213.
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term is open do debate; the term “several” is probably more appropri-

ate. Among the chroniclers he refers to but does not cite is Henry
Knighton’s chronicle, which, however, takes a more complicated view:
it mentions “the Second Pestilence ‘in which great and less died, but
especially young men and children.’ ”75 Knighton appears to have made
quite a composite observation of the social pattern of supermortality
and by implication of submortality among various social classes and
other demographic categories. He certainly emphasizes supermortality
among children, but also among young men who, being differentiated
from children, must be assumed to be older than twelve or fourteen
years and thus to have lived through the Black Death, and also among
the upper classes and the lower classes, and it is a relative emphasis, not
a description of more or less overwhelming dominance of children. It
is intriguing to consider why young men should have had much less
immunity than young women? And what happened to the middle
classes? What is it that Knighton observed, if that is what his text
reflects?
Even a quick glance at Shrewsbury’s presentation of this second
British plague epidemic provides a much more complicated picture of
contemporary observations of the pattern(s) of mortality in this plague
epidemic of 1361. “Adam of Murimuth calls it a great mortality and
records that ‘of it there died in England some outstanding people
and noblemen, and a very large number of churchmen, both secular
and regular.’ ” The chronicle called “The Brut notes that it especially
slaughtered men, whose wives ‘as women out of control,’ proceeded to
consort with any men that were available.’ ” John of Reading describes
the mortality pattern as sexum masculinum valde consumens, meaning
that the plague had a very strong predilection for, or to a very high
degree consumed or destroyed the male sex, which again raises the
question of why men should be much less immune than women. In the
Calendar of the Close Rolls, which is not a chronicle but which in this
case provides a contemporary observation of much the same character,
it is stated on 10 May 1361: “great multitudes of people are suddenly
smitten with the deadly plague now newly prevailing as well in the city
of London as in neighbouring parts, and the plague is daily increas-
ing.”76 Jean de Venette, the prominent contemporary French chronicler,
75
Shrewsbury 1971: 128.
76
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224 chapter six
asserts that there was substantial mortality in Paris, “notamment parmi

les pauvres”=“especially among the poor.”77 As can now be readily seen,
it is possible to select a number of chroniclers’ statement on the differ-
ential social impact of this plague epidemic to the effect that it espe-
cially swept away men or adults or the poor. Taken together, the
chroniclers’ statements could also be interpreted to indicate that this
plague epidemic hit seriously various main social categories with
respect to age, gender and social class, but perhaps not so much women.
However, women apparently tended to be present in the chroniclers’
minds primarily as morally weak or outright immoral sexual beings
and to be out of focus as a demographic category, which may raise
doubts and inspire source-criticism or outright source-scepticism.
There will be occasion to return to Cohn’s statement cited above.
It is important to remark that the scholarly meaning of the concept
of “infectious child disease” is not, as Cohn would like us to believe, a
disease with disproportionately high distribution of epidemic cases
among children. Most modern medical textbooks on child infectious
diseases do not consider the term “infectious child disease” or “infec-
tious paediatric disease” to mean a disease with an imbalanced distri-
bution of cases between different age groups. Instead, they define
infectious child diseases as diseases spreading among and between
children independent of proportions in different age groups.78 Thus,
there are two highly different concepts of infectious child disease with
very different operational properties, and Cohn’s intuitive understand-
ing of the concept is not self-evidently valid, but it does serve his pur-
pose. In the present discussion, this intuitive meaning will be the focus
of endeavours to clarify its scientific, medical and demographic con-
notations and validity.
According to Hatcher, Christ Church Priory in Canterbury was vis-
ited by plague during fourteen years between 1413 and 1507, that is on
the average once every 6.7 years; if we take into account the fact that on
two occasions the same plague epidemic appeared also a second con-
secutive year, the number of epidemics was twelve and plague epidem-
ics recurred on the average every 7.8 years.79 If the plague epidemics
were as frequent among the population from which the monks were
recruited, which must be a rather cautious assumption, many monks
77
Glénisson 1968–9: 32.
78
See for instance Donowitz 2003: 17.
79
Hatcher 1977: 17; Hatcher 1986: 29–30.
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must be presumed to have survived at least one, often two plague epi-
demics as a child, before they entered cloistered life (age at profession
for all novices was eighteen years80). However, the monks suffered great
mortality from plague. So what happened to immunity?
In his huge corpus of wills produced in southeastern England in the
period 1430–80, Gottfried registered evidence of eight plague epidem-
ics in these fifty-one years which correlate well with other contempo-
rary registrations of plague epidemics; on average, a new epidemic
occurred every 6.4 years.81 And there are many large collections of wills
from this period which exhibit tremendous increases in numbers dur-
ing periods of plague.82 But why would adults abruptly start making
wills in the face of a threatening plague epidemic if they mainly
were immune? And surely the pervasive immunity of those who had
survived plague in childhood or adolescence must have been conspicu-
ous, people must have observed that those who had survived the
plague rarely contracted the disease again? Mortality of children would
not be relevant to adult fear of dying intestate. So what happened to
immunity?
In Norway, there were three grave plague epidemics in the years
1521–9(−30); in 1525 and in 1529 the epidemics were in the southeast-
ern region, and both must have started in Oslo and spread out of the
town over the region. So what happened to immunity?83 In my history
of plague in Norway, I have registered as fully as possible all plague
epidemics in Norway, England, the Netherlands and northern Germany
in the period 1348–1666, which made it possible to create comparative
tables for the periods 1348–1500 and 1500–1666.84 I registered four-
teen plague epidemics in England in the 1500s, on the average a new
wave of epidemics every 7.2 years, and seven epidemics in the period
1600–66 indicate on the average a new epidemic every 9.5 years. Much
the same pattern occurred in the other countries. Norway mostly
imported plague from England and thus showed much the same tem-
poral rhythm.
80
Hatcher 1986: 27.
81
In the period 1430–80, there appear to have been seven epidemics of plague in
England of a national or extra-regional scale, in 1433–4, 1438–9, 1452–3, 1457–9,
1463–4, 1467, 1471–3, and 1478–80; locally there were many more.
82
Some of them are mentioned or presented in Benedictow 2004: 81, 106, 119, 121,
135–7, 178, 197–8, 272, 336.
83
Benedictow 2002: 131, 146–56.
84
Benedictow 2002: 102–09, 129–37.
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226 chapter six
In the period 1500–1666, the quality and quantity of textual sources

increased greatly, which is reflected in modern archives. So why has no
earlier scholar asserted that the historical plague epidemics of the
period exhibited the general pattern of child disease and acquired
immunity? The answer is very clear, because there is overwhelming
demographic evidence that this was not the case, that the mortality
rates among the adult population were usually tremendous in all of
these epidemics, which also explains the very strong correlation
between the mass production of wills and plague epidemics. This is the
reason that scholars who have made comprehensive in-depth studies of
historical plague epidemics have not so much as hinted that post-Black
Death plague epidemics took on the character of child disease. Since
Cohn mainly bases his assertion on this point on English and Italian
material, it must be emphasized that E. Fiumi, M. Livi-Bacchi, L. Del
Panta and C.M. Cipolla, the highly admired Italian historical demogra-
phers, have not observed plague as a child disease at any time during
the plague period in Italy. This seriously undermines Cohn’s assertion
on this point and may also serve to explain his ill-natured attacks on
Cipolla’s work85 and why the important works by Fiumi, Livi-Bacchi
and Del Panta are passed by in silence. No Italian historian has formed
such an opinion; it is Cohn’s arbitrary idea. The same is true of all of the
prominent scholars of English medieval and early modern demogra-
phy and epidemic history, Postan, Russell, Shrewsbury, Hatcher, Slack,
Schofield, and Wrigley. Prominent French and Dutch scholars in this
field of research like Biraben, Dubois, Nordergraaf and Valk have also
failed to note any such development, and this is also the case with the
authors of the first volume of Histoire de la population française,86 the
authoritative summary of French demographic history. Nordergraaf
and Valk have registered a plague epidemic somewhere in the
Netherlands about every year from the time their registration starts in
1450 until the last plague epidemic in 1668. In some urban centres
plague epidemics broke out in quick succession, in Amsterdam for
instance in 1550, 1554, 1557, 1558, and 1559, and in 1616, 1617, 1618,
1623, 1624, 1625, 1626, and 1629.87 So what happened to immunity?
This evidence and perspective makes it urgently necessary to exam-
ine Cohn’s evidence. However, in order to understand the significance
85
Above: 60–1, 209, 226, 293–4, 352–3, and in subsequent contexts.
86
Dubois 1988: 324–66.
87
Nordergraaf and Valk 1996: 225–8.
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of his evidence, suitable analytical tools are needed. Unavoidably

and centrally, the concept of child disease must be clarified. Such a
clarification is crucial since the concept of child disease in the loose
sense suggested by Cohn’s intuitive (and self-serving) use of it only
implies that children constituted something like a highly dispropor-
tionate part of the total mortality in plague epidemics. It also entails the
corollary that this highly unproportional mortality among children
reflects widespread or comprehensive acquired immunity among the
adult population who had survived earlier epidemics of the disease,
this manifestation being the hallmark or defining feature of viral dis-
ease. In order to acquire a more accurate and operational concept of
child disease, it is necessary to make explicit some central demographic
aspects of medieval population structure, especially the proportion of
children among the living and the dying in normal populations both
in normal circumstances and in plague epidemics. Only on the basis
of such information can a realistic and operational definitional notion
of the disproportionality of child mortality as evidence of child disease
be considered.
The concept of child disease according to Cohn’s notion must relate
to epidemic morbidity and mortality rates among children of ages
c. 0–14 as proportions of concomitant morbidity and mortality rates
among the older segments of the population. Or more accurately: the
demographic and epidemiological concept of child disease must relate
to or reflect a notion of the proportion of sick and dying children usu-
ally caused by an epidemic disease which differentiates it from con-
cepts of population mortality or adult mortality in a way that makes it
useful as an analytical tool. Since Cohn has not provided any idea of
these proportions and their relative dimensions, his conceptual notion
is obviously as impressionistic and intuitive and unanalytical and there-
fore unscientific as the impressions of the chroniclers on which he
bases it, and can as such be summarily rejected as useless as an analyti-
cal tool.
Greenwood provides some of the data needed for the definition of
the proportional concept of (infectious) child disease in an historical
perspective, when he states:
as recently as 1851–60 the rate of mortality [in smallpox] in no age
group later than 5–10 amounted to one-fifth the rate in the age
group 0–5, and the mortality at 5–10 was one-quarter the mortality at
0–5. In the epidemic of 1881–2 the relative predominance of the first
age group was considerably lessened; the mortality at 5–10 was half
that of 0–5 […],
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228 chapter six
and so on.88 This shows that when Cohn does not specify the constitu-
ent definitional elements and their interrelationships, that is, the cor-
relates of his definition of the concept of infectious child disease, it
clearly becomes well-nigh impossible to test the material tenability or
relevance of his assertion. Without real testability, not only the tenabil-
ity but also the validity of his assertion can be rejected.
Notions of disproportionality of morbidity and mortality according
to age in the face of epidemic disease relate by implication to notions of
normal proportions. Any serious approach to this definitional problem
must therefore also take into consideration the fact that these relation-
ships or notions of interrelated proportions are not constant but vary
with social structures. Any realistic and useful definition of child dis-
ease derived from studies of epidemic child mortality as a proportion
of adult mortality in modern Western society will be highly different
from an historical definition derived from studies of relative propor-
tions of child mortality in medieval or early modern populations, and
would therefore be unusable for the study of this topic in these socie-
ties. This is the case for several crucial reasons:
(1) because there are vast differences in demographic structures, and
in particular, children constitute far smaller proportions of the
populations in modern Western society;
(2) because the incidence, prevalence and effects of epidemic diseases
in modern and old-time society are tremendously different;
(3) because normal levels of population mortality in these periods are
extremely different;
(4) because the pattern and distribution of normal mortality accord-
ing to age are extremely different.
This means that the definition of an operational concept of child disease
or child mortality according to the distribution of cases by age in a pop-
ulation will vary greatly with changing demographic and other societal
structures and historical periods, a fact all too often overlooked.
Therefore, concrete data of the proportion of children in populations
at the time is needed in order to gain knowledge of the relative size of
the pools of children and older age categories which are exposed to
epidemic disease and epidemic death. Only on this basis can mortality
rates in particular age groups which are out of proportion with their
88
Greenwood 1935: 240.
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numerical representation in the population be identified and analyzed

for an understanding of causal factors. Intuitive, impressionistic and
other arbitrary or subjective notions of such conditions must be rejected
as methodologically invalid and materially untenable.
Since Cohn focuses on Italian material, it will be reasonable and fair
to put a certain emphasis on Italian demography here in an otherwise
general discussion. Life expectancy at birth in the Late Middle Ages
and the first half of the sixteenth century appears to have been twenty
and twenty-five years, respectively.89 Belletini indicates the same life
expectancy as normal in old-time Italy, “oscillating usually between
twenty and twenty-five years, rarely reaching the limit of thirty years.”90
A useful point of departure for a realistic understanding of demo-
graphic structures under such circumstances can be seen in Table 1
which is a life table, Model South level 3,91 showing life expectancy and
mortality at various ages in a population of females with life expect-
ancy at birth (eo)92 of twenty-five years, the number of deaths at each
age level and the number alive at the start of each age level out of an
original population of 100,000 persons. Among other things, this life
table shows that 54.6 per cent of all children born died at ages 0–14,
and over one-fourth of all children born died as infants, in the first year
of life. This pattern of child mortality corresponds to Belletini’s view on
child mortality in old-time Italy: “normally a fourth of all new-born
babies (neonatus) died in the first year of life, but that the death toll
not rarely reached or exceeded one-third of births, while half of the
89
See the summary and discussion of normal levels of mortality in the Middle Ages
in Benedictow 2004: 250–6. Since the work on this monograph was finished in 2003,
two very important works on the subject have been published. The first is Hatcher’s
outstanding and, one must hope, final breakthrough in the understanding of late medi-
eval demography, Hatcher 2003: 83–130. In 2006 Hatcher Piper and Stone published a
study of monastic mortality in Durham Priory in the period 1395–1529. The latter
work accords with Hatcher’s study of late medieval monastic mortality at Christ Church
Priory in Canterbury and Harvey’s study of monastic mortality at Westminster Abbey
in about the same period. These studies accord with and corroborate my presentation
of medieval mortality in my monograph. Cf. Benedictow 1996b: 36–42.
90
Belletini 1973: 494. My translation from Italian.
91
Coale and Demeny 1983: 11–2, 31–4. For a similar table of Model West, see Coale
and Demeny 1983: 43, or Benedictow 2004: 249.
92
The differences between this table and a similar table for males are negligible in
this context. eo is a standard abbreviation in demography meaning life expectancy at
birth, e being an abbreviation of the Latin word eta(ti)s (aetas/aetatis) in nominative
and genitive cases meaning (of) age, o referring to age at birth. Life expectancy at other
ages, at age 15, for instance, would correspondingly be written e15.
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230 chapter six
Table 1. Life table, model south, level 3: life expectancy and mortality
at various ages in a population of females with life expectancy at birth
(eo) of 25 years, and the number of deaths at each age level and the
number alive at the start of each age level out of an original population
of 100,000 persons
Age Number of deaths Number alive Life expectancy
0 26433 100000 25.00
1 22263 73567 32.85
5 3799 51304 42.57
10 1892 47505 40.80
15 2490 45613 37.38
20 2931 43123 34.39
25 2935 40192 31.71
30 2836 37257 29.00
35 2759 34421 26.18
40 2588 31662 23.23
45 2519 29074 20.07
50 2980 26555 16.73
55 3572 23575 13.52
60 4810 20003 10.47
65 5335 15193 7.96
70 5029 9858 5.86
75 3319 4829 4.26
80 1193 1510 3.13
85 286 317 2.24
90 30 31 1.59
new-born babies of a generation did not live beyond the fifth year of
age.”93 This means that at the time, according to this life table, of 100,000
persons born, 54,387 would die before their fifteenth birthday while
45,613 would not. That is, among death’s normal yearly harvest in a
normal population, almost 55 per cent were children of ages 0–14.
At the time, the normal level of mortality in a normal population
under normal circumstances should, thus, be expected to have a large
93
Belletini 1973: 494. My translation from Italian.
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component of child mortality according to modern notions of the rela-

tive distribution of mortality. In other words, in the period under con-
sideration the proportion of normal child mortality in a population
would easily qualify as the outcome of a very serious child disease
according to modern notions. Contemporaries considered this, on the
contrary, to be the normal distribution of mortality among the various
constituent age groups of the population under normal circumstances.
Carmichael is right when she points out that 50–60 per cent of those
dying from plague in the epidemic of 1400 were children, and that “this
was close to the proportion of children in the population.”94
The usefulness of a realistic understanding of the normal rates of
child mortality at the time can be demonstrated in relation to Cohn’s
discussion of the first part of the Necrology of the Dominican monas-
tery in Siena containing burial lists for the cemetery in Camporegio
1336–1430. Cohn asserts, for instance, that it contains representative
information on child mortality when the entries of interments, accord-
ing to his inaccurate figures, produce a child mortality rate of 9 per cent
in the year of the Black Death, 1348, and (erroneously, as can be seen
from Appendix 1 and Tables 4–5 below) one-third in 1363,95 the year of
the next plague epidemic. Comparison of these data with Table 1, Life
table, Model South, level 3, life expectancy at birth (for females) of 25
years, makes it clear that Cohn’s assertions are completely untenable as
assertions of demographic reality in the meaning of registrations of the
deaths in a normally constituted contemporary population at the time,
whatever its social-class composition, pattern of territorial location,
types and structure of habitation or occupational structure.
This can be put in a realistic perspective by considering more fully
the Necrology as a source on contemporary child mortality in Siena. As
can be seen from Tables 4 and 5 below,96 in all non-plague years in the
period 1337–78, thirty-nine years out of forty-two years, the average
proportion of child burials is 7.6 per cent and never exceeded 11.3 per
cent but could be as low as 2.5 per cent. In the three plague epidemics,
the proportions of child burials were 11.0, 46.6 and 59.6 per cent,
respectively, according to the Necrology. The figure for the Black
Death is obviously without contact with reality, in the two following
94
Carmichael 1983: 514.
95
Cohn 2002: 212.
96
Below: Table 4, 254, Table 5, 258. The material on which these tables are based is
cited in Appendix 1.
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232 chapter six
epidemics the figures are within the realm of normalcy, and in the last
epidemic within the higher reaches of the range of normal levels of
mortality. The strong increase from the Black Death to the two subse-
quent epidemics is interesting and will be addressed below. However,
Cohn’s claim that this Sienese cemetery population reflected the
normal process of dying in a normal parish population can be uncere-
moniously rejected.
The very high normal mortality rates among children imply that
children constituted a much higher proportion of the population in
medieval society than in modern society, and the very high normal
mortality had to be balanced by high fertility or the population would
diminish and become extinct. This is what Table 1, Life Table, Model
South level 3, predicts. Few direct demographic studies of the composi-
tion of medieval populations according to age are available for empiri-
cal testing of the prediction. Herlihy and Klapisch-Zuber have presented
material on the age structure of the population in Florence in 1427.
Since this population is affected by plague epidemics and the effects of
plague on populations is at the heart of this discussion, this material is
methodologically problematic as it would tend to invite a circular argu-
ment. However, as it is, it implies a proportion of children ages 0–14 of
45–50 per cent. In my analysis of the studies of medieval skeletal popu-
lations in Scandinavian cemeteries in my monograph on Nordic medi-
eval demography, I reached the same conclusion, that the proportion
of registered children in these ages was 45–50 per cent.97 In addition,
there is always a significant and even serious problem of underregistra-
tion of infants and young children both in population registers and in
cemeteries, as the bones of infants and the youngest children would
tend to disintegrate beyond any possibility for registration or recovery.
For this reason, the real proportion of children under age fifteen con-
stituted probably a significantly higher proportion of the population
than fifty per cent, which figure accords with the predictions of Life
Table, Model South, level 3. Taking into account normal variation, a
normal medieval mortality rate among ages 0–14 can be estimated at
50–60 per cent. Taken as they are, these registrations show that the very
high normal rates of child mortality at the time, constituting 50–60
97
Herlihy and Klapisch-Zuber 1978: 427, cf. also p. 456 where the probability of
underregistration and underestimation is pointed out. Benedictow 1996b: 29–36, cf.
p. 156–9, 162.
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per cent all mortality, occurred in a population where children below

the age of fifteen constituted around half of the population. This con-
firms the impressionistic notions of mortality in the minds of the con-
temporaries and that they were extremely different from modern
notions or impressions. To the irreparable and irremediable damage of
Cohn’s views on immunity, he has avoided to address the crucial ques-
tion: How much increased relative mortality among children would be
needed for the chroniclers to consider a disease a child disease, accord-
ing to their impressionistic notions of such matters? Only an opera-
tional answer to this question can serve as a base for possible inference
to immunity.
This conclusion must be seen in the perspective of available histori-
cal and other relevant knowledge of the relative impact of plague on
children, which will be the next point to consider. Generally, children
are particularly vulnerable to infection due to immaturity of the
immune system.98 A clinical study of plague among Vietnamese chil-
dren of ages 0.25–16 years compared with adult cases published in 1973
concluded that adults resist the disease better than children: “the usual
illness was more fulminant in children, and the mortality seemed to be
higher.”99 A study of plague patients over six years of age in Vietnam
from 1970 concluded thus: “The adolescent age group were most affected
and were also the most toxic […]. These age correlations suggest that
younger patients may be more susceptible to infection and to the toxic
manifestations of the disease.”100 Clearly this indicates that children
and adolescents tend to have weaker innate resistance to plague infec-
tion, are therefore relatively more likely to succumb to plague infection
than older persons and will, thus, suffer higher lethality rates and
supermortality in plague epidemics for this biological reason. In fact,
this was observed in the Black Death: Chalin de Vinario, one of the
pope’s personal physicians, points out that children and youngsters fre-
quently died quite suddenly,101 which accords with the fulminant course
of plague disease in children and youth due to weaker innate resistance
to plague infection relative to adults observed by modern physicians.
However, children also suffer supermortality for social reasons,
because they were especially vulnerable to the detrimental effects of the
98
Donowitz 2003: 17.
99
Burkle 1973: 296.
100
Butler 1972: 274.
101
Sticker 1908: 58.
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234 chapter six
breakdown of families visited by plague. Many children, especially in

the age brackets up to about 10–2 years, would succumb for lack of
nourishment and normal care, even if they were not infected. In his
study of the plague epidemic in the provincial English town of Colyton
in 1645–6, which is based on family-reconstitution of the population
according to parish registers (see above), Schofield addresses this ques-
tion. His study shows that if the father survived and the mother died,
nine out of ten children died; if the mother survived and the father
died, nine out of thirteen children died; if both parents survived, eleven
out of forty-seven children died, corresponding to mortality rates of
90, 70 and 23 per cent respectively.102 Thus mortality among children in
plague epidemics was a variable dependent on the fate of parents. This
point is also made by Del Panta in his history of epidemic disease in
Italy.103 However, this point is not taken into account by Cohn, although
he has read Schofield’s study, albeit with ill-will (see above); scholars in
the field may be surprised that he evidently has not read Del Panta’s
standard work on Italian epidemic history, since so much of Cohn’s
material is Italian.
In modern plague epidemics, the incidence of plague mortality
among older children and youngsters is much higher than their relative
proportion of the population. This was observed in India, China and
Manchuria in the first decades of the twentieth century. Later, the same
observation was made also in the U.S.A. where 55 per cent of all plague
cases in the period 1950–79 were children aged 0–16 years. Clearly, in
plague epidemics children and youth are strongly overrepresented in
relation to their proportion of the population and the relative number
of age classes that they represent. The plague epidemics in Vietnam
during the war in the 1960s and early 1970s were the most recent to
produce many thousands of cases which permitted a thorough demo-
graphic analysis. In 1967 there were 5,547 recorded plague cases,104 and
children and youth under twenty years constituted between half and
two-thirds of all plague cases.105 The researchers explain this skewed
distribution of plague cases according to age by the play-oriented
behaviour and generally active behavioural patterns of children and
youngsters which increase the level or intensity of their exposure to
102
Schofield 1977: 118–9. See also, for instance, Hirst 1938: 690.
103
Del Panta 1980: 48.
104
Reed, Palmer, Williams et al. 1970: 467.
105
Marshall, Joy, Ai et al. 1967: 605, 612.
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infection relative to most other parts of the population.106 Supermortality

among children in plague epidemics is also a function of children’s and
adolescents’ behavioural patterns which entail increased exposure to
infection relative to adults. This point is also made by Del Panta.107
Thus, children should be expected to suffer substantial supermortal-
ity in plague epidemics for biological and social reasons. Carmichael
found that the Florentine Books of Dead “give strong evidence of heavy
mortality among dependent children during the early fifteenth century,”
and that “during epidemic years [in the decades around the mid-1450s]
more than 70 per cent of those dying from all causes were children.”
She is surprised that in the plague epidemic of (1429–)1430, “the rela-
tive losses of children exceeded the percentages that would be expected
if plague alone were the principal determinant of mortality patterns,
since there is no reason that bubonic plague would selectively affect the
young.”108 As shown above, there is no ground for her surprise, because
for various reasons plague produces supermortality in children and
adolescents; instead her findings confirm what should be expected.
This proportion of child mortality in plague epidemics would defini-
tionally be distributed over only fourteen age groups, whilst the remain-
ing well under half of all deaths would be distributed among the
remaining about fifty significant age groups. No doubt, this pattern of
mortality according to age would easily produce an impression among
contemporary observers that plague caused extraordinary high mor-
tality among children which could, according to their culture and mean-
ing of words, permit or inspire the use of the expression “child disease.”
The assumption that such impressions constitute certain evidence of
immunity among the adult population is clearly unwarranted.
Plague according to Social Class, Age and Gender
These preliminary conclusions can be considered as a hypothesis to be

tested on the Black Death which, being the first plague epidemic, hit a
so-called naïve population (without prior contact with the contagion)
in which no population element could enjoy the alleged advantage of
106
Wu Lien-Teh 1936c: 399–400, 417, Pollitzer 1954: 503; Payne, Sandwell and
Hennessy 1946: 993; Reed, Palmer, Williams et al. 1970: 470, 472–7.
107
Del Panta 1980: 48.
108
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236 chapter six
acquired immunity. If chroniclers or other contemporaries observed

supermortality among children, this constitutes corroborative empiri-
cal evidence to the effect that supermortality among children is a nor-
mal aspect of the mortality effects of plague epidemics which is
unrelated to acquired immunity among other sections of the popula-
tion. In this context, M.R. Cazelles’ study of the differential social
impact of the Black Death in France (excluding Languedoc109) accord-
ing to chroniclers and other contemporary observers takes on particu-
lar importance. Its title speaks loudly about his findings, that the
Black Death was an “Épidémie prolétarienne et enfantine,” that is, an
“Epidemic of proletarians and children.”110
Cazelles cites, among others, Simon of Couvin, whose account of the
Black Death in verse Cohn knows and cites falsely in his attack on
Hankin.111 In this case, Cohn does not attribute to Simon de Couvin a
statement he does not make, but passes in silence by his statement on
the particularly great mortality afflicted on the “splendid youth” by the
Black Death. He also passes in silence by Simon de Couvin’s poetic
description of the particularly fulminating course of the disease among
the young which led to death in a day: “who perishes before a day is
over like a flower which born in the field, in the morning greening
flowers, in the evening completely withers.”112 Instead, Cohn refers to
Simon of Couvin’s work on another aspect of the differential social
impact of the Black Death: “all doctors of Montpellier perished in the
plague of 1348.”113
Cazelles cites to the same effect other prominent chroniclers of the
time, prominent in the sense of being among the most often cited
because their chronicles are considered among the most valuable of
their kind, namely those of Jean de Venette and Gille le Muisit.114 In
Histoire de la population française Dubois cites most of Jean de Venette’s
account of the Black Death, including the statement that “All this year
109
Cazelles employs the old geographical term “Langue d’oïl” which denotes the
main part of France where the word for “yes” is “oui,” in contrast to “Langue d’oc” where
the word for “yes” is “oc,” derived from Latin hoc. Languedoc is not included because
contemporary chroniclers there held other views, but because they do not provide
views or observations pertinent to the matter in question.
110
Cazelles 1962/1965: 293–305.
111
Above: M26–7.
112
Littré 1840–1: 233: Illic strata jacet hominum speciosa juventus,/ Quæ perit ante
diem quasi flos qui natus in agro/ Mane virens floret, et vespere totus arescit;. My transla-
tion from Latin.
113
Cohn 2002: 121.
114
Cazelles 1962/1965: 304–5.
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and the next, the mortality of men and women, of the young even more
than of the old, in Paris and in the Kingdom of France, and also, it is
said, in other parts of the world, was so great that it was almost impos-
sible to bury the dead.”115 In fact, Cohn cites this chronicler quite often
in his monograph, twelve times, and even cites the following sen-
tence,116 but on a minor point and without taking interest in the chroni-
cler’s view on the Black Death’s predilection for young persons or
children. Also Gille le Muisit, Abbot of St Martin’s in Tournai (modern
Belgium), states in his chronicle that in Tournai more young persons
than old perished in the Black Death. Cohn has used also this chronicle
and cites it twice on points regarding differential social mortality,
namely on the supermortality of the beneficed parish clergy and to the
effect that “neither the rich, the middling sort, nor the pauper was
secure.”117 Thus, all three chroniclers are well known by Cohn118 who
pretends, nonetheless, that he has overlooked their statements on the
supermortality of young persons or children in the Black Death.
Conspicuously, Cohn knows and cites Cazelles’s paper but pretends
to know only half of the paper’s title and half of its conclusion, writing
that “Raymond Cazelles, has claimed that from the beginning the Black
Death was ‘a proletarian epidemic.’ ” Thus, Cazelles’s view that also chil-
dren, according to the chroniclers, suffered conspicuous supermortal-
ity from the Black Death is deleted and the author’s opinion is
misrepresented. In the same vein, Cohn goes on to state falsely (foot-
note included in brackets):
but more convincingly others, such as Geneviève Prat and Edouard
Perroy, relying on local studies with land registers and fiscal records,
have corroborated the message heard from the mass of the chroniclers:
initially the Black Death was egalitarian in its onslaught [fn. 207:
“Carpentier, ‘Famines et épidémies,’ pp. 1069–70, summarises this
historiography.”]119
This short statement contains three assertions:
(1) that empirical evidence like “land registers and fiscal records” rep-
resents the most valuable and crucial material for the study of the
Black Death;
115
Dubois 1988: 317; The Chronicle of Jean de Venette 1953: 48.
116
Cohn 2002: 110, cf. p. 310.
117
Cohn 2002: 121, 126.
118
Cohn 2002: 310, 312, 316.
119
Cohn 2002: 127.
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238 chapter six
(2) that the Black Death was “egalitarian in its onslaught”;

(3) that the studies based on manorial registers and fiscal registers
corroborated the assertions or statements of the “mass of chroni-
clers” to this effect, that there is full agreement or identity between
the information provided by these two categories of sources on
this point.
As emphasized several times above, Cohn is a scholar who consistently
avoids documentary empirical evidence like population registers, tax
registers, and manorial rolls. As shown in my monograph on the Black
Death, there are available almost 200 demographic studies of mortality
in the Black Death based on such material, but Cohn has not taken
interest in any of them. Instead, Cohn relates to the problem of the
nature of historical plague as a cultural historian attempting to make
his case primarily on the purported amassment of chroniclers’ views,
enumerating in his bibliography 407 “chronicles, annals and calendars.”
This is the material that constitutes the basis for his main argument for
an alternative theory of the microbiological nature of the Black Death.120
Thus, the thrust of Cohn’s remarks just cited is quite astonishing: if
documentary empirical evidence like censuses, tax registers, and mano-
rial rolls are considered superior medieval demographic sources, then
any serious scholarly study of the Black Death, its mortality, differential
social impact according to social class, age and gender, and the ques-
tion of the microbiological nature of historical plague epidemics would
be very different from Cohn’s, as my monograph is for exactly this
reason.
The assertion that a mortal epidemic disease like “the Black Death
was egalitarian in its onslaught” is at variance with epidemiological and
social sciences’ general observation of epidemic diseases’ characteristic
predilection for particular sections of populations, for the poor and
destitute, for the old and the elderly, for infants and children, and so on.
It must be treated with caution and even suspicion. In my monograph
on the Black Death which takes into consideration all relevant studies,
it is shown that the disease was socially selective and non-egalitarian
(see below).121 Hence Cohn’s assertion must be materially untenable,
and it is important to take a closer look at his arguments and support-
ing references.
120
Cohn 2002: 99 and bibliography: 255–73.
121
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Prat’s work of 1952 is a study of the Black Death in the city of Albi on
the basis of two registers in which the population is recorded according
to household and their assets are surveyed in order to assess their taxes,
including those who were too poor to pay taxes who are registered only
by name without tax assessment (compoix d’Albi). Thus, her sources
record households according to householders, always adult persons,
overwhelmingly men.122 Unsurprisingly, her paper does not mention
the words “child” or “children,” does not contain a single reference to a
chronicler, and does not show mortality according to various social
divisions and, thus, certainly does not argue that the “Black Death was
egalitarian in its onslaught.” However, Prat’s paper contains a compari-
son with the compoix of 1357 which shows that the proportion of those
who were too poor to bear any tax assessment had fallen from 42 per
cent in 1343 to 28 per cent in 1357, which could legitimately be taken
to indicate considerable supermortality among the poorest classes of
the city. Cohn’s assertion with respect to Prat’s conclusions, cited just
above, is misleading.
Perroy’s paper of 1949 “On the Origin of a Contracted Economy:
The Crises of the Fourteenth Century”123 likewise does not mention the
words “child” or “children” or use or refer to chronicles or argue that
the Black Death was socially egalitarian in its onslaught. Cohn’s asser-
tion is misleading.
Prat’s and Perroy’s papers are not entered in Cohn’s bibliography. For
support of his assertion and two scholarly references, Cohn refers in
the accompanying footnote to a paper by E. Carpentier published in
1962 which he asserts “summarizes this historiography.” Carpentier
wrote a synthetic paper on the significance of famines and epidemics in
the fourteenth century; she does not mention the mortality of children
in the Black Death, she does not maintain that mortality in the Black
Death was “egalitarian in its onslaught” or that mortality did not vary
according to social class, gender, or age, neither on pages 1069–70 to
which Cohn refers nor anywhere else in the paper. She does not sum-
marize the views of chroniclers, as they are peripheral to her material.
She refers to chroniclers three times, twice in relation the famine and
epidemics of the years 1315–6, and once to make the point that chroni-
clers enumerated the plague epidemics, the first plague, the second
122
Benedictow 2004: 265, 332–3.
123
My translation from French, see bibliography for the original French title.
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240 chapter six
plague, and so on, to show that the Black Death and subsequent plague
epidemics by contemporaries were perceived as representing a new
disease.124 Everything Cohn states about Carpentier’s paper is simply
misleading.
The assertion that Prat, Perroy and Carpentier in these papers “cor-
roborated the message heard from the mass of the chroniclers” is there-
fore wrong in all tree cases. Cohn’s use of false references to these early
papers on these subjects, which are good in their own right, must serve
a need and a purpose. A possible explanation could be that if the Black
Death did not ravage the populations in an egalitarian way, various
social categories would, according to his line of reasoning, suffer differ-
ent rates of morbidity and mortality and, consequently, contain higher
or smaller proportions of persons with immunity, which in subsequent
plague epidemics should be observed with marked consistency by
chroniclers. This would seriously complicate and potentially under-
mine his argument on differential immunity and the development of
plague as a child disease.
In view of the topic of immunity and purported development of
plague into a child disease that allegedly was very clear in the second
plague epidemic, it is a conspicuous feature of Cohn’s argument that he
avoids or evades presenting the two most important papers on the sub-
ject of what happened to children in the Black Death and the subse-
quent epidemic, namely Cazelles’s paper of 1962 on the fate of children
in the Black Death which I have discussed above, and J. Glénisson’s
paper of 1968–9, the most important paper on the second plague
epidemic of 1360–3. In his paper, Glénisson accepts Cazelles’s finding
of supermortality among children in the Black Death according to
the chroniclers.125 Although these two papers are central in relation to
the question of the pattern of mortality of children in the Black Death
and in the second plague epidemic, they do not appear in Cohn’s
bibliography.
Cohn has also avoided presenting the findings of any of quite a
number of papers and monographs based on manorial records and fis-
cal records which were published after Prat’s, Perroy’s, and Carpentier’s
and which show that children and the poor suffered considerable
and even dramatic supermortality in the Black Death. In order to
124
Carpentier 1962: 1072, 1081–2.
125
Glénisson 1968–9: 35.
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emphasize this point, a small sample of these studies will be presented

in detail instead of just enumerating them; I also invite the reader to
consult my monograph on the Black Death.
In his study of the manor of Halesowen (Worcestershire), Z. Razi
found evidence showing that “child mortality in the Black Death was
very heavy,” in fact, “child mortality in the plague must have been
catastrophic.”126 His perspective is also very different from Cohn’s in
relation to the subsequent epidemics: “it would seem that infants
and children were as susceptible to these plagues as they were to the
pestilence of 1349.”127
M. Ecclestone’s study of mortality among the “garciones,” the (all-
but-)landless men aged twelve and older at seventeen of Glastonbury
Abbey’s manors, uncovers considerably higher mortality among this
rural proletarian class than among the customary tenants, the land-
holding classes of peasant society.128
On some manors of the bishopric of Winchester, the (all-but-)land-
less classes were liable to pay death duties in the form of small money
payments called heriots in order to obtain the right to transfer cottages
and tiny plots of land to inheritors. Heriots are thus a special type of
death duty that would reflect the number of deaths or level of mortality
among this proletarian social class. The heriot registers appear to be
complete from 1270 through the time of the Black Death. The studies
of these registers reveal very high supermortality among this proletar-
ian class relative to that suffered by the customary tenants.129
In three parishes near Chambéry in the County of Savoy in south-
eastern France, mortality in the Black Death has been studied on the
basis of records registering small money payments made by the house-
holds for permission from the lord to collect firewood. These lists
record most of the landless classes who also needed firewood for cook-
ing and heating. New lists of these rural householders were produced
each year, also in the year of the Black Death, and they reflect directly
the impact of the Black Death. The study of these lists reveals clear
supermortality among the poor and proletarian classes.130
126
Razi 1980: 104.
127
Razi 1980: 129.
128
Ecclestone 1999: 6–29. See also Benedictow 2004: 265, 364 fn. b, 368, 374–6.
129
Ecclestone 1999; Postand and Titow 1958–9: 408; Ohlin 1966: 84–9; Benedictow
2004: 259, 364–5 fn. g, 376–7. Cf. Arthur 2005: 113–20, 123–7.
130
Brondy 1988: 88. See Benedictow 2004: 259, 264–5, 320–1.
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242 chapter six
Thus, Cohn’s assertion that studies based on fiscal and manorial

sources confirm the socially egalitarian character of the Black Death’s
onslaught is three times false,
(1) false because such studies generally prove the contrary,
(2) false because the studies he cites do not provide evidence to this
effect, and
(3) false because Prat’s paper provides good evidence for the opposite
view, namely that the poor and proletarian social classes suffered a
marked supermortality in the Black Death. The Black Death’s
onslaught was socially non-egalitarian both according to social
class and according to age.
In the page preceding the quotation under discussion, Cohn himself
cites several chronicles which clearly demonstrate that the social impact
of the Black Death exhibit a highly varied and differential social pat-
tern, i.e. that it was non-egalitarian. He asserts that
The Paris Medical Faculty, Geoffrey le Baker, the Abbot at Tournai [Gille
le Muisit: my insertion], and Henry of Hervordia even saw the first plague
striking down the strong and rich in greater numbers than the weak and
ill.131
This is seemingly the opposite of Cazelles’s findings of chroniclers’
observations on the differential social impact of the Black Death pre-
sented above. However, the Paris Medical Faculty is not a chronicler
and has not addressed differential mortality but rather the cause of the
Black Death.132 Cohn refers to two chroniclers. As usual he has only
picked what suits his case and thus has produced a skewed impression
of the opinion expressed in the source. What Le Baker really states is,
according to Creighton, that:*
Few of the first rank died, but of the common people an incalculable
number, and of the clergy and the cleric class a multitude known to God
only. It was mostly the young and strong who were cut off, the aged and
weakly being commonly spared.133
Clearly, Le Baker gives quite a complicated picture of differential
mortality, and he obviously agrees with Cazelles or rather Cazelles’s
131
Cohn 2002: 126–7.
132
This statement is cited with valuable introductory comments in Hoeniger 1882:
149–56. Cf. Sticker 1908: 60–2.
133
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informants among French chroniclers that the Black Death also visited
the poor and proletarian classes with particular ferocity. It can be
proven that Cohn knows better since almost a hundred pages later he
refers directly to Creighton’s text on this page, but again in a way that
misrepresents not only Le Baker’s statement but also Creighton’s ren-
dering of it, namely:
Similarly, Creighton, History of Epidemics in Britain, p. 122, found that
the plague of 1348–9 in England carried off able-bodied young adults
and not the young, weak or elderly.134
Here, Cohn paraphrases, or more accurately apparently paraphrases
Creighton’s view on the differential social impact of the Black Death,
but deletes Creighton’s emphasis on the great supermortality among
the poor thus producing a great distortion of Creighton’s view.
Cohn states that “Various chroniclers claimed that the first wave of
plague hit populations indiscriminately, regardless of age, sex, or social
class,”135 in other words in a socially egalitarian way. Conspicuously, in
the accompanying footnote he succeeds in mustering only two chroni-
clers for support,136 while as seen above he inadvertently provides four
references for an entirely different view among chroniclers or contem-
porary observers and, as demonstrated by a correct paraphrasing of Le
Baker’s statement on the matter, this material could easily be aug-
mented. According to my experience, it would be possible to find two
or more chroniclers who express a particular opinion on any conceiv-
able point, which means that Cohn’s references in this case can only
have illustrative function and serve as a basis for formulating working
hypotheses. Thus, a quick look at Cohn’s documentation shows that he
is not able to provide significant evidentiary support for his central
assertion: “the message heard from the mass of the chronicles: initially
the Black Death was egalitarian in its onslaught.” It is one of his numer-
ous arbitrary assertions formed to serve his great objective, his great
134
Cohn 2002: 212, fn. 73.
135
Cohn 2002: 126.
136
Cohn 2002: 126. He also supports this view by citing Matteo Villani who main-
tained, or in Cohn’s unfortunate choice of word “suggested,” that the poor were espe-
cially severely hit but also called the Black Death “a pestilence among men of every
condition, age and sex.” However, there is no logical or factual contradiction between
maintaining that the poor were especially severely hit and that all social classes, ages
and both genders suffered severe losses; it means that the Black Death did not take an
equal toll among all main social categories of people and therefore was not egalitarian
in its impact.
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244 chapter six
revolutionary ambition, an alternative theory of the nature of the Black

Death. His misrepresentation of Prat’s, Perroy’s, Carpentier’s, and
Cazelles’s paper and Le Baker’s views reflects the grave problems he has
with his sources and the means he must employ in order to form a
semblance of supporting evidence.
The reference to “message heard from the mass of the chroniclers” is
fundamentally a statistical assertion implying a very large number of
persons. Central to Cohn’s assertion is the implied claim that he has
gathered the views or opinions on the matter of such a large number of
chroniclers that it constitutes a mass of material. Whether 407 chroni-
clers constitute a mass of persons according to the terminology and
conceptual notions of historical science and social science more gener-
ally is a definitional question open to debate and dispute. However, the
sociological term “mass [of persons]” should satisfy also other criteria
than numbers, for instance, “a very diverse population that has no
social organization,” which makes it unlikely that chroniclers would
constitute a mass of persons according to formal sociological criteria,
since they tend to be interconnected with respect to social class, educa-
tion, ideology, values and norms, frame of mind and outlook on life.
If ordinary sociological demands for definitional clarity and specifi-
city are left aside, it must be pointed out that the meaning and statisti-
cal implication of the expression “message heard from the mass of
chroniclers” is unclear. Primarily, it must be taken to mean that con-
temporary chroniclers as a mass, massively, held a certain opinion. This
is obviously untenable, since chroniclers held a great variety of opin-
ions, as documented above. However the expression could possibly
with maximum goodwill be understood to mean that the vast majority
of chroniclers held a certain opinion. In this context, expressions like
“the (great) mass of ” or “the vast majority of ” must mean that the pro-
portion holding this opinion must be very high, at least 75–80 per cent,
in order to discern the expression notionally from formulations like
“over half,” “the majority,” “the substantial majority” or even “the great
majority,” so that the implied meaning would at least approach some-
thing like “the overwhelming majority.” Thus, Cohn’s assertion must be
taken to imply that at least 300–25 chroniclers should have expressed
this specific opinion. Of course, anyone knowledgeable of medieval
chronicle(r)s will know that this is taken out of thin air in order to
serve Cohn’s argumentative objective. If Cohn’s assertion were to have
any scholarly relevance or significance in the form of any level of ten-
ability, it would need to be underpinned by explicit and systematic
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empirical data: the relevant statements of the (mass of) chroniclers

must be quoted and marshalled in some type of table or register which
renders the vital statements with footnotes which alone can satisfy the
crucial criterion of testability. Only in this way can the assertion be
made methodologically valid and materially tenable. These citations,
which would have been useful both for his supporters and his critics,
could have been presented in a fourth appendix and be used for cross-
references in his monograph. Cohn has refrained from performing this
work although he asserts that he has the material at his disposal.
Scientifically and methodologically, his approach is arbitrary, his argu-
ment invalid and untenable.
However, any scholar knowledgeable of the cultural attitudes of con-
temporary chroniclers to the Black Death would know that many of
them, quite possibly the majority of them, do not mention the Black
Death,137 and that the great majority of those who mention the epi-
demic do not provide any information on differential social mortality,
but make only some terse statement about great mortality. Only a tiny
fraction will mention the Black Death and also provide opinions on the
social distribution of mortality. Cohn’s reference to 407 chroniclers and
the opinions of the mass of chroniclers constitutes fictitious evidence
which is unavoidably misleading and forms the basis of quasi-
statistics.
In fact, chronicles can rarely be used for the study of generalized or
sociological aspects of social, demographic or epidemic reality. To the
extent that their writings attract interest, it is usually in connection
with the study of cultural history, medieval mentality and outlook on
life, and in some cases of political history. Their statements on demo-
graphic or soci(ologic)al issues must be exposed to relentless and mer-
ciless source-criticism and be testable on independent material, tests
they regularly (but not always) fail to pass.
A Demographic Case Study: The Necrology of the Monastery of

San Domenico in Camporegio
Cohn also argues his case for immunity on the basis of a purported
demographic study of a necrology associated with the Dominican
monastery of San Domenico in Siena which was mentioned above.
137
Benedictow 2004: 192–4, 207.
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246 chapter six
Since he ascribes great importance to the evidentiary value of his study

of this Necrology, especially with respect to immunity and its great sig-
nificance for the understanding of the microbiological nature of the
disease, it should be taken seriously. As a medievalist historical demog-
rapher, I have taken upon myself the task of producing a responsible
study of the central part of the Necrology which can be usefully com-
pared with Cohn’s study and serve as a base for a serious discussion of
the purported facts.
First, the medievalist demographer must make some highly special-
ized initial comments. A necrology is not a burial register comparable
to parish burial registers as Cohn gives the impression. The typical
necrology is a monastic (or ecclesiastical) death-roll or register contain-
ing entries of the deaths or more usually, as in this case, burials of per-
sons which was usually kept in the chapter’s assembly hall where it was
used for brief commemorations of the dead in the morning. Such com-
memoration services were normally associated with honourable places
of burial in the cemetery or monastic buildings and normally required
significant payment. Consequently, persons entered in a necrology did
not constitute a normal population of dead persons but were over-
whelmingly persons who could afford such investment in a better after-
life in relation to God and to prestige among the local population.
Interments in the cemetery of the monastery of San Domenico in
Siena are known by name in lists running from 1336 when it was started
and are published as I Necrologi di Siena di San Domenico in Camporegio.
As pointed out repeatedly, a conspicuous aspect of Cohn’s monograph
and his approach to scholarly work is his lack of interest in taking into
account many of the central works of Italian historical demography on
the late medieval period. This Necrology has been briefly studied in
relation to the Black Death by two of Italy’s leading historical demogra-
phers of the twentieth century, Professor M. Livi-Bacchi and Professor
L. del Panta in central works of Italian historical demography, namely
Livi-Bacci’s La société italienne devant les crises de mortalité [Italian
Society in the Face of Mortality Crises], and Del Panta’s standard
work Le epidemie nella storia demographica italiana (secoli XIV–XX)
[Epidemics in the Demographic History of Italy (Fourteenth to Twen-
tieth Centuries)]. These works remain unmentioned in both Cohn’s
book and his bibliography, and he discusses the Necrology as if he has
discovered it and pioneered research on it.
I have made a complete demographic registration of all entries from
the first full year, namely 1337, to 1378, that is, for forty-two years and
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through three plague epidemics, in all 1644/46 persons, with accurate

registration of all demographic vital information on age, gender, day of
burial, and so on. The material is summarized in Table 5 according to
year, gender and age; in order to ensure easy testability all of the material
is presented in Appendix 1. The Necrology contains ample information
showing that burials normally took place on the day of death or the
following couple of days, a delay which is of no significance for this type
of study. The editor of the Necrology has enumerated the acts of inter-
ments but not the number of interred. Since there is an incidence of two
or more simultaneous burials in the same grave and also other “irregu-
larities,” use of the enumeration for production of numerical data will
lead to inaccurate figures, which is the case for all three scholars.
According to Agnolo di Tura, the Black Death broke out in Siena in
May,138 which may quite likely be when it became observable to con-
temporaries. To the historian’s prying eyes there is, however, a suspi-
cious sprinkling of burials in the Necrology starting 12 April and which
by 7 May comprised eight interments139 corresponding to about ten in
a month or 120 burials a year, about four times the yearly average in the
ten preceding normal years. This can be considered the endemic phase
of the incipient plague epidemic, the ten interments on 10 May repre-
senting the start of burials from the initial epidemic phase.
It is useful to see how prominent Italian historical demographers
relate to this source and the problems associated with it in order to put
Cohn’s handling of it in perspective. In the words of Del Panta who has
enlarged on some of Livi-Bacchi’s original findings, over a hundred
deaths were recorded
in the period including 10 May and 6 June [1348];140 then, abruptly, the
registrations break off and are not taken up again with regularity until the
end of August. If the curve is extrapolated for the period in which there
are no registrations, we reach an estimate (obviously only suggestive) of
about 400–20 deaths in the whole year.141
Del Panta clearly includes the whole part of the Necrology which
covers continuously the course of the plague epidemic until it breaks
138
Cited in The Black Death. A Turning Point in History? 1971: 13. Cf. Del Panta
1980: 112; Benedictow 2004: 92, 94.
139
Nos. 739–46.
140
The correct figure is 111 persons buried: there are a number of burials of two or
more persons in the same grave.
141
Del Panta 1980: 115. My translation from Italian.
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248 chapter six
off 6 June; only a few episodic interments are registered later, two on
12 June, three 17 June, three 6 August, four single interments in the
days 28 August–2 September, and only three more burials for the rest
of the year. These ten episodic entries in the second half of 1348 can-
not be taken as evidence that systematic registration of burials was
resumed. The four entries performed around 1 September are not dif-
ferent from the previous three instances of entries of burials and are
followed by only three burials for the rest of the year, only a fraction of
the usual number of burials for normal years before the Black Death
(see Table 5). This must be taken to indicate that regular registration of
burials was discontinued after 6 June for the rest of the year. Instead,
the ten episodic interments in the cemetery in the second half of the year
can be usefully seen in the light of the personal tragedies so graphically
described by the city’s well-known chronicler Agnolo di Tura who bur-
ied his five children with his own hands, and also relates that “none
could be found to bury the dead for money or for friendship. Members
of a household brought their dead to a ditch as best they could, without
priest, without divine offices.”142 Table 2 shows that, in 1348, there were
seven burials in April, fifty-five in May and sixty-four or sixty-six in
June, in all 126/128, which all may be presumed to reflect the effects of
the Black Death. Quite likely this was also the case with six burials in
August and two burials in September, so in all there were 134/136
plague-related burials. In the whole year there were 144/146 burials.
As can also be seen, the registration of burials breaks off at a time
when the number of daily and weekly burials was rising steeply, that is,
it breaks off before the first epidemic phase was completed by reaching
the apex of epidemic intensity. Thus, the burials recorded in the
Necrology reflect only a small part of the plague period and lack the
remaining part of the phase of increasing epidemic intensity, the whole
period of maximal intensity and the decline of the epidemic to its final
phase and end. In fact, the lacuna is so huge and devastating for the
Necrology as a source on the Black Death that the number of burials
recorded in the year of the Black Death is considerably smaller than in
the severe year of dearth and hunger-related epidemics of 1340 when
176 persons were buried in the cemetery, and much smaller than in the
subsequent plague epidemics when 328 persons were entered in the
142
Rendered in The Black Death. A Turning Point in History? 1971: 13. Cf. Bowsky
1964: 15; Del Panta 1980: 112; Benedictow 2004: 91.
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Table 2. Interments by month and week in the Dominican cemetery in

Siena in 1348
Month Week No
1 2 3 4 5
January 0 0 2 1 0 3
February 0 0 1 0 0 1
March 0 0 1 2 1 4
April 0 3 1 2 1 7
May 2 5 14 21 13 55
June 57/59 4 3 0 0 64/66
July 0 0 0 0 0 0
August 3 0 0 1 2 6
September 1 0 1 0 0 2
October 0 1 0 0 0 1
November 0 0 0 0 0 0
December 0 1 0 0 0 1
Total number of
interments 144/146
Necrology in 1363 despite three lacunae, and 231 persons in the epi-
demic of 1374, as will be seen from Table 5 and Appendix 1.
Cohn mentions that the Necrology is not complete for the time of
the Black Death,143 but over forty pages from where he presents most of
the results of his purported demographic study of it,144 at quite a safe
distance, presumably, for the memory of most readers, and in a way
that seriously understates the size of the lacuna and its numerical sig-
nificance.145 He does not anywhere in his monograph specify the grave
significance of this lacuna or include it in his discussion. He does not
mention at any time that there are three large lacunae in the Necrology
for the time of the next plague epidemic of 1363, as will be seen from
Table 3, or that there is also a probable but not clearly significant lacuna
in connection with the third plague epidemic of 1374. Instead, he uses
143
Cohn 2002: 171.
144
Cohn 2002: 211, 212.
145
Below: 256–7.
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250 chapter six
Table 3. Interments by month and week in the Dominican cemetery in

Siena in 1363
Month Week No
1 2 3 4 5
January 0 1 1 1 3 6
February 0 0 2 0 2
March 1 1 8 0 1 11
April 5 5 12 9 3 34
May 10 14 20 16 9 69
June 39 28 4 0 0 71
July 22 17 13 5 2 59
August 2 2 24 34 10 72
September 0 0 2 0 0 2
October 0 0 0 0 0 0
November 1 0 0 0 0 2
December 0 0 0 1 0 1
Total number
of interments 328
crude and inaccurate figures summarizing the entries on these three

plague epidemics for comparative purposes, making strong inferences
as to immunity and differential mortality, which are obviously meth-
odologically invalid and materially untenable (see below).
A plague period for the Black Death of only four months for such a
large city, according to Del Panta’s assumption, would be highly unusual.
In fact, there is, as mentioned, really no reason to assume that normal
burial practice and regular registration of burials in the Necrology was
resumed at the end of August, and the four single interments around 1
September have, as mentioned, the same character of episodic or inci-
dental interments as those made 12 June, 17 June and 6 August. This
means that there is no real empirical basis for assuming that normal
keeping of the Necrology was resumed before the start of the next year.
This source-critically based view can be empirically supported with an
important piece of information given by Agnolo di Tura, namely that
the epidemic continued in full force “until September.”146 Thus, more
146
Cited after Bowsky 1971: 14.
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likely the epidemic began to decline some time in September and

petered out during October, quite likely ending with a few endemic
cases sometime in November, the epidemic lasting, as one would
expect, eight months (at least). This time perspective corresponds
much better to the size of the city of Siena and the time needed for a
plague epidemic to spread effectively across it, a time perspective well
known from other plague epidemics in big(ish) cities at the time. This
means that the lacuna is much larger than assumed by Del Panta and
that his extrapolation is much too small. An extrapolation along more
realistic lines suggests a much higher number of persons who poten-
tially would have been recorded as being interred in the cemetery if the
process of registration had not broken down: over 600 potential burials
seems more realistic on these premises. The estimated number and dis-
tribution of burials according to these extrapolations are based on gen-
eral knowledge of the pattern of development and duration of plague
epidemics and on a Necrology recording only the main part of the first
phase of the epidemic as reflected in interments in this cemetery.
Obviously, the empirical basis is weak and the extrapolation is hypo-
thetical. These mortality figures can usefully be seen in the perspective
that the population loss in Siena in the Black Death appears to have
been of the same order as in Florence, namely about 60 per cent.147
Del Panta erroneously claims that the number of yearly interments
entered in the Necrology in the previous years was, on average, twenty,
which means that he assumes that the mortality in the Black Death
increased by a factor of twenty or twenty-one. Since the average yearly
number of interred persons in the ten normal years preceding the Black
Death was 31.2,148 the increase, according to Del Panta’s extrapolation,
would be around thirteen times the average of normal years. A more
realistic period of extrapolation would suggest an increase in the poten-
tial number of burials of at least around twenty times or somewhat in
excess of 600 burials, if the system had not broken down and inter-
ments in the cemetery and entries in the Necrology had proceeded as
usual. Instead, only 144/146 interments are recorded in the Necrology
147
Benedictow 2004: 299–300; Carmichael 1983: 514.
148
See Table 5 and Appendix 1. In the decade 1338–47, 438 persons were interred in
the cemetery, a yearly average of 43.8 persons. If the severe crisis year of 1340 is deleted
(176 burials) and substituted by the interments in the normal year 1337, the number of
interred persons in the ten normal years would be 312, and the average number of in-
terred persons in normal years would be 31.2.
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252 chapter six
for the whole year or an increase of only 4.6 times relative to the previ-
ous ten-year average. This shows again that the lacuna has devastating
effects for any demographic use, a point which Cohn disregards at the
cost of making all his assertions and statistics and comparisons based
on the Necrology untenable.
The outcome of this analysis of the registrations relating to the Black
Death appears more realistic also when compared with the next plague
epidemic of 1363 which was generally much smaller than the Black
Death and generally caused much lower mortality rates. This is the cru-
cial epidemic for Cohn’s argument that survivors of the Black Death
acquired persistent and good immunity according to the pattern of
viral diseases and that plague’s consequent development into a child
disease was reflected now for the first time. According to the Necrology,
this second plague epidemic lasted at least six months in Siena, namely
March to August. In this period, as shown in Table 3 and Table 5, 328
persons were interred in the cemetery, 182 more persons or 25 per cent
more interments than were registered in the Black Death, which cer-
tainly does not support a notion of widespread immunity among the
survivors. However, in January 1363 there are six registrations of inter-
ments in the cemetery, the largest number recorded in the Necrology
for this month from the first full year in 1337 to the end of my demo-
graphic registration forty-two years later in 1378. This indicates that
plague contagion arrived in the late autumn and that the epidemic was
in incipient development but was slowed down almost to a halt by
chilly or cold winter weather. In this phase, its presence took on the
character of a smouldering epizootic spreading among the rat colonies,
a process manifesting itself in a few episodic human cases and prepar-
ing the ground for a rapid epidemic rise with the advent of warmer
early spring weather. This explains the early start of the plague epi-
demic in the middle of March.
However, as can be seen in Table 3 and Appendix 1, the Necrology’s
registration of burials also broke down in the 1363 epidemic, three
times, the first breakdown started 16 June and lasted fifteen days until
1 July when registration was resumed; a new breakdown started 26
July149 and lasted for twenty-one days, during which time there
were only seven episodic burials, until 16 August when systematic
registration of burials were resumed, but only for fifteen days until the
149
Or perhaps 27 July, since there is one burial 26 July.
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registration again broke off 30 August, this time for good. In the two
weeks preceding the first breakdown of registration there had been
twenty-eight burials, in the fifteen days following the resumption of
burials there were sixty-eight entries. This shows that the registrations
first broke off when the epidemic was in a process of intensification,
that it was resumed at the height of the epidemic, and that it broke
down completely and finally when the epidemic was still at its apex. It
may also suggest that during the twenty-two days of intermission of
registration there may have been a loss of 50–60 potential burials. The
third and final breakdown came at a point when the epidemic appar-
ently still raged with full force. Indisputably, these three lacunae are so
large and disastrous for the Necrology as a demographic source also for
this plague epidemic that to present any crude figure for burials in the
cemetery as reflecting the reality of mortality and to use it for compari-
son and inferences to immunity and differential mortality by gender or
age is clearly fallacious and misleading.
This source-critical demonstration of the comprehensive lacunae in
the Necrology and their devastating effects on its usability as a demo-
graphic source for the study of plague mortality is not the only devas-
tating blow. Even a quick glance at Tables 4 and 5 and Appendix 1 will
show, as documented above, that the proportion of child burials in the
cemetery does not reflect the normal process of dying in a local soci-
ety/parish society. In the eleven years preceding the Black Death, from
the first full year of the Necrology in 1337 to 1347, thirty-two interred
persons could have been children below age fifteen;150 in the same
period a total of 519 burials were registered in the Necrology, so chil-
dren constituted consequently a very low 6.1 per cent of the interred.
This period includes the severe dearth year of 1340 with a greatly
enhanced number of burials, namely 176, about five times the average
number of burials in the ten normal years of the period 1337–47, how-
ever, the number of children interred was only nine and the proportion
of children 7.4 per cent. Correspondingly, children constituted 8.2 per
cent of the interments in the inter-plague period of 1349–62. In the
next inter-plague period, 1364–73, the percentage of child burials was
8.2 per cent, in the following four post-plague years the percentage was
11.3. As shown in Table 5, in all of the non-plague years 1337–78 taken
together, the total number of burials was 938, the total number of child
150
See Appendix 1.
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254 chapter six
Table 4. Proportion of child burials in the cemetery of Camporegio in

Siena, 1337–78, according to the Necrology. Non-plague years (N.P.),
crisis year 1340, plague years (P.Y.), in italics 1348, 1363, 1374.151
Period Burials Adults Children %
1337–39 119 116 3 2.5
1340 176 163 13 7.4
1341–47 224 208 16 7.2
1348 144/46 128/30 16 11.0
1349–62 208 191 17 8.2
1363 328 175 153 46.6
1364–73 158 143 15 9.5
1374 233 94 139 59.6
1375–78 53 47 6 11.3
Total 1643/45 1265/67 378 23.0

Total N.P. 938 868 70 7.6
Total P.Y. 705/07 397/99 308 43.6
burials was seventy, so the proportion of child burials was 7.6 per cent.
Even in the Black Death, the proportion of child burials was only 11
per cent. Since normal child mortality in ages 0–14 in normal years at
the time would be in the range of 50–60 per cent of total mortality, this
makes it entirely clear that the cemetery population was grossly unrep-
resentative of populations in normal local societies or parishes and that
its recruitment did not reflect the normal process of dying in a normal
population. Clearly, this age structure reflects special cultural and reli-
gious attitudes and practices associated with social class within a
broader context of civilization. The great majority of the children of the
adults interred in the cemetery must have been buried elsewhere, pre-
sumably in the cemeteries of the parishes in which their parents’ habi-
tations were located, whilst their parents purchased expensive and
religiously attractive burial places in the cemetery of the Dominicans.
Obviously the increase in the proportion of child burials from the Black
Death to the two subsequent plague epidemics is interesting and will be
addressed below. However, the fact that the proportion of child burials
151
The material on which this Table is based, is presented in Appendix 1.
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reverted nearly to the pre-Black Death level in the normal years between
the plague epidemics is also interesting, and must also be explained.
The central point of Cohn’s argument is that he claims to have suc-
ceeded in proving that the plague epidemics repeatedly ravaging Siena
in this period caused immunity in the surviving adult population and
that this is what is reflected in the greatly increased percentages of child
burials in the plague epidemics following the Black Death. What should
now be clear is that the material he cites is grossly deficient, that the
entries in the Necrology generally cannot support realistic demo-
graphic statistics or Cohn’s mortality statistics more specifically. The
facts are that all child mortality statistics based on this source are meth-
odologically invalid and factually untenable: the percentages of child
burials before the Black Death and in the inter-plague periods repre-
sent only a tiny proportion of normal child mortality, and the percent-
ages of child mortality for the plague years, disregarding for a moment
the fact that they are not based on valid source material, are all within
the range of normalcy of child mortality in normal years at the time
and provide therefore no specific empirical reflection of child mortality
in plague epidemics.
Cohn’s statistics are quasi-statistics, they resemble statistics but are
not. They are quasi-statistics because the registration breakdowns at an
early stage of the Black Death and covers only a minor part of the epi-
demic. They are quasi-statistics because Cohn avoids pointing out and
taking into account that there are three large breakdowns of the regis-
trations in the Necrology in relation to the next plague epidemic of
1363. Cohn pretends that he can compare a grossly deficient part of the
Necrology relating to the Black Death with another grossly deficient
part relating to the second plague epidemic without having any possi-
bility for identification of the missing parts in order to produce correc-
tions that could make it feasible to establish tenable comparability. This
is obviously methodologically fallacious independent of the phoney
character of his mortality statistics. In English historiography, the term
‘bastard feudalism’ is applied to situations that resemble feudalism but
are not, for instance, enlistment in royal armies of gentlemen warriors
for longer periods of service than the forty days associated with feudal
obligations or services given by a retainer to his lord in exchange for a
fee and livery.152 In this sense, we have here bastard statistics, what
152
See for instance Hicks 1995; Bellamy 1989.
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256 chapter six
resemble statistics but are not. And this is only the beginning of bastard
statistics, there is much more to come.
When this presentation of the Necrology’s burial register is com-
pared with Cohn’s handling of it, interesting and revealing aspects can
be observed. It may be useful to start with Cohn’s presentation of the
register and its contents and then we will examine the demographic
information he maintains to have extracted from it:
For burials of the laity in Dominican grounds at Siena, the figures for
1348 show the same seasonal trajectory: they mounted in May, jumping
from seven to 54, and continued to climb in June (66 burials), but for July
the scribes ceased their reporting, perhaps turning to unrecorded mass
graves or dying themselves. When the register was resumed in August, its
count had returned almost to normal (6).153
Cohn maintains that he has found 127 burials in the register in the
months from April to June before it breaks off, which is quite correct
(126/28), but also maintains that the number of interments in the whole
year is 136,154 which is not correct, as can be seen from Tables 2 and 5,
and reflects a pervasive tendency of looseness with his figures. In this
citation, the crucial point is that Cohn endeavours to make the period
of registration seem much longer and by implication the lacuna much
shorter than in fact is the case and, thus, to upgrade its quality and
potential usability far beyond the limits that source-criticism will allow.
He neglects to inform his readers that it broke off 6 June, misleadingly
and erroneously implying that instead it continued throughout June
and did not break off until some time in early July, about a month later.
He also pretends that normal registration of burials was resumed in
August, while the reality is that there was an episode of three burials 6
August which was followed by a lacuna lasting to 28 August, when
there was a new episode of four registrations, followed by a breakdown
lasting for the rest of the year when only four episodic burials are
recorded. Cohn’s account would clearly tend to suggest to the unsuspi-
cious mind that registration was resumed quite early in August and
that the epidemic had declined radically at this point. For this reason,
Cohn cannot inform his readers that the “66” (64/66) burials in June
(Table 2) occurred in the first six days of the month and that, in fact,
half of the total number of deaths for the whole epidemic as recorded
in the Necrology are from these six days and, consequently, can
153
Cohn 2002: 171.
154
Cohn 2002: 211.
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represent only a small fraction of total mortality in this month. This is

a point of crucial importance since it shows that the epidemic was
under explosive development when the register broke off. This indi-
cates also that the keeping of the Necrology was discontinued because
the great mortality at the time affected the monastic administration
and made the organization of prestigious individual interments in the
cemetery (well-nigh) impossible.
Thus, Cohn’s presentation of the registrations of this Necrology for
the time of the Black Death appears to be profoundly characterized by
misinformation. While the lacuna in the form of absence of regular
registration of burials lasts for the rest of the year, Cohn makes it seem
as if it lasts about thirty-five days. Presumably his motive is to increase
the register’s seeming value as a demographic source in order to make
his “data” appear more plausible when he presents, forty pages later, the
essence of his purported “demographic” findings or data in the form of
quasi-statistics (in this quotation the footnotes are in brackets; for the
correct figures, see Table 5):
lay burials at Siena’s Camporeggio bear out even more forcefully the same
patterns. In 1348, men and women were buried in almost equal numbers,
the same as in non-plague years. [fn. 65: I Necrologi di Siena di San
Domenico, 66 of 136 were female, or 49 per cent] But, with the plagues of
1363, 1374, 1383, 1400, and 1411, women consistently fared better than
men, accounting respectively for 43, 45, 42, and 43 per cent of the burials,
[fn. 66: In 1363, 143 of 331 were women; in 1374, 104 of 233; in 1383, 110
of 260; in 1400, 78 of 182; and 52 of 120 in 1411.]155
Unusually, and in an obvious and amateurish breach of demographic
terminology, Cohn claims to have registered women when he also has
included female children, which would require use of the term
“females.”
The records of Camporeggio (Siena) are the only ones I know to record
the burials of the laity across the plague experience from the Black Death
of 1348 to the fifteenth century. Here we witness a remarkable transfor-
mation. Of 136 Sienese buried in the Dominican cemetery in 1348, only
12 or under 9 per cent, were identified as children (simply filii or filie
without their own names) [fn. 73].156
155
Cohn 2002: 211.
156
Cohn 2002: 212: “Similarly, Creighton, History of Epidemics in Britain p. 122,
found that the plague of 1348–9 in England carried off able-bodied young adult and
not the young, weak, or elderly.” This citation is commented on above: 243, and shown
to be false.
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258 chapter six
With the second strike in 1363, their proportion increased to 116 of 331,
over a third of the plague burials. The change corresponds with what
chroniclers across Europe were saying. As we saw earlier with sex and
social class, they emphasised the plague’s indiscriminate killing in 1348.
Matteo Villani called it “a plague among men of every condition, age, and
sex.” [fn. 74: Matteo Villani, Cronica, I, p. 9.]157
Instead of 1361 [sic! (should be 1363), my insertion] being exceptional,
the burials plot this second plague on a trend-line of increasing propor-
tions of childhood deaths through the fourteenth century. In the third
plague of 1374, the death of children in Siena increased from a third to
over a half (136 of 233).158
Table 5. Proportion of child and female burials registered in the necrol-

ogy of the Dominican cemetery in Siena, 1337–78. Non-plague years
(N.P.), crisis year 1340, plague years (P.Y.) 1348, 1363, 1374. A = Adults,
F = Females, C = Children
Period Burials A FA F A % C % FC FC % All
F%
1337–39 119 116 59 50.9 3 2.5 1 33.3 50.4
1340 176 163 91 55.8 13 7.4 8 61.5 60.7
1341–47 224 208 103 49.5 16 7.2 7 43.8 49.1
1348 144/46 128/30 15964 52.9 16 11.0 8 50.0 52.6
1349–62 208 191 69 33.1 17 8.2 6 35.3 36.1
1363 328 175 66 37.7 153 46.6 75 49.0 43.0
1364–73 158 143 71 49.7 15 9.5 4 26.7 47.5
1374 233 94 40 42.6 139 59.6 62 44.6 43.8
1375–8 53 47 20 42.6 6 11.3 5 83.3 47.2
Total 1643/45 1265/67 583 46.0 378 23.0 176 46.6 46.1
Total
N.P. 938 868 413 47.6 70 7.6 31 44.9 47.3
Total
P.Y. 705/07 397/99 170 42.6 308 43.6 145 47.1 44.6
157
Cohn 2002: 212–3.
158
Cohn 2002: 214–5.
159
The number of adult men and women is smaller than the number of adults be-
cause in two cases of simultaneous burials of three and 4–6 persons respectively the
gender of the interred is not given, no. 796–3, and no. 839–4/6, which give 64 women
and 57 men. Thus, the population of gendered burials in 1348 is 137 persons when
children are included, of whom women are 64 plus eight female children, in all 72.
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One should note that the Latin terms filius and filia do not mean “child”
as maintained by Cohn but “son” and “daughter.” This is a point of some
of importance in the present circumstances since all human beings are
sons or daughters, including adults, but not all sons and daughters are
children. Latin has words specifically denoting children or youngsters,
for instance, natus, infans, puer/ puella, parvulus/ parvula, juvenis. The
five last words are employed by the Dominican scribes, but only in
twenty-eight cases160 or 1.7 per cent of the burials in the period. This
confirms that neonatals, infants, toddlers and young children were not
normally buried in the cemetery, although they constituted a large part
of total normal mortality, probably about 45 per cent (see Table 1).
Even as a point of departure for a realistic discussion of child mortality,
this should be taken to suggest that also older dead children were often
not buried in the cemetery with their parents or relatives. These termi-
nological considerations agree completely with the empirical picture of
the proportions of child mortality provided by the Necrology for nor-
mal years and the crisis year 1340. On the other hand, since sons and
daughters also are children, many of them, quite possibly a large major-
ity of those who are registered without indication of marital status or
other indications of adult age, will be children. Importantly, there can
be no doubt that the identification of all entries of unnamed sons or
daughters as children will produce an unrealistically high figure, but
since there is no means of “sieving” this material, it is probably best to
do as Cohn does and identify them all as children, as I have also done.
However, Cohn neglects to inform his readers about his choice and its
consequences (see Appendix 1). One should also note that the term
juvenis meaning “youth” could also denote persons of age 15 and a few
years older, but this problem is of no real significance since it used only
in five cases.161
As can be seen from Table 5 and substantiated by the presentation of
the underlying material in Appendix 1, Cohn’s figures are inaccurate to
the point of being erroneous and misleading: the number of recorded
burials in 1348 is 144/46, not 136, and the number of children is six-
teen, not twelve. In 1363 the number of burials is 328 and the number
of children is 153 and not 116, seventy-eight boys and seventy-five
160
I Necrologi di San Domenico 1337: Nos. 466, 843, 881, 896, 913, 976, 996, 1176,
1189, 1212(1229), 1224, 1227, 1231, 1233, 1234, 1425, 1427, 1450, 1509, 1839; 1116–2,
1550; 1054, 1070–2, 1071, 1667.
161
I Necrologi di San Domenico 1337: Nos. 1054, 1070–2, 1071, 1667.
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260 chapter six
girls; the proportion of child burials is thus 46.6 per cent and not 33 per
cent. This discrepancy is so large that it is inexplicable as the outcome
of serious research but could possibly be explained on the assumption
that Cohn wishes to produce a larger rise in the proportion of immune
persons in the population as the logical consequence of repeated plague
experience.
Further comments must start with elementary source-criticism
which predictably levels more devastating blows at Cohn’s use of the
Necrology. It is not true, to put it in the mildest possible terms, that the
Necrology of San Domenico at Camporegio contains continuous
records of the “plague experience from the Black Death of 1348 to the
fifteenth century.” Cohn knows, and the readers now know, and also
know that he knows, that for most of the period of the Black Death
there are no registrations in the Necrology, simply because the registra-
tion of burials broke down early in the development of the epidemic162
and that there are three large lacunae in the Necrology for the period of
the plague of 1363.
Cohn does not subject his purported demographic data from the
Sienese Necrology to the usual source-critical and analytical tests by
presenting and addressing crucial questions: Did the burials in this
prestigious cemetery recorded in the Necrology really reflect the
normal process of living and dying in a normal population of a local
parish? Could they have been affected by religious and social prestige,
social class and cultural notions which attracted deceased for burial
from elsewhere or from special segments of local population or the
Sienese population? Could the interred for these reasons be socially
skewed also according to age or gender? True, ten pages before his
presentation of his purported demographic data from this source he
states:
the demand to be buried in Siena’s Dominican cemetery also appears to
have risen in tandem with the rising prestige of the Dominicans in post-
plague Siena, as illustrated in the pious choices of the laity in their last
wills and testaments.163
In a much used technique, Cohn separates this important source-
critical information from his discussion of the source and presentation
162
Here it is not of significance whether or not this reflected the actual breakdown
of the process of interments.
163
Cohn 2002: 200–1.
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of his purported demographic results. This reveals that Cohn recog-

nizes that the cemetery population was not recruited from the local
parish population, at least to a considerable extent, but attracted people
living elsewhere, in other localities and parishes, for religious and devo-
tional reasons in the hope that a burial place there would enhance their
afterlives and also out of social ambition associated with prestigious
religious burial places in those days. The Necrology contains much
material showing that burial places were often expensive, and the scribe
functioning in the years c. 1368–74 provides a particular abundance of
such information.164
In this context, Cohn supports his argument by stating: “the number
of burials recorded at Santa Maria Novella in Florence during the sec-
ond plague of 1363 also outstripped those of 1348 (90).”165 Cohn
neglects to mention that this burial register also breaks off during the
peak of the Black Death and therefore is grossly incomplete, a fact that
the responsible historical demographer Livi-Bacchi conscientiously
underlines. He also scrupulously underlines the very special character
of this burial list, namely that it recorded those interred with the
Dominican habit, a ceremony performed with some pomp, an honour
that only devoted upper-class people could afford.166 These central
source-critical facts are also carefully emphasized in my discussion of
this source and its potential usefulness in my monograph on the Black
Death.167 Thus, this register is socially unrepresentative as well as highly
incomplete, and Cohn’s use of it is misleading and fallacious. The buri-
als of persons in the habit of the Dominicans in the cemetery of Santa
Maria Novella in Florence was not unique; according to the Sienese
Necrology this was also the case with quite a number of those interred
in the Dominican cemetery there. Unfortunately, this information can-
not attain further source-critical function since Cohn does not discuss
this Dominican cemetery’s religious and social prestige before the
advent of the Black Death but links it directly to his presentation of his
purported demographic data from the Necrology. Although it is not
stated explicitly, it seems that this was a prestigious burial ground also
before the Black Death; according to Cohn its religious prestige
increased in post-plague Siena, but perhaps it would be more accurate
164
I Necrologi di San Domenico in Camporegio 1937: 104–22.
165
Cohn 2002: 154.
166
Livi-Bacchi 1978: 14.
167
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262 chapter six
to say that it continued to increase.168 There is strong evidence for

assuming that the cemetery population was skewed not only by age,
but also by social class.
Also Cohn’s claim that “women consistently fared better than men”
in subsequent plague epidemics according to the Necrology of San
Domenico in Siena, in the meaning that they suffered lower mortality
rates, is obviously fallacious and untenable. The distribution of burials
of female and male adults and female and male children in the period
1337–78 are shown in Table 5 below and in Appendix 1. The Necrology’s
burial figures from the time of the Black Death cannot be compared
with later burial figures for two independent sufficient reasons. Firstly,
the comparison is fallacious for the fundamental source-critical and
methodological reason that it represents only a small fraction of the
Black Death and cannot, therefore, be compared with purportedly
complete but, in fact, also grossly incomplete registrations of burials in
the 1363 epidemic or with the registrations of burials during the subse-
quent plague epidemic of 1374. Secondly, the comparison is fallacious
as the social origin and composition of the population of living which
was recruited into the cemetery population has not been usably clari-
fied. It is clearly not a normal local population or parish population as
is overwhelmingly demonstrated by the gross deficit of children in nor-
mal years. These two conditions represent two independent sufficient
conditions for concluding that it is fallacious to maintain that the
somewhat lower proportions of women’s burials in subsequent
plague epidemics reflect lower female mortality. Instead, the small ten-
dential underrepresentation of females could reflect the fact that men
in this society were considered more important than females and that,
for this cultural reason, males were more often given prestigious and
costly burials. Thus, what the Necrology’s burial lists quite probably
show is not that “women consistently fared better than men” in plague
168
Cohn ignores the usual source-critical question of the extent to which the seem-
ing increase in this burial ground’s prestige is real, and not affected by other factors, for
example, by the fact that wills and testaments which he refers to for substantiating his
point became more usual in the period following the Black Death (and subsequent
plague epidemics), which resulted in larger numbers of inheritances and increased the
affluent proportion of the population, and/or also as a consequence of intensive changes
in culture and mentality associated with the development of Renaissance society.
Perhaps even more important were the lessons learned from the difficulties of making
wills during such a tremendous mortality crisis as the Black Death, emphasizing the
importance of preparing for calamities of a new dimension.
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epidemics but that they consistently fared worse than men with respect
to getting burials in prestigious burial grounds. Only this explanation
contains a causal factor and must therefore be deemed superior. As
underlined above, it is fallacious not to take into account the fact that
social, cultural and religious factors could affect the cemetery popula-
tion and the relative distribution of burials according to the main
socio-demographic divisions of social class, gender and age which may
produce alternative explanations.
The social unrepresentativeness of the cemetery population stands
out in glaring clarity when child mortality, which is at the heart of the
matter under discussion here, is considered more closely.169 As shown
above in Table 5, in all non-plague years 1337–78 taken together the
proportion of child burials was 7.6 per cent. In the Black Death, the
proportion of child burials was only eleven per cent. Since normal child
mortality in ages 0–14 in normal years at the time would be in the
range of 50–60 per cent of total mortality, the recorded level of child
mortality is clearly grossly unrepresentative of normal local societies
or parishes at the time and the recruitment of the cemetery population
was not the result of the normal process of dying in a normal parish
population, but reflects special cultural and religious attitudes and
practices associated with social class and a wide(r) catchment area. As
pointed out above, the great majority of the children of the adults
interred in the cemetery must have been buried elsewhere, presumably
in the cemeteries of the parishes in which their parents’ habitations
were located, while their parents purchased expensive and religiously
attractive burial places in the cemetery of the Dominicans. Obviously,
the strong increase in the proportion of child burials from the Black
Death to the two subsequent plague epidemics from 11 per cent in the
Black Death to 46.6 per cent in the second plague epidemic and 59.6
per cent in the third epidemic is interesting and must be explained.
However, also interesting is the fact that the proportion of child burials
in the second and third plague epidemics does not exceed the level of
normal child mortality at the time of 50–60 per cent, which shows that
these strongly increased mortality rates do not reflect or indicate spe-
cific levels of plague mortality. The fact that the level of child mortality
reverted nearly to the pre-Black Death level in the normal years between
the plague epidemics must also be explained.
169
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264 chapter six
Cohn asserts that in the plague of 1400 in Florence, the “gravedig-

gers identified two-thirds” of burials as children, however, he does not
provide a footnote.170 Despite considerable efforts, I have not been able
to identify the possible source with certainty, but it could be a table in
Carmichael’s monograph.171 As mentioned above, Carmichael found
that the Florentine Books of Dead “give strong evidence of heavy mor-
tality among dependent children during the early fifteenth century,”
and that “during epidemic years [in the decades around the mid-1450s]
more than 70 per cent of those dying from all causes were children.”172
Thus, it may appear that Cohn understates the significance of
Carmichael’s findings and that the threat they represent to his alterna-
tive theory may be the reason for his unreasonable attacks on her work
which is, in fact, of high scholarly standards (see above). Also the pur-
ported further increase in the proportion of child burials in the next
plague epidemic of 1374 to over half reflects underregistration of child
mortality as a proportion of normal mortality in plague epidemics,
since children are particularly at risk in plague epidemics and child
mortality increases as a proportion of total mortality, but also this
mortality rate is within the range of normal child mortality in normal
years. Obviously, the proportions of child burials according to the
Necrology are gravely deficient and grossly unrepresentative, they can-
not serve as evidence of the real level of child mortality in normal years
or in plague years or be taken to demonstrate any change in children’s
proportions of mortality between the two first plague epidemics or in
relation to later plague epidemics. Consequently, the increases in regis-
tered proportions of child burials in the two post-Black Death plague
epidemics in this cemetery do not constitute evidence that this devel-
opment represents increasing levels of immunity among survivors so
that groups of children born after the previous epidemic constituted
increasing proportions of the susceptible part of the population.
Instead, one must consider other reasons for the increase, especially
changes in religious attitudes and practices under the traumatic psy-
chic impact of the Black Death. When the Sienese chronicler Agnolo di
170
Cohn 2002: 215.
171
Carmichael 1986: 94. Cf. however, Carmichael 1983: 514. In Herlihy and
Klapisch-Zuber 1978, which would be a likely source for such information, the entries
on gravediggers = becchini/(fossoyeurs) match with “peste 1400” only on pages 453
and 456 where nothing to this effect is stated. I have also checked all pages which the
index indicates contain references to gravediggers or to “peste 1400.”
172
Carmichael 1986: 91–2. See above: 235.
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Tura informs his readers that he buried his five children with his own
hands, we can only attempt to understand the psychic trauma, and
since this terrible experience, according to his account and other con-
temporary accounts, appears to have been quite usual, its generalized
psychological effects on Sienese mentality and culture must also be
taken into account. It is also important to take into account the fact that
these informal burials were unlikely to have been registered anywhere,
and the possibility cannot be excluded that Agnolo di Tura buried them
in the cemetery of San Domenico in Camporegio.
Of particular importance in this context is the following quotation
from Agnolo di Tura, which shows that not only the mind-boggling
mortality of the Black Death but also the breakdown of burial services
impressed itself on contemporary observers:
And so they died. And none could be found to bury the dead for money
or friendship. Members of a household brought their dead to a ditch as
best they could, without priest, without divine offices. Nor did the death
bell sound. And in many places in Siena great pits were dug and piled
deep with the multitude of dead. And they died by the hundreds both day
and night, and all were thrown in those ditches and covered over with
earth. And as soon as those ditches were filled more were dug. And I,
Agnolo di Tura, called the Fat, buried my five children with my own
hands. And there were also those who were so sparsely covered with
earth that the dogs dragged them forth and devoured many bodies
throughout the city.173
The last rites were a necessary condition for salvation according to the
teachings of the Church, as was burial in a consecrated burial ground,
and a proper funeral was considered indispensable for the profoundly
religious and devotional minds of contemporary medieval persons.
Nothing worse could happen to them than the events so graphically
described by Agnolo di Tura, that the dead were unceremoniously
thrown into ditches. Agnolo di Tura’s account does not stand alone:
other contemporary chroniclers, for instance Marchionne di Coppo
Stefani in Florence described the social scene in a similar way:
All the citizens did little else except to carry dead bodies to be buried;
many died who did not confess or receive the last rites; and many died by
themselves and many died of hunger […]. At every church they dug deep
pits down to the water-table; and thus those who were poor who died
173
Cited in The Black Death. A Turning Point in History? 1971: 13. Cf. Del Panta
1980: 112; Benedictow 2004: 92, 94.
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266 chapter six
during the night were bundled up quickly and thrown into the pit. In the
morning when a large number of bodies were found in the pit, they took
some earth and shovelled it down on top of them; and later others were
placed on top of them and then another layer of earth, just as one makes
lasagne with layers of pasta and cheese.174
Evidently, the most frightening features of this enormous demographic
disaster in the authors’ mind are, in accordance with the religious
beliefs and mentality of the time, that people died without priestly
administration of the last rites, and, thus faced perdition and eternal
punishment, and that their loved ones were unceremoniously and
humiliatingly thrown into mass graves or, even worse, unconsecrated
ditches, which was an independent sufficient condition for perdition
or at least prevented salvation. There is every reason to believe that
such very frightening and humiliating events on a mass scale would
have jolted many persons into action to save themselves and their
spouses and children and other loved ones from such a fate in the future
and there is every reason to believe that the representatives of the
Catholic faith, both the secular and regular clergy, took the same view
and also considered how this could be avoided in the future. In other
words, when the second plague epidemic and subsequent plague
epidemics arrived, there was a mental and practical preparation of all
parties concerned for a tremendous onslaught, among the laity as well
as the clergy. This explains the tremendous efforts by the Dominicans
of San Domenico in Camporegio to re-establish the functioning of the
Necrology and burials during the second onslaught of plague, twice
succeeding in reorganizing a functioning administration after break-
downs. This explains on source-critical grounds some peculiar features
of the Necrology over time: it seems that parents who had pur-
chased costly and prestigious burial places in the Dominican cemetery
acquired the right to have their children buried properly there and
preferably in their own graves or sepulchres in order to be certain that
their children would not be unceremoniously thrown into mass graves
or unconsecrated ditches if they died when they were sick themselves
or after they had died and were unable to take care of the children’s
burials.
In this perspective, it is also important to take into account the
fact related so graphically by contemporary chroniclers that the
174
Cited after Henderson 1992: 145.
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mind-boggling mortality in the Black Death had the effect that many
survivors received inheritances and acquired a new wealth or good for-
tunes, and many also entered good economic positions due to oppor-
tunities created by the epidemic. Survivors of the Black Death and later
plague epidemics were quite likely to be lucky twice. Agnolo di Tura,
for example, states that “all money had fallen into the hands of nou-
veaux riches,”175 which is certainly logical: when a great proportion of
the population, probably over half, dies in a few months, many of the
survivors must receive an inheritance and often multiple inheritances.
This meant that many people could now afford not only to raise their
standards of living substantially but also acquired the means to raise
the standard of their afterlife by the purchase of attractive burial places
for themselves and their spouses and ascertaining that also their dead
children would be properly taken care of when the burial process in
their local parish cemeteries broke down, as it so often did in the Black
Death. This is only a well-founded explanatory hypothesis which, how-
ever, integrates much important material and many important per-
spectives of the contemporary scene, is not a variance with known
facts, and is a methodologically and materially tenable hypothesis,
which Cohn’s immunity theory is not. Crucially, this hypothesis is
materially testable, and I can only hope that historians of contempo-
rary culture and mentality will address it from a scholarly basis that I
do not possess.
This discussion of the material bearing on Cohn’s alternative theory
to the effect that plague was a viral disease, that survivors acquired
strong and persistent immunity and that plague epidemics subsequent
to the Black Death developed into a child disease can now be summa-
rized. Much of the purported material from chroniclers and burial lists
which Cohn produces to support his theory is not valid and must be
rejected as evidence for his theory. At a closer look much of his mate-
rial does not agree with his theory or is incompatible with it. It has also
been necessary to cite a number of studies and much material left out
by Cohn which is at variance with his theory. It has also been made
clear that Cohn does not base his discussion on adequate demographic
competence, as reflected in the absence of realistic notions of normal
levels of child mortality in medieval society and the normal proportion
of child mortality of total mortality, and in his flawed terminology.
175
The Black Death. A Turning Point 1971: 15.
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268 chapter six
It has also been shown that he has not taken into account the frequent
fulminant course of plague disease in children and youth with a conse-
quent increased level of lethality or their supermortality from second-
ary catastrophic effects in plague epidemics, which increase children’s
relative proportion of mortality above the normal proportion of 50–60
per cent in normal times. Unsurprisingly, it is possible to find chroni-
clers who make this point, that children and youth also suffered a dis-
proportional level of mortality or supermortality in the Black Death. In
addition, Cohn has ignored or neglected Cazelles’s study on this point
as well as Glénisson’s study of the second epidemic. Cohn has not pre-
sented tenable evidence to the effect that the relative or absolute level of
child mortality increased from the Black Death to subsequent plague
epidemics. Cohn has also neglected to take into account several impor-
tant pieces of research with direct bearing on his theory of immunity
effects associated with historical plague: the material on re-infections,
the stability of lethality rates, the pattern of clustering of plague cases
according to size of family, and so on, which represent further evidence
that historical plague could not have been a viral disease spreading by
cross-infection. Cohn’s assertions to the effect that plague epidemics
subsequent on the Black Death took on the character of a child disease
are untenable.
The Real Problem and its Solution: Marriage Rates and Fertility Rates
after the Black Death
In the chronicles it is possible to discern a stronger emphasis on the

perceived level of child mortality in the second plague epidemic than
in the Black Death. This impression is, then, the real problem to be
addressed which has been overlooked or ignored by Cohn since it does
not imply any potential for support of his great revolutionary alterna-
tive virus-based theory.
A real interest in this impression and a scholarly will to examine and
explain it in its own right rather than turning it into a case for a revolu-
tionary new theory could usefully start with another point made by
chroniclers. As pointed out by Glénisson, “The contemporaries have
noted that, after the plague epidemic [the Black Death], there was an
epidemic of marriages and the number of births rose.”176 Jean de
176
Glénisson 1968–9: 30. My translation from French.
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Venette’s description of how survivors of the Black Death reacted to the

post-plague social scene and the new sociology of opportunity can be
a useful point of departure:
After the cessation of the epidemic, pestilence, or plague, the men and
women who survived married each other. There was no sterility among
the women, but on the contrary fertility beyond the ordinary. Pregnant
women were seen on every side. Many twins were born and even three
children at once.177
Jean de Venette claims to have observed that, in the wake of the Black
Death there was a great upsurge in marriages and a great consequent
increase in fertility. As usual, chroniclers’ statistics cannot be taken lit-
erally, and there is no biological reason to accept that sterility among
women disappeared in the wake of the Black Death, or that there was
an increase in individual natural fertility, or that there would be any
increase in the incidence of births of twins or triplets, but one may take
serious interest in the generalized impression of great increase in mar-
riage rates and a consequent strong increase in fertility rates.
Chroniclers’ statements in this regard can be taken seriously because
this type of development should be expected for three main reasons. In
the decades before the advent of the Black Death life was difficult for
the great majority of common people both in the towns and in the
countryside. Great population pressure on the resources for produc-
tion and income made it difficult for young adults to find work and
income that could serve as a base for sustaining a family, thus there was
a pool of young persons ready to marry and on the lookout for oppor-
tunities. This is a Malthusian explanation based on comprehensive eco-
nomic and social research and appears to be tenable for most of Europe,
from Norway in northern Europe to Spain in southern Europe, from
England and France in Western Europe all the way to Poland178 in
Eastern Europe.179 Secondly, great mortality entails that many people
will receive inheritances, often from more than one relative, so the
177
The Chronicle of Jean de Venette 1953: 51.
178
See for instance Pelc 1937. His price history of Krakow agrees completely with
the price history of Western European countries and both reflect great Malthusian
pressures before the Black Death and a late medieval fall in grain prices and increase in
wages which must reflect a great contraction of the population which allowed peasants
and their lords to concentrate grain growing on the best and most productive lands
while the demand for workers produced an upwards pressure on wages. Cf. Benedictow
2004: 219–21, 387–94.
179
Benedictow 2004: 177–9, 388–91.
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270 chapter six
economic situation of survivors would tend to be strongly improved.

Thirdly, the social situation would now be very favourable for marriage
because great mortality creates attractive vacant positions in the labour
market and the housing market.180 Young adults entered them, acquir-
ing the economic ability to realize marriage ahead of plans, often even
making dreams come true. Thus, not only would young widows and
widowers soon remarry and keep up normal reproduction, but also
many young unmarried persons would now be in a good position for
entering into matrimony producing in due time a large increase in
realized fertility, a baby boom, that would produce a corresponding
increase in the proportion of infants and children in the population.
The period from the Black Death to the second plague epidemic covers
the whole span of child years, ages 0–14, as in Siena where the Black
Death raged in 1348 and the second plague raged in 1363, or almost
the whole span of child years in Norway, where the main year of the
Black Death was 1349 and the second epidemic raged in 1360.181
In fact, quite a number of studies of various plague epidemics reveal
that a strong increase in marriage rates was a characteristic feature of
post-plague social developments. With the usual time-lag, birth rates
increased briskly.182 There is also significant and important empirical
evidence associated with the aftermath of the Black Death. This pattern
is clearly reflected in the only extant parish marriage register from the
time of the Black Death, that of Givry in Burgundy. In the years 1336–
41, for which the register appears to be complete, the mean number of
marriages was 17.5, varying between eleven and twenty-nine. In 1348,
the year of the Black Death, no marriages were recorded in this small
Burgundian town, either because the keeping of the register broke
down or because the ravages of the Black Death had made it impossible
to arrange new marriages either for the hopeful or for the parish priest
and his auxiliary personnel. However, in 1349, the number of regis-
tered marriages was eighty-six, a quintupling of the pre-plague mean.
And for a number of subsequent years the number of marriages was
considerably higher than in the pre-plague period: in the year 1350
there were thirty-three marriages, and the number did not fall under
180
Cf. Herlihy and Klapisch-Zuber 1978: 194–8.
181
Benedictow 2002: 44–81, 91–2, 115. Cf. Benedictow 1993/1996: 73–102, 141–5.
182
Bickel 1956: 515; Russell 1958: 41–2; Le Méné 1964: 196, 209; Croix 1967: 77;
Croix 1981: 264–345; Dupacquier 1972: 199–204; Clark and Slack 1976: 88–9; Hatcher
1977: 56–7; Herlihy and Klapisch-Zuber 1978: 208; Perrenoud 1978: 265–88; Vaquer
Bennassar 1987: 133; Weiner 1970: 50–1.
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the pre-plague level until 1355, when there were twelve marriages fol-
lowed by ten marriages in 1356.183 Since the post-plague population
must have been much smaller than before the plague, the marriage rate
was quite likely still significantly higher in 1355–6 than before the Black
Death. The same was the case in Florence after the Black Death: “The
memories of the Florentine families show well the cascades of marriage
contracts which followed a great epidemic.”184
The same development has been noticed in England by several schol-
ars. T. Lomas found that at the manor of Norton in County Durham
“there were a great many grants of licence to marry [merchets] in
1350.”185 J. Ravendsdale found in his study of the manor of Cottenham
in Cambridgeshire
a rush to the altar (or should it be the church door) in 1349 [which] rep-
resented marriages that would have been postponed even longer but for
the plague, the average age at marriage would have been depressed, thus
bringing increased fertility within marriage.
The crop of marriages in 1349 must have been followed by a baby boom
among the villeinage.186
In his study of the manor of Halesowen (Worcestershire), Razi found
that in the three-year period which immediately followed the Black
Death, “proportionally more marriages were contracted in Halesowen
than in any other three-year period in the fourteenth century.”187
The number of marriages in Halesowen “rose sharply again in the
years 1361–3 as a reaction to the second visitation of the plague,”
which is evidence that mortality among adult members of the manorial
community was high. If mortality had been concentrated among
children because many or most of the adults were immune, the sec-
ond plague would not have been followed by an upsurge in new mar-
riages. It is also evidence to the effect that supermortality among
children is a general feature of plague epidemics. Razi concludes that
“during the first two decades following the Black Death the marriage
rate in the parish was high […] the birth rate must have been at a high
level.”188
183
Gras 1939: 303.
184
Herlihy and Klapisch-Zuber 1978: 196. My translation from French.
185
T. Lomas 1984: 260.
186
Ravensdale 1984: 212, cf. 209.
187
Razi 1980: 132–3.
188
Razi 1980: 134.
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272 chapter six
This means that in the years following the Black Death, the propor-
tion of children (ages 0–14) in society would have increased consider-
ably and even substantially above the normal level of around 50–60 per
cent. Since children constituted a considerably or substantially higher
proportion of the population at the time of the second plague than
before the Black Death, children would also constitute a correspond-
ingly higher proportion of total mortality than in the Black Death. If
child mortality normally constituted 65–70 per cent of population
mortality in the Black Death, this explains why some chroniclers
noticed a relative increase in child mortality in the second plague com-
pared with what they had seen in the Black Death. A substantially
increased proportion of child mortality above this level would readily
affect the impressions of contemporary observers, and this is what
probably occurred in relation to the second plague epidemic. On this
solid background of facts and studies, the fact that some chroniclers
designated the second wave of plague epidemics as a child disease can
reasonably be taken to reflect a perception of a real phenomenon: chil-
dren below the age of fifteen constituted an unusually high proportion
of the population, and children in general died in correspondingly
higher proportions which also were affected by the additional specific
increase related to plague disease, and produced an impressionistically
observable higher proportion of the victims than people were accus-
tomed to.189 These impressions reflected social and demographic reality
but had nothing to do with immunity among survivors in the Black
Death or subsequent epidemics. This is a sufficient and satisfactory
explanation of the tendency among chroniclers to emphasize the high
proportion of child mortality in the Black Death and the stronger ten-
dency to emphasize the high proportion of child mortality in the sec-
ond plague epidemic.
This resolution of the problem addressed in this chapter corresponds
also to the observations by chroniclers of the socio-demographic dis-
tribution of mortality in the second plague epidemic, for instance, by
Knighton:
Eodem anno mortalitas generalis oppressit populum quae dicebatur pestis
secunda. Et moriebantur tam majores quam minores, et maxime juvenes et
infants. Et de congregatione nostro xi canonici mortui sunt.
189
Benedictow 1993/1996: 144–5. Cf. Bridbury 1973: 591.
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This year a widespread mortal disease visited the population which is

called the second plague. Both the upper and lower classes died, and
especially youth and children. And in our congregation eleven canons
died.190
As can readily be seen, the contemporary observer Knighton was of the
opinion that all main social classes suffered serious mortality; adults
were not spared, as is also shown by the Dominican Necrology of Siena,
but children and youth suffered even higher proportions of mortality
than in the Black Death. This is what should be expected according to
ordinary demographic and sociological considerations and has noth-
ing to do with acquired immunity in any part of the population. This
account explains the phenomenon in the basic scientific meaning that
all relevant evidence can be satisfactorily incorporated within a normal
demographic explanatory framework based on ordinary demographic
developments in the wake of plague epidemics.
After I first pointed out this resolution of this problem in my doc-
toral thesis,191 I have noted that both L. Genicôt and A. Bridbury have
suggested a similar explanatory model and it seems also to be implied
in Herlihy’s and Klapisch-Zuber’s study of late medieval Florence.192
Cohn discusses quite a number of points mentioned in my doctoral
thesis and exhibits quite comprehensive knowledge of it. One may
again note with interest that his reading is selective, and he takes no
notice of the sections on immunity and on the inverse correlation
between population density and mortality in modern as well as and
historical in plague epidemics, epidemic manifestations with eviden-
tiary powers of falsification of his alternative theory.
190
See Shrewsbury 1971: 128; Russell 1948: 229 and fn. 24.
191
Benedictow 1993/1996: 141–5.
192
Genicôt 1966: 675–5; Bridbury 1973: 591; Herlihy and Klapisch-Zuber 1978:
195–7.
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PART FOUR
DEFINING FEATURES
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INTRODUCTION: CONCEPT OF DEFINING FEATURE
In principle, all diseases are identified by comparison with known

defining properties or a set of characteristic features according to a
level and range of compatibility. A standard case definition serves as
the base for description of the epidemiology of a disease or health
event. This comparative methodological approach must also be used in
all endeavours to identify historical diseases, including the question
whether or not historical plague epidemics were bubonic plague or had
a different microbiological identity according to any of the alternative
theories.
In the Part 3 above, it has been decisively shown that all fundamental
requirements for the rise and spread of bubonic plague epidemics were
operative in medieval and early modern Europe. It has also been shown
that the central aspects of spread and mortality were not at variance
with the observations on bubonic plague made by the IPRC when
proper account is taken with respect to the extent and modernity of the
epidemic countermeasures implemented in India at the time. It has
also been clearly demonstrated that the pattern or dynamics of spread
and the level or social distribution of mortality did not militate against
the disease being bubonic plague. All assertions of the advocates of
alternative theories of historical plague to the contrary were shown to
be untenable. The fact that the fundamental requirements for bubonic
plague were operative in European society at the time obviously sug-
gests the possibility of epidemics of bubonic plague.
A defining feature of an epidemic disease is characteristic only of
that disease and permits therefore certain identification. In medical or
epidemiological terminology, the term is “pathognomonic feature” or
also “cardinal feature,” while in the terminology of social science it is a
“defining feature,” a self-explaining term that will be used here. Defining
features can be ordinary clinical and epidemiological manifestations of
a disease caused by a specific infectious pathogen and its process of
transmission or demographic manifestations in the form of a unique
level or pattern of morbidity or mortality according to age, gender,
social class or population density.
Positive identification of the microbiological agent of historical
plague epidemics can be achieved by direct positive identification of
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278 introduction
the genetic or biological material, the DNA or proteins of Yersinia pes-

tis, taken from skeletal remains in plague graves of the past. Such find-
ings will constitute evidence to the effect that the pathogen of bubonic
plague was present at the time and was spread in epidemic form and,
consequently, independently make a strong or decisive case for the
identity of historical plague epidemics with bubonic plague. This topic
will be discussed below in the chapter “Defining Feature 5: Reclamation
of Yersinia pestis from Plague Cemeteries or Graves.” It can also be
identified by unique clinical or epidemiological properties like, for
instance, the normal occurrance of buboes or latency periods.
Defining features can also have a composite character, that is, they
can consist of two or several characteristic features each of which may
not be unique to a specific disease but which taken together constitute
a unique combination of concomitant manifestations which satisfy the
definition of a defining feature.
Shrewsbury is very clear and firm on this point on page 1, specifi-
cally in connection with the identification of historical diseases:
The confirmatory evidence that is required to identify a pestilence in
olden times as an epidemic of bubonic plague may be either a contempo-
rary description of the clinical picture of the pestilence that is pathogno-
monic of plague or a conjunction of certain observations that are exclusive
to the epidemiology of plague. Unless, one—and preferably both—these
conditions are fulfilled the assumption that an ancient pestilence was an
epidemic of bubonic plague is not justifiable.
These general comments on the concept of defining features pave the
ground for presentation and discussion of some specific reflections or
manifestations of bubonic plague that constitute a definitional feature
suitable for comparison with historical plague for the purpose of iden-
tification of the nature of the disease. These features can, as mentioned,
usefully be divided into clinical, epidemiological, and demographic.
This provides a basis for presenting a sample of cases suitable for iden-
tification of historical plague.
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CHAPTER SEVEN
DEFINING FEATURE 1: LATENCY PERIODS
Bubonic plague epidemics have a distinctive temporal pattern of devel-

opment from the introduction of plague contagion into a rat colony in
a locality to the first human case or cases which can usefully be divided
into several phases (see also Appendix 3):
(1) The temporal pattern of plague-infected rats and fleas
(1a) Normally, when an infective rat flea of the usual species
Xenopsylla cheopis has been introduced into a rat colony, it
takes ten to fourteen days before the rat colony has become
so decimated that it is difficult for the great numbers of fleas
which have gathered on the remaining but soon-to-die rats
to find new hosts.1
(1b) After about three days of fasting, hungry rat fleas will turn
on human beings in their immediate surroundings.2
This initial epizootic phase of a bubonic-plague-epidemic-
to-be lasts thirteen to seventeen days.
(2) Temporal pattern of the first human case or cases
(2a) Time of incubation: When human beings have been infected
with bubonic plague, the infection takes on average three to
five days to incubate before the disease breaks out.
(2b) Duration of illness: The course of illness takes on average
another three to five days before the diseased in most cases
die.3 Thus, the development of a human plague case from
1
IPRC 1907g: 764; Lamb 1908: 21, 51; Wu Lien-Teh 1936b: 222.
2
IPRC 1907g: 765; Lamb 1908: 52; Wu Lien-Teh 1936c: 387; Pollitzer 1954: 485.
3
IPRC 1907g: 765; Lamb 1908: 52; Chun 1936: 309–10, 313; Wu Lien-Teh 1036c:
387; Pollitzer 1954: 409–11, 418, (485). The IPRC estimates the average duration of
illness in fatal cases at 5.5 days. This figure is the outcome of the fusion of two sets of
figures, namely the average duration of illness of 100 fatal cases reported on their case
cards, which was 3.6 days, and the average of 64 hospital cases which was 7.5 days.
I cannot agree with the IPRC that the average duration of illness according to these two
sets of figures is 5.5 days: instead the average is 5.12, which should be rounded to five
days. In my opinion, this estimate is probably flawed also for methodological reasons.
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280 chapter seven
infection to death takes usually six to ten days, on average,

eight days.
(3) Latency period, first part
From the introduction of plague contagion among rats in a
human community it normally takes nineteen to twenty-seven
days, on average around twenty-three days, before the first per-
son dies from plague. This time lag or latent period between the
importation of contagion and the first human case(s) is one of the
defining features of bubonic plague: no other epidemic disease
exhibits a similar pattern of early development. New research has
fully clarified the biological premises.4
(4) Endemic phase
Since this process will have to be repeated by the spread of infec-
tive rat fleas (by contiguous spread or metastatic spread) to other
rat colonies where the disease will develop in a similar way, the
development of a plague epidemic is characterized by a slow,
incipient initial phase, an endemic phase, with only a sprinkling
of cases while the underlying epizootic processes acquire increas-
ing momentum and eventually become manifest by several con-
comitant deaths and cases of severe illness.
(5) Transition from the endemic into the epidemic phase and the full
latency period
The transition into an epidemic phase takes around forty days
after the introduction of plague contagion into a rat colony in a
human community. In this phase the epidemic developments
become more immediately observable and recognized in village
Quite likely, cases arriving at hospitals would tend to live longer and have a better
social background than the average of Indian plague cases. One misses therefore con-
siderations relating to questions of social and illness-related representativeness. The
numbers of patients constituting the two sets of figures appear to be used unweighted
according to notions of representativeness and the reasons for the great discrepancy
between the two figures are not commented on. Taken together, these factors represent
significant methodological problems. I prefer therefore later estimates which also take
into account subsequent experience, namely that the duration of illness is normally
three to five days, which also corresponds better to the information taken down on the
IPRC’s case cards. Since the IPRC gives a shorter average period of incubation (three
days) than later estimates (three to five days), the duration of these two elements taken
together does not differ significantly from the average represented by later estimates. If
the small correction noted above is taken into account, the figures will be identical and
average eight days. In a later study of the duration of the course of illness, the
Commission estimated the average for thirty-eight fatal cases at “a little over four days.”
IPRC 1907j: 943. This accords with Pollitzer’s information.
4
Appendix 3: 682–7.
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latency periods 281
communities. In larger towns, cities and metropolises, the pro-

cess of recognition will be delayed from a few days up to two
weeks according to the size of the city, because the immediate
observability of the early epidemic developments will be affected
by increased social and territorial distance between the first cases
and the great majority of the population and representatives of
the social classes who would note the occurrence in writing in
some form that eventually might be available to historians.5 This
delay from the first death to an early epidemic situation charac-
terized by several or more concomitant deaths and severely dis-
eased persons is therefore also social in construction, and more
complex social contexts require a higher degree of epidemic
development before the epidemic becomes more generally
observable and obviously significant to the observers. The epi-
sodic occurrence of deaths in epidemic disease was a fact of daily
life in medieval and early modern society, in urban society as well
as in rural society. This period while plague disease rages among
house rats up to the time the epidemic flares up and becomes
readily observable and recognizable is called the (full) latency
period and “is characteristic of plague of rat origin.”6 For these
reasons, epidemics of rat-based bubonic plague are generally also
characterized by protracted duration in the same locality.
The recognition of the existence of a latency period belongs to the very
early days of modern plague research. It was first noted by
P.L. Simond, the pioneer French epidemiologist who, in a paper pub-
lished in1898, noted that plague had a latency period of usually around
twenty days between the introduction of infection into a locality and
the epidemic outbreak. Simond points out that this feature is incom-
patible with inter-human spread of a disease. Hankin knew Simond’s
paper a few years later and put his observation to good use in his
endeavours to understand the Indian plague epidemics in the years
around 1900. In these early days, terminology as well as the under-
standing of the mechanisms of spread of bubonic plague were rudi-
mentary, but the reality is clear when Hankin states in a chapter called
“Simond’s Latent Period in the Locality”:
This undeniable fact of the frequent occurrence of a long period of
incubation in the locality independently of the incubation period in
5
Benedictow 2004: 57–9, cf. 124–5. See also Sticker 1910: 369.
6
Hirst 1953: 125.
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282 chapter seven
the human body, indicates that, as a rule, plague spreads not by simple
contagion from patient to patient, but by some deep-seated and perhaps
complicated method.7
Here for the first time the term “latent period” emerges, but is not estab-
lished in the community of scholars and presumed to be unfamiliar to
the readers and is therefore pedagogically explained by Hankin as an
incubation period of the locality which precedes the incubation period
in the infected person. Clearly, these two incubation periods corre-
spond quite closely to the term of the first latent period. Hankin illus-
trates the point by an account of the introduction and first development
of bubonic plague in the village of Mahlgahla in the Punjab in 1898:
The infection was introduced by a woman who was attacked by the dis-
ease, and who on the day following her attack, with her whole family, was
removed from the village to an isolated camp. Twenty-one days later
seven of the inhabitants of the village were attacked […] disinfection of
the evacuated quarters of the village in which no human cases had
occurred, was commenced. Numbers of dead rats were found in each of
these quarters […].8
The latent period is also described by the IPRC, now with an accurate
temporal and factual description of the epizootic process among the
rats, the consequent release of infective fleas, their subsequent attack
on human beings in their proximity, and the duration of the incubation
period and the course of illness.9 These findings by the IPRC confirmed
and explained Simond’s and Hankin’s observations of a latency period
and their view that this latency period ruled out the possibility that
bubonic plague was spread by cross-infection.
In the second volume of his standard work on historical and modern
plague published in 1910, Sticker emphasized the significance of the
latent period, “Latenzzeit” or “Latenzperiode,” as a defining feature of
rat-based plague.10 He illustrates his point by several case histories. Its
status as a defining feature was also pointed out by Hirst who also
employs the term “latent period.” Both the first phase of the latent
period and the full latent period reflect a plague of “rat origin,” both
these temporal manifestations of the pace of development of rat-based
plague are unique and function independently as defining features.
7
Hankin 1905: 63–4.
8
Hankin 1905: 71.
9
IPRC 1907g: 764–5 and fn. 6 above; Lamb 1908: 51–2. Cf. Wu Lien-Teh 1936c:
387.
10
Sticker 1910: 220, 227–32.
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Thus, latency periods as defining features of bubonic plague were

such an obvious characteristic manifestation of bubonic plague that
the phenomenon was observed by the first modern scientific medical
scholars who studied the outbreaks of plague at the end of the nine-
teenth century and was soon conceptually and materially clarified
and entered in the standard works on plague. The broad negligence of
the significance of latency periods as defining features of bubonic
plague by the advocates of alternative theories is thus all the more
remarkable.
The exception is Twigg who has noted Shrewsbury’s presentation of
the latency period, how it reflects rat-based plague,11 and he under-
stands its grave implications for his alternative theory.12 In contrast to
Cohn and Karlsson, he does not pass this problem by in silence, but the
way he goes about handling it is disappointing. Shrewsbury gives a his-
torical case illustration of a latency period based on an account by
Bishop Gregory of Tours of the development of plague in Marseilles in
588 as it was hit by the fourth wave of epidemics in the Justinianic pan-
demic of 541–766. The bishop relates that the contagion had been
introduced into the harbour of Marseilles by a merchant ship. Many
citizens purchased goods from it, and soon the contagion broke out
among a family of eight who died rapidly and the house stood empty.
However, the disease did not go on to spread through the residential
quarter, there was “a certain interval,” and “then, like a wheat field set
on fire, the entire town was suddenly ablaze with the pestilence.”13 What
Bishop Gregory without any knowledge of rat-based plague had
observed and what puzzled him was the latent period while plague
worked its way through adjacent rat colonies and, as it seems, also
through rat colonies in houses at a distance where rat fleas might have
been introduced in visitors’ clothing, until the rat fleas released from
dead rats began to attack human beings in their proximity and plague’s
presence re-emerged among the inhabitants in the form of dramatic
human mortality.14 Shrewsbury correctly points out that “plague did
not spread immediately after its introduction to a town, as a disease
that is spread by human contacts would do.” This point must be empha-
sized: no disease spread by cross-infection would for any reason exhibit
11
12
Twigg 1984: 172–5.
13
Little 2007: 11; Twigg 1984: 35.
14
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284 chapter seven
an interval with no epidemic activity, and certainly not anthrax which

is mainly spread by the eating of un(der)cooked contaminated meat:
such diseases would develop according to a bell-shaped continuous
curve. Twigg focuses on Bishop Gregory’s dramatic description of the
development of the epidemic, maintaining that the plague in India
did not produce “epidemics that flared in that way” and avoids in this
way to relate seriously to the significance of the description of the
latency period. He does not discuss the idea that Bishop Gregory’s
choice of words could have anything to do with rhetorical dramatiza-
tion,15 although dramatic rhetorical figures of speech were a central
part of classical education and they lived on in the medieval world as
an ordinary part of chroniclers’ writings.
The central methodological point is that in order to preserve his
theory Twigg is required to reject the fact that a silent interval, a latent
period, is an ordinary part of bubonic plague, and to document that a
latent period was characteristic of anthrax disease and explain how this
feature sprang from this disease’s properties. He appears not to have
noted that the Indian epidemics, according to the IPRC, were charac-
terized by this silent interval or latency period(s), as shown above.16
Sticker who had studied plague in India points out that this epidemio-
logical feature was observed in Mumbai in 1896 at the very start of this
plague period in India, and in Hubli in 1897, and so on.17 This means
that Twigg’s argument on this point is not based on the work of the
IPRC or earlier plague researchers in India and must be considered
unfounded.
Next, the way Scott and Duncan address this topic must be consid-
ered. It begins with their study of post-medieval plague in Penrith
(Cumbria) during 1597–8 based on parish records which provide good
data on the early epidemic developments of mortality as reflected in
the burial records, which in the case of medieval epidemics tend
to remain more or less veiled to the historian’s prying eyes. The first
victim of plague was a stranger named Andrew Hogson who was bur-
ied 22 September 1597. Conspicuously, the next burial did not occur
until 14 October, twenty-two days later, and the epidemic progressed
slowly in the following couple of weeks.18 Obviously, the stranger had
15
Twigg 1984: 35–6.
16
Twigg 35–6.
17
Sticker 1910: 228.
18
Scott and Duncan and Duncan 1996: 3; Scott and Duncan 2001: 116, 128.
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latency periods 285
introduced plague contagion into the small town; he must have been a
fugitive from some locality in the region where outbreaks of plague
were quite widespread at the time.19 The delay between the two first
burials is a defining feature of bubonic plague corresponding exactly
to the first latency period, and the ensuing slow developments are
compatible with the whole latency period and as such also a defining
feature of bubonic plague.
Scott and Duncan decline to take these basic facts into account,20
they remain unacknowledged and ignored in all of their works. This
may indicate that they do not have basic knowledge of bubonic plague’s
temporal structure of development and are unable to add up the dura-
tion of the various subphases. However, several aspects of their mono-
graph make it difficult to accept the idea that they have no knowledge
of bubonic plague’s typical latency period(s). In their monograph of
2001, they refer, for instance, to Shrewsbury and his monograph 116
times, or on almost 20 per cent of the pages, and often more than once
on a page,21 and Shrewsbury presents this feature of bubonic plague at
the very beginning of his monograph, on page 3, giving the first latency
period the self-explanatory name of “lag interval.”
In their account of the plague epidemic at Eyam, they do not test
their theory according to usual methodological principles. Instead of
providing the time of the first deaths and examining whether or not it
could be compatible with bubonic plague, they introduce as fact an
invalid estimate of an incubation period of thirty-two days for filo-
viridal disease (Ebola and Marburg diseases), a figure unknown in the
modern literature on these diseases, which will be discussed below. On
this arbitrary basis, they proclaim that the first victim had been infected
“about 1 August” and that the “first secondary infection took place on
16 August.”22 The crucial methodological point is that they do not test
their material according to the known properties and characteristics
19
Scott and Duncan and Duncan 1996: 12.
20
Scott and Duncan 2001: 128, 137.
21
Scott and Duncan 2001: 6, 14, 16–2, 18, 80–3, 81–3, 89–2, 90–2,91–4, 94–2, 95,
96, 98, 99–4, 100–3, 101, 102–3, 104, 106–2, 110, 111, 112, 113–2, 114, 115, 122, 149,
151–2, 152–6, 153–5, 154, 163, 165, 166–4, 167, 168, 176, 177, 179, 181, 182,193, 202–
2, 204, 205, 207–2, 209, 212, 215, 220, 232, 233, 238–2, 245, 247–2, 250–2, 253, 256–2,
257, 258, 261, 262–2, 265–2, 284, 357, 359–3, 360–2, 374, 375, 377, 380, 395. First
figure is page number, and the number after the hyphen indicates the number of times
Shrewsbury is referred to by name on the page.
22
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286 chapter seven
of bubonic plague and prove that they are incompatible with the events
of the epidemic. The first victim died 6 September after three days of
illness when he developed swellings in the groin and neck and the fatal
token, the plague spot. The clinical manifestations and the duration of
the course of illness are typical of bubonic plague, buboes are a defining
feature of bubonic plague and have not been observed in relation to
cases of filoviridal disease (see below).23 None of these features con-
forms to the theory of filoviridal disease according to currently availa-
ble medical information. The duration of the course of illness takes the
case history back to 3 September. Assuming that the disease was
bubonic plague, a normal assumption of incubation period indicates a
time of infection c. 31 August. According to local oral tradition taken
down in writing about 1840, the first victim was a tailor who received a
box with cloth from London where the last great plague was raging.
This account is credible in so far as transportation of plague in cloth(ing)
over considerable distances is, as shown above, a usual mechanism
of metastatic spread, and an infective rat flea (or more) could have
emerged when the box was opened, and, desperately hungry and
thirsty, have bitten the tailor and next searched for its natural host, a
black rat. If this traditional information is reasonably correct, this
would constitute an ordinary scenario of the beginning of a plague epi-
demic which would manifest itself in a sequence of epidemic events
characteristic or defining of bubonic plague. It is therefore of crucial
importance that the second victim, who lived in the same house, was
interred 22 September, twenty-three days after the beginning of the
process of infective transmission.24 As can be seen, this is a very fine
match for the general time structure of the two first cases of an epi-
demic of bubonic plague, and the twenty-three day period is the first
latency period which is a defining feature of bubonic plague, and as
such represents sufficient evidence that the epidemic disease under
development at Eyam was bubonic plague. Thus, even the introductory
evidence displays two defining features of bubonic plague, namely the
buboes and the duration of the first latency period. The other serious
scholars who have made in-depth studies of the epidemic at Eyam have
readily recognized this.25
23
See below: 652–3.
24
Bradley 1977a: 64–5.
25
Shrewsbury 1971: 523; Bradley 1977a: 64–5, 69–71, 73; Coleman 382–3.
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latency periods 287
What about Slack’s observation in relation to the plague epidemic in

Devonshire in 1546–7, which he makes on the basis of extensive empir-
ical evidence: “the apparent slow movement of disease from place to
place, burials rising in one village a fortnight or a month after they had
done so in another a few miles away”? Does this not constitute interest-
ing evidence of short-range metastatic leaps and the latent period, con-
forming to and reflecting the rhythm of development and pattern of
spread of bubonic plague?26
These grave flaws in their argument perhaps explain why Scott and
Duncan fill their book with declamatory assertions of the truth of their
findings and of the great weaknesses of the work of other scholars, as if
to veil the realities behind a verbal smoke-screen: “the details of the
epidemic demonstrate clearly again, as at Penrith in 1597–8, it is a bio-
logical impossibility that Yersinia pestis was the causative agent”; the
conditions at Eyam “would be completely unsuitable for the establish-
ment of a colony of black rats”; and the usual disparaging remarks on
the incompetence of historians “who all assume without question that
this was an outbreak of bubonic plague,” and once “blind acceptance of
bubonic plague has been abandoned, the sequence of events […] fit
readily into the pattern of a ‘standard’ infectious disease which was
transmitted person-to-person.”27
Their principal monograph contains several similar instances—
examples of epidemics with latency periods that clearly suggest bubonic
plague as the disease in question—that remain ignored and unrecog-
nized. For instance, they discuss an epidemic in 1665–6 in Neston, a
small port on the R. Dee, about 16 km north of Chester, and give some
examples of “spread of the infection within households”:28 “George
Leene (son of William Leene) brought the infection into his family and
died on 13 September 1665. He infected other members immediately
at the end of his latent period and they died on 24 (father), 25 (sister),
26
Slack 1985: 84.
27
28
Scott and Duncan 2001: 252–5. This epidemic is not mentioned by Shrewsbury
and it is not clear on what material Scott’s and Duncan’s account is based. It could pos-
sibly be a pre-modern amateur work by W.E.A. Axon, “Chronological Notes on the
Visitations of Plague in Lancashire and Cheshire”, Transactions of the Lancashire and
Cheshire Antiquarian Society, 12 (1894): 52–99. This paper is used by Shrewsbury who,
as it seems, does not let any epidemic go unmentioned, but does not mention the al-
leged outbreak at Neston. Since I have not have succeeded in identifying the paper and
acquiring it, I have not been able to examine the account.
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288 chapter seven
26 (brother), 26 (‘base child which William Leene’s wife nursed’),

28 (sister) September. On this basis, Scott and Duncan announce
“35 days as the minimum duration of the latent and infectious peri-
ods.”29 If it is assumed that this was bubonic plague and deduct an aver-
age of eight days for incubation and duration of illness, George Leene
would have been bitten by an infective flea 5 September, the flea would
then have searched for its natural host the black rat and triggered a rat
epizootic that, according to the first latent period, would manifest itself
in human cases nineteen to twenty-seven days later, which fits abso-
lutely with the sequence of epidemic events and deaths in the family.
This sequence of events corresponds perfectly to a defining feature of
bubonic plague, namely the first latency period. Scott’s and Duncan’s
assertion that George Leene infected the other family members imme-
diately at the end of his latent period is unconvincing for several rea-
sons. The sequence of events does not fit with an incubation period of
thirty-two (here thirty-five) days according to their invalid assertion
on this point for filoviridal diseases: no such latent period or extraordi-
nary long incubation period has been observed in research on filo-
viridal diseases (see below). Scott and Duncan have not only invented
this imaginary incubation period of thirty-two days (see below), but
have also taken out of thin air the idea that infected persons in this
period were extremely contagious. This is yet another assertion which
they are unable to document or prove30 for the obvious reason that all
medical research on the two filoviridal diseases agrees that there is not
a “carrier state” and that infection requires direct transmission of living
cells.31 This is an awkward and inefficient mode of transmission which
explains why this type of disease “typically appears in sporadic out-
breaks” which are also typically small. This makes it surprising that
Scott and Duncan should not have met with latency periods as a char-
acteristic feature of bubonic plague.
29
30
Scott and Duncan 2001: 384–9 (or anywhere else in the monograph).
31
www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 2; www.who
.int/inf-fs/en/fact103.html 2003: 1; Dowell, Mukunu, Ksiazek et al. 1999.
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CHAPTER EIGHT
DEFINING FEATURE 2: INVERSE CORRELATION BETWEEN

MORTALITY RATE AND POPULATION DENSITY
Introduction
At the heart of modern epidemiological theory is the notion that E.M.

Burnet, the Nobel Laureate, in his standard work Natural History of
Infectious Disease formulates thus:
no matter by what method a parasite passes from host to host, an
increased density of the susceptible population will facilitate its spread
from infected to uninfected individuals.1
A representative sample of Cohn’s unfair discussion of Hankin’s paper
of 1905 has been commented on above. The central reason for Cohn’s
misrepresentation and disparagement of Hankin as a scholar is his
(Hankin’s) discovery that Indian epidemics of bubonic plague caused
higher mortality rates in villages than in urban centres and that the
Black Death in England appeared to follow the same pattern and, thus,
also was bubonic plague.2 This strange phenomenon, that mortality
rates did not increase with increasing population density but, on the
contrary, decreased, is at variance with the central tenet of epidemiol-
ogy and must reflect a very special or unique mechanism of transmis-
sion and dissemination. Observation of a unique feature of bubonic
plague is of particular importance, because a unique feature is obvi-
ously synonymous with a defining feature and can, as such, serve as a
sufficient criterion for identification of the disease and invalidation of
all theories based on other diseases. Clearly an inverse correlation
between morbidity or mortality rates and population density is incom-
patible with and falsifies all alternative theories of the identity of his-
torical plague epidemics based on diseases spread by interhuman
1
Burnet and White 1972: 11. This standard work was written by Burnet, the 4th
edition is revised by White.
2
Hankin 1905: 48, 57–8. Above: 21–3.
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290 chapter eight
cross-infection, primarily Cohn’s, Scott and Duncan’s, and Karlsson’s

alternative theories.
In a paper published in Population Studies in 1987, I developed
Hankin’s point by introducing much more evidence to the same effect
and also succeeded in presenting an explanation for it that so far, over
twenty years later, appears to have been generally accepted. The gist of
this paper was presented in my doctoral thesis of 1993, which Cohn
knows, but nonetheless he ignores this point in his monograph of 2002.
However, since the gist of this paper is also presented in my mono-
graph on the Black Death and the cat is out of the bag, so to speak,
Cohn attacks my findings in his “review” of my monograph in The New
England Journal of Medicine (see below).
It is interesting to note how the advocates of alternative theories
relate to this epidemic evidence. Cohn’s efforts to misrepresent and
belittle Hankin as a scholar are commented on above. Twigg admits
that Hankin’s finding can be correct for India, but maintains on quite
speculative grounds, as it may seem, that “constraints of climate and
other factors might have resulted in a different situation in northern
Europe.” The comparative evidence Hankin gathered on the Black
Death showing the inverse pattern of correlation in England and addi-
tional European historical evidence to the same effect presented later
by other scholars are ignored.3 Scott and Duncan do not discuss this
point. This allows Scott and Duncan to construct a line of argument to
the effect that historical plague epidemics were density dependent in
their restricted meaning of the term, i.e. that mortality rates increased
with population density (as if the inverse correlation is not also a struc-
ture of density dependence), which seemingly satisfies the epidemio-
logical principle for diseases spread by cross-infection formulated by
Burnet.
This makes it important to perform two tasks: (1) to present an
outline of the evidence passed over in silence by all advocates of
alternative theories which provides proof that the inverse correlation
was a characteristic feature of historical plague epidemics; and (2) to
consider Scott and Duncan’s attempt to make a case for the positive
correlation of levels of population density and mortality in histori-
cal plague epidemics, which will be carried out in a subsequent
subchapter.
3
Twigg 1984: 55–6.
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mortality rate and population density 291
More Data on the Inverse Correlation in India and Historical Europe
In India the inverse correlation to the effect that “plague is much more
severe in country villages than in towns” was so obvious that it was
mentioned briefly in passing by Bannerman a year after Hankin pub-
lished his findings.4 In the following year (1907) the IPRC published a
study of the relationship between population density and mortality in
various sections in Mumbai, i.e., an intra-city study, and to their sur-
prise noted that
there is no relation between the severity of plague in these sections and
any of the facts which contribute to overcrowding of the population
[…].
Viewing the evidence as a whole we are of [sic] opinion that there is no
relation between overcrowding and plague incidence.5
This observation is an important contribution to the study of the inverse
correlation because it strengthens and expands the systematic or per-
vasive character of the phenomenon from an urban-rural dimension
by showing that it also holds good in an intra-urban perspective. This
instils it with a generalized character which must reflect important
basic factors in the mechanisms of spread of bubonic plague which
permits us to establish the concept of the principle of inverse correla-
tion for the pattern of distribution of mortality rates according to pop-
ulation density in bubonic plague epidemics, decreasing with increasing
population density. Interestingly, the IPRC’s observation suggests that
the principle of inverse correlation should also be a structural density-
dependent feature in the countryside, that is, that mortality rates should
be higher in hamlets and small villages than in large villages. Empirical
data to this effect would make the principle of inverse correlation com-
pletely generalized, a hypothesis that must be tested on relevant data as
they become available. If it is not substantiated, a separate explanation
would be called for.
However, for some years, the study of the inverse correlation slipped
out of the IPRC’s focus. In 1911, Major Greenwood, the epidemiologist
and also the statistical specialist of the IPRC, published a study “on
some of the factors which influence the prevalence of plague” in the
4
Bannerman 1906: 195. Later, it was observed also in China, see Wu Lien-Teh
1936c: 396–7.
5
IPRC 1907g: 780–1.
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292 chapter eight
Punjab, where he found that “given an equal period of exposure to

infection, small villages suffer more severely from plague than large
ones.” “These curious and interesting facts” caught his attention exactly
because they were at variance with the central principle of epidemiol-
ogy, and being an eminent scholar he asked the pertinent methodo-
logical question whether “the same or similar circumstances have been
noticed before.”6 This led him to Hankin’s observation of a similar or
closely related pattern, that villages outside “Bombay Presidency” had
much higher mortality rates than towns, which corroborated the cen-
tral aspect of his own finding. In view of Cohn’s negative assertions and
characteristics, it is of particular interest that Greenwood then points
out that “Hankin also called attention to the probable occurrence of a
similar phenomenon in the Black Death,” showing that it is not difficult
for a fact-oriented scholar to cite Hankin’s pioneering finding correctly
on this comparative point. He then proceeds to test also Hankin’s his-
torical finding:
In Appendix I,7 I deal with such statistics as I could obtain bearing on the
historical plagues: it will be found that these, so far as they go—unfortu-
nately not very far—bear out Hankin’s suggestion. They lend some sup-
port to a belief that we here have to deal with a general epidemiological
phenomenon […].8
it would appear probable that the rule deduced from the Punjab village
statistics, viz. that the rate of plague mortality tends to increase as the
absolute population of the infected community diminishes, may apply to
European epidemics.9
Concluding, Greenwood points out that his own study enlarged on the
knowledge of the observed phenomenon in so far as “the difference is
found to be carried further and still to prevail amongst communities of
the same general type,” i.e., among villages (of various sizes).10
Suprisingly, Twigg displays knowledge of Greenwood’s first report
on plague in the Punjab, IPRC 1910b: 349–443 + 48 maps, “On the
Spread of Epidemic Plague through Districts with Scattered Villages,”
but in his bibliography he discloses that he refers only to Part II (pages
416–42) constituting 28 per cent of the running text,11 which means
6
Greenwood 1911b: 74–5.
7
Greenwood, IPRC 1911b: 93–6, 150–1.
8
Greenwood, IPRC 1911b: 75.
9
Greenwwod 1911b: 95.
10
Greenwood, IPRC 1911b: 74–5.
11
Twigg 1984: 187, 243.
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that he avoids having to admit knowledge of metastatic spread of

bubonic plague from this paper. He displays no knowledge of the
important second and especially third reports on plague in the Punjab
published the next year where metastatic spread is the central topic
(see above).12
As can be readily seen, Cohn’s, Twigg’s and Scott and Duncan’s asser-
tions that the inverse correlation between population density and mor-
tality has been observed only in relation to modern bubonic plague are
not correct: both Hankin and Greenwood adduced evidence of the
same pattern in historical epidemics. Clearly, Hankin’s discovery is
important and valid and strengthened by Greenwood’s similar finding
on independent material. The problem confronting Hankin and
Greenwood was the early and low level of development of historical
plague research which restricted the level of tenability that it was pos-
sible to achieve by the comparative approach, but tenable their results
were, and taken together, at a significant level both with respect to
plague in India and with respect to historical plague epidemics in
Europe.
Cohn enters Greenwood’s study of 1911b in his monograph’s bibli-
ography and can therefore be assumed to know it, although he refrains
from mentioning it in his text. Despite this silence it can be assumed
that Cohn also knows that Greenwood addressed Hankin’s finding that
the inverse relationship between levels of plague mortality and popula-
tion density appeared to be characteristic also of historical plague epi-
demics, and that Greenwood adduced significantly more historical
evidence to the same effect and strengthened the empirical status and
level of tenability of this observation.
More evidence showing the main outline of the same pattern of
inverse correlation between levels of mortality and population density
in European historical plague epidemics was published around 1980.
In their monographs of 1978 and 1981 respectively, both R.S. Gottfried
and C.M. Cipolla noted the basic point: the effects of plague epidem-
ics were at least as severe in rural areas as in urban centres in
fifteenth century England and seventeenth century Italy, despite
much lower population densities.13 Cohn knows Cipolla’s monograph
(Fighting the Plague in Seventeenth-Century Italy), since he refers to
12
IPRC 1911a: 47–61; IPRC 1911b: 62–156.
13
Gottfried 1978: 138–54, 226–7; Cipolla 1981: 102.
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294 chapter eight
page 14 in it,14 although at a safe distance from page 102 where Cipolla
addresses this subject. Thus, Cohn has again overlooked significant
evidence bearing on this important point which undermines his alter-
native theory and corroborates the bubonic plague theory. He does not
enter Gottfried’s monograph in his bibliography, which is surprising
from an author who accuses his adversaries for “highly selective” read-
ing of the scholarly literature (see above and below). Cohn’s comments
on Cipolla’s work have been discussed also above and shown to be mis-
leading: Cipolla is not an historian “squaring the circle.” Unfortunately,
Cipolla is not in a position to defend himself against these unjustified
accusations.
While working on my monograph on the Black Death and making
my way through the Spanish studies of historical plague epidemics, I
noted that three scholars, P. Vilar, M.V. Shirk, and M. Berthe had
observed that the Black Death ravaged the countryside even more
severely than the towns in the Spanish regions for which there was
mortality data, namely Catalonia and the Kingdom of Navarre.15 Cohn
has overlooked all three studies.
In 1985, Paul Slack published his large and important monograph on
plague in Tudor and Stuart England where he unreservedly identifies
the demographic and epidemiological patterns and clinical descrip-
tions of the epidemics as bubonic plague, and is for this reason severely
criticized by Cohn, who also criticizes a number of other notable schol-
ars, including me, albeit on untenable grounds, as shown above.16 Since
Slack had not discovered Hankin’s and Greenwood’s pioneering studies
on the inverted relationship between population density and mortality
rates in plague epidemics, he was unprepared for making the same
curious finding. However, he has used Greenwood’s standard work of
1935 on epidemic diseases and has also read the chapter on plague,
actually citing it on a point five lines before the following statement:
“the smaller the community the greater the rate of mortality if it
becomes infected.”17 Being a historian, not an epidemiologist, and
expecting a conventional pattern, Slack treated this curious finding
14
Cohn 2002: 14, fn. 75.
15
Vilar 1962: 464; Shirk 1981: 365; Berthe 1984: 314.
16
Cohn 2002: 28–9. See above: 56.
17
Slack 1985: 94; Greenwood 1935: 300–1. Greenwood’s italics. Cohn also enters
this work in his bibliography and refers to it once in the text, but does not cite the
chapter on plague and the statement on the inverse relationship between plague mor-
tality and population density.
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with circumspection, and, as it seems, uneasy disbelief. However, his

in-depth studies of plague in Devonshire in the years 1546–7 based on
a broad sample of parish registers showed that
the variations in mortality […] appear to bear no relation to the size of
the community involved. The epidemic was as bad in the small parish of
Bridford, south-west of Exeter, consisting mainly of scattered farms, as it
was in the large village of Ugborough […] and it was less serious in the
market town of Colyton in east Devon than in either of these […].
Incidentally Slack might also have said that it was less serious than in
Exeter. Clearly, mortality was higher in villages than in urban centres
and there was also clearly a general inverse correlation between the size
of communities involved and the level of mortality. Slack also made
in-depth studies of the effect of plague in quite a number of parishes in
Devonshire in the period 1568–1626. The gist of his findings is revealed
in his Table 4 and show a similar pattern: small rural parishes like
Widworthy and Dean Prior suffered extreme mortality, much higher
than urban centres like Exeter, Tiverton or Plymouth.18 Thus, the same
pattern emerges in mid-sixteenth-century England that was first
observed by Hankin in India, that village mortality was much higher
than in towns.
Deeper insights into the matter could have been achieved if Slack
had organized the material in a table according to the size of the com-
munities and the mortality rates they suffered. As it is, Slack has con-
tributed valuable historical evidence to the effect that mortality rates in
epidemics of bubonic plague did not increase with size of community
in sixteenth-century England but, on the contrary, tended to be (much)
higher in villages than in towns. The significance of this observation
is clear: these historical plague epidemics did not spread by cross-
infection but by some other mechanism which produced this inverse
correlation of mortality rates and population density or, at least, pre-
vented correlation of mortality rates with increasing population den-
sity. Finally, I think it is fair to point out the central role of British
scholars in the discovery and development of this topic.
Shortly before Slack’s monograph appeared, I was setting up tables of
plague mortality in Italian localities in 1630–2 and in French localities
in southern France in 1720–2, when it struck me that village mortality
was much higher than that in towns. Next, I remembered that Hankin
18
Slack 1985: 88–9, 94.
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296 chapter eight
and Greenwood had noted the same peculiar pattern which they, how-
ever, were unable to explain, and I delved eagerly into this exciting
problem. In order to avoid methodological problems from possible dif-
ferences between morbidity rates, which directly reflect the dynamics
of the epidemic process of spread, and mortality rates, which might
vary according to lethality rates, I endeavoured to collect all available
information on morbidity rates. I also collected some series of mortal-
ity rates and at the end of the day it was clear that these two types of
data was similar, reflecting the historical stability of plague lethality.
Inevitably, this emphasis on the quality of data in the form of morbidity
rates had the effect that my data was associated with quite late histori-
cal epidemics of bubonic plague in Europe, namely the Italian epidemic
of 1630–2 and the French epidemic in 1720–2. However, these data
expanded substantially in time and geography the English data of
Hankin and Greenwood on the Black Death, Gottfried’s data on epi-
demics in fifteenth-century south-eastern England, and Slack’s on
sixteenth-century England. It emerged that the mortality data of these
two epidemics showed the same pattern and contributed to the forma-
tion of a systematic pattern covering the whole of the plague period
from the Black Death to the last, the French epidemic of 1720–2. The
inverse correlation was a systematic characteristic feature of historical
plague. Since this feature was a characteristic feature of bubonic plague
epidemics both in India and in historical Europe it constituted indis-
putable evidence to the effect that historical plague epidemics were epi-
demics of bubonic plague.
The outcome of my endeavours was published in a paper in the
demographic journal Population Studies in 1987 and it contains a broad
range of historical evidence. It shows a systematic inverted correlation
between levels of population density and mortality, that mortality rates
are highest in small villages, tend to fall with increasing village size, and
fall abruptly in towns (urban centres with 1000–9999 inhabitants). It
thus confirms the hypothesis constructed on the basis of the IPRC’s
paper of 1907f that the inverse correlation held at the level of villages or
rural settlement more generally. Since the vast majority of European
populations lived in the countryside in relative small agricultural set-
tlements, this finding also conforms with the extreme mortality of the
Black Death. However, in the evidence I studied the mortality rates
start to increase in the big cities and the metropolises of the time, so
that a bimodal pattern emerges. This means that the expression “inverse
correlation” is inaccurate. My data is summarized in Figure 1, where
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Morbidity rates (per cent) France 1720-2 Morbidity rates (per cent) Italy 1630-2
80 80
70 70
60 60
50 50
40 40
30 30
20 20
10 10
0 0
Small Village Large Small Samll Town City Metro Small Village Large Small Samll Town City Metro
village village town 1 town 2 village village town 1 town 2
Figure 1. Population density and morbidity (epidemics of plague)
they produce a sort of bimodal correlative histogram. Specification of

data and source-critical points is presented in my paper; see the foot-
note here for demographic explanation of the terms describing the
sizes of the settlements.19
A detailed summary of this study is given in my doctoral thesis.20
Cohn has apparently read it not only in a biased way, but also in a selec-
tive way, since he failed to notice my discussion of this phenomenon in
a separate subchapter aptly called “The Problem of Population Density”
complete with Figure 1 and a conclusion written in bold type to under-
line its importance (see below).
This topic is also discussed and enlarged upon in my monograph on
the Black Death, first in a subchapter called “Can It Be True that Plague
Spreads More Effectively in the Countryside than in Urban Areas?”21
All mortality data was tested for further evidence on the matter. In the
19
Settlements and population centres are categorized in an approximate fashion
according to demographic and sociological criteria taking into account contemporary
societal realities and cultural notions: a village has up to 1000 inhabitants; a town from
1000 to 10,000 inhabitants; a city 10,000 to 100,000 inhabitants; a metropolis 100,000
inhabitants and upwards. Metro = metropolis. The French data refer to the following
numbers of inhabitants: small village = 74–109; village = 213–450; large village = 540–
850; small town 1 = 1,000–1,750; small town 2 = 2,000–3,000; town 2 = 4,200–6,000;
city = 22,500–24,000; metropolis = 100,000. The Italian data: village = 190–640;
town = 2,025–3,900; city = 12,000–76,000; metropolis = 130,000–140,000.
20
Benedictow 1993/1996: 177–80.
21
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298 chapter eight
case of Spain, it is pointed out that several scholars have noted that the
Black Death ravaged the countryside even more severely than the towns
in the regions for which there is mortality data, namely parts of the
Kingdom of Navarre and Catalonia, an observation my work con-
firmed.22 The Italian mortality data on the Black Death is too few to
constitute a good material for this discussion. In San Gimignano, mor-
tality in the town was higher than in the countryside, in Prato the data
suggests that mortality was about the same in the city and in the coun-
tryside, and the mortality rate in a number of villages in Valle Susa in
the Piedmont was about 52.5 per cent. Taken together, it appears
that the available Italian data indicates about the same level of mortal-
ity in the urban centres as in the countryside, which still is incompati-
ble with the epidemiological principle that mortality rates should
increase with increasing population density and, thus, support the
inference that it was bubonic plague.23
In the case of France, a similar pattern of mortality in the Black
Death appears in Provence where the data comprises nine urban cen-
tres, which according to the registration of household(er)s containted
roughly 1350–6700 inhabitants, and seven villages with roughly
130–650 inhabitants. For urban centres and rural communities the
mortality rate of householders was about 52–3 per cent, and measured
as part of the population about 60 per cent. However, a closer look at
the rural data makes it possible to discern a pronounced tendency
towards higher mortality rates among the smaller villages and lower
mortality among the larger villages. Despite the fact that the lowest rate
is found in the smallest village, the two second smallest villages, both
with forty householders, lost more than 70 per cent of them, while the
two largest villages comprising 144 and 122 household(er)s lost 48 and
46 per cent of their householders respectively.24 The material for vil-
lages in the County of Savoy also shows a tendency, albeit quite weak,
to the same effect, the largest villages or small towns lost a somewhat
smaller proportion of their population than medium-sized and small
villages, and there is no tendency to the positive correlation on which
Cohn’s and Scott and Duncan’s alternative theories depend.25 This evi-
dence tends to support the prediction (above) that mortality rates in
22
23
24
25
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bubonic-plague epidemics should tend to be higher in small rural set-

tlements than in large villages.
The available English mortality data on the ravages of the Black
Death does not include information on urban populations and cannot
be used for ascertaining relative levels of mortality between urban and
rural environments. It is, however, hard to envisage that urban mortal-
ity can have exceeded the average mortality rate among seventy-nine
manorial communities of about 55 per cent among the householders of
the customary tenantry, and over 60 per cent (c. 62.5%) among the
rural population as a whole, quite likely the highest rate in Europe. The
mortality rates among landless or all-but-landless men are known for
seventeen of the manors of Glastonbury Abbey. They show a tendency
to higher mortality rates on manors of under-average size than on
those of over-average size.26
Thus, even in these early days in the development of medieval
demography the surprisingly numerous and territorially quite widely
dispersed mortality data that is available for populations visited by the
Black Death shows a consistent pattern to the effect that the epidemic
either ravaged the countryside even more harshly than urban centres
or that the mortality rates may have been at about the same level. They
also indicate that population losses were more severe in small villages
than in large villages. Since this monograph appeared after Cohn’s
monograph, he may be excused for not knowing it, but not for ignoring
all of the relevant data or for his misleading comments in his “review”
of the monograph, when he realized that the cat was out of the bag and
the issue had to be addressed.27
In this chapter it has been empirically shown at a high level of tena-
bility that a mainly inverse correlation between levels of mortality and
population density in epidemics of bubonic plague is an inherent, his-
torically stable and unique property of this disease, at least this is the
case for communities up to the size of big cities or metropolises of the
Middle Ages. For this reason, it is also incompatible with and invali-
dates all alternative theories of the microbiological nature and mecha-
nisms of spread of the Black Death and subsequent plague epidemics
based on assumptions of interhuman spread, specifically the alterna-
tive theories of Karlsson, Scott and Duncan, and Cohn.
26
27
Cohn 2005: 1354–5.
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300 chapter eight
However, the question remains of whether this defining feature can

be explained on the basis of unique aspects of the epidemiology of
bubonic plague which set it epidemiologically apart from all other epi-
demic diseases. The point of departure must be that the central tenet of
epidemiology predicts in a sweeping and general fashion that no matter
by what means or method a disease is transmitted from person to per-
son, morbidity and mortality rates will increase with increasing density
of the susceptible population. If this general prediction can be shown
on solid empirical grounds not to be fulfilled by an epidemic disease,
but that the disease, on the contrary, exhibits a pattern of mortality that
is inversely correlated with or unaffected by population density, as is
the case with bubonic plague, the reason or cause must be sought in
the only reservation, namely that this is generally true only of
diseases spread by cross-infection. Consequently, diseases that are not
disseminated or transmitted directly from person to person can, in
principle, exhibit other types of correlation. In this context, it is also
important to emphasize that the study of the correlation between levels
of mortality and population density did not exhibit a linear decreasing
development along the population-density axis, but unexpectedly and
conspicuously began to increase when population density reached the
level of the big cities and metropolises of the Middle Ages. This pecu-
liar feature must also be explained by a satisfactory explanatory model
or theory.
In my paper on the inverse correlation between levels of morbidity/
mortality and population density in bubonic plague epidemics, an
explanatory model or theory was presented that so far has not been
criticised or countered. In the interest of encouraging regular scholarly
discussion and development of the topic, the compressed version given
in my doctoral thesis will be cited at quite some length:
We have also been able to demonstrate that this seemingly unique, accord-
ing to basic epidemiological theory inverted relation between morbidity
rates and population densities, may be explained only by assuming that
epidemics of plague reflect epizootics among commensal rodents. In
other words, it reveals that the rat flea is of paramount importance for
dissemination and transmission of plague among human beings. In the
case of diseases spread by cross-infection, the density pattern is, so to
speak, one-dimensional, comprising only humans; the density of suscep-
tible humans will, accordingly, in the main decide the powers of spread.
In the case of rat-based plague, the density pattern is three-dimensional,
comprising the density not only of humans but also of rats and rat fleas.
The latter two density-factors will tend to co-vary strongly and, therefore,
to override the significance of the density of humans.
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Rats are social animals defending territories. This means that in the
countryside at least one rat colony will normally co-reside with a house-
hold, whereas in urban environments several households will usually
crowd together within the territory of a rat colony. The ratio of humans
to rats and fleas will, accordingly, tend to be lower in urban environments
than in rural, there would be more persons to share between them the
dangerous rat fleas let loose from an afflicted rat colony.
This epidemiological model provides a basic explanation why plague
may wreak havoc after having arrived at some small-scale residential
unit, and why, in the case of plague, severity of impact on human popula-
tions does not increase with mounting density of human settlement. This
finding is of crucial importance. Only an epidemic disease with these
disseminative properties could possibly have brought about the demo-
graphic developments observed in the Nordic countries in the Late
Middle Ages (and also in most other European countries). Thus, another
necessary condition has been identified as being fulfilled.28
In this summary, one point is not included, namely the tendency of
mortality rates to rise again in large cities and metropolises as shown in
Figure 1. Again a reasonable explanation can be found within the the-
ory of rat-and-flea-based bubonic plague. In large late medieval and
early modern urban centres, often surrounded by walls, the price of
building sites would induce building of multi-storey houses, quite often
with two or more living units at the same level. This would create new
ecological niches or habitats for black rats where colonies would settle
in the space provided by floors, in the walls between living units and in
the ceiling or roof, according to a pattern observed in India and com-
mented on by the IPRC,29 “the fact that R. rattus lived at all levels of the
houses and therefore in close contact with man.”30 This would produce
the effect of increasing the number of rats and fleas relative to the
human population within the territories of rat colonies, causing mor-
bidity and mortality rates to rise again and surpass the level character-
istic of small or middle-sized towns.
Scott and Duncan and the Correlation between Population Density

and Mortality
In their monograph of 2001, Scott and Duncan refer to my paper on

the inverse correlation twice:
28
Benedictow 1993/1996: 179–80.
29
See, for instance, Lamb 1908: 22–3.
30
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302 chapter eight
(1) “Naples, with about 300,000 inhabitants, suffered 150,000 deaths

in 1656. The morbidity in the countryside has been estimated at
66% (Benedictow, 1987).”31 First, one should note the juxtaposi-
tion of mortality and morbidity data without mediation of lethal-
ity data that would allow real comparison of mortality—and
lethality data is provided in the paper. Unfortunately, the morbid-
ity rate of 66 per cent in the countryside given by Scott and Duncan
with reference to my paper is erroneous and therefore misleading
for two reasons: because it is taken from a table which does not
contain morbidity data on the epidemic of 1656, but on the epi-
demic of 1630–2, and because these data does not relate to the
countryside around Naples as asserted by Scott and Duncan, but
to Tuscany almost a generation earlier.32 Disquietingly, the combi-
nation of these two sets of erroneous data can hardly be acciden-
tal; they are carefully selected from page 405 and page 424 in the
paper, twenty pages apart. As shown above, mortality rates start to
increase again in the big cities and increase further in the metrop-
olises of the time, and Naples is obviously one of the largest
metropolises of the time with correspondingly high(er) relative
mortality. This constellation of selected data serves to conceal the
fact that morbidity data is also generally higher in the countryside
than in urban centres in Italy. Scott and Duncan could have
avoided the misleading combination of data from two different
epidemics by choosing from the page that contains the piece of
information on Naples the brief passage on Venice, for instance.
The mortality in Venice in the epidemic of 1575–7 was consider-
ably higher than in the next epidemic of 1630–1 when the popula-
tion had fallen by about a quarter; it is also pointed out that urban
mortality rates in Venice and Terrafirma were considerably lower
than rural plague mortality.
(2) “During the 17th century, there is evidence that the mortality and
relative severity of the plagues in London were declining slightly
(Sunderland, 1972; Benedictow, 1987).”33 The citation is accurate,
and the reference to Sunderland is taken from my brief discussion
of this minor or rather peripheral point in my paper. However, the
31
32
Benedictow 1987: 405–8, 413–5, 418–24.
33
Scott and Duncan 2001: 377. Cf. Benedictow 1987: 424.
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heart of the paper, the presentation of comprehensive historical

evidence from Spain, Italy and France and other countries show-
ing a strong tendency of inverse correlation between levels of mor-
tality/ morbidity and population density up to the level of large
cities or metropolises, when the tendency reverses, a pattern con-
stituting a defining feature of bubonic plague, remains ignored.
Thus, Scott and Duncan ignore all historical evidence for the inverse
correlation between levels of mortality and population density in
plague epidemics, although they cannot have avoided acquiring knowl-
edge of it. Their silence on this topic seems to produce a clean sheet
that, apparently enables them to make a case that the powers of spread
and mortality of historical plague epidemics in England were positively
correlated with increasing population density. A positive correlation
would, as they emphasize repeatedly and correctly, constitute proof
that historical plague epidemics were spread by cross-infection, and
thus proof that these epidemics could not have been bubonic plague. In
view of the broad empirical documentation of the inverse correlation
supplied in the preceding subchapter, these endeavours deserve a closer
examination.
Scott and Duncan’s highly divergent and self-contradictory opinions
on this phenomenon in India indirectly provide an impression of being
shattered, as it were, for instance:
Bubonic plague in India was primarily a disease of the smaller towns: the
intensity of an outbreak in 1897–8 was inversely proportional to the size
of the community, with the maximum mortality in the villages rather
than towns (Hankin, 1905).34
Thus, within this sentence Scott and Duncan state that bubonic plague
in India was primarily a disease of small towns and also that the levels
of mortality in the epidemic of 1897–8 were highest in villages. Scott
and Duncan isolate this purportedly observed self-contradictory fea-
ture to one epidemic wave and, thus, reduce its significance by avoiding
mentioning that Hankin found the same characteristic feature in two
earlier Indian waves of plague epidemics, in 1812 and 1836 (above).
This was, therefore, a general feature of Indian plague epidemics in the
nineteenth century. In view of the fact that India’s population was over-
whelmingly rural at the time, the plague epidemics would obviously
34
Scott and Duncan 2001: 77–8, 103.
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304 chapter eight
also have to be mostly rural, the pattern mainly being that plague first
arrived in urban centres and from there fanned out into the surround-
ing countryside. In fact, this point is not unknown to Scott and Duncan
about a hundred pages later:
[…] authentic outbreaks of bubonic plague in India, where it is essen-
tially a rural disease of village communities.35
They also maintain that
Endemic bubonic plague is essentially a rural disease because it is an
infection of rodents. The Black Death, in contrast, struck indiscrimi-
nately in the countryside and in the towns.36
Here, Scott and Duncan compare endemic bubonic plague with epi-
demic plague, actually the largest plague epidemic ever to visit human-
kind called the Black Death. Clearly, in this context these two
phenomena are not comparable, are not in pari materia, and the juxta-
position and comparison on this basis is fallacious. They maintain that
endemic plague was essentially a rural disease because it is an infection
of rodents without presenting arguments for why rodents in the form
of rats (mice?) were not generally amply present in urban centres, and,
as so often, they fail to provide a supporting footnote. It has been an
accepted opinion among English plague researchers for some time that
plague developed a more or less continuous endemic presence in the
larger English cities, which can especially be clearly discerned with the
advent of bills of mortality around 1550 when systematic registration
of deaths discloses the quite continuous incidence of plague cases.37
Slack points out that plague “was certainly endemic for long periods in
major towns, in Norwich as well as in London,” and after the last great
plague in London 1665–6, cases of plague continued to occur until
1679. The only periods of any length when the country appears to have
been free from epidemics of plague were the period 1612–24 and the
period 1654–64.38 Scott’s and Duncan’s assertion that endemic plague
was a phenomenon of rural districts seems unfounded and the lack of
supporting footnote or reference is explicable.
Before proceeding, it is useful to compare the previous citation with
another citation from Scott and Duncan’s monograph, this time on the
35
36
37
Slack 1985: 239–45.
38
Slack 1985: 68–9, 133.
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epidemic that broke out in Marseilles in 1720 and spread over large
parts of southern France in the following couple of years, and which
they recognize as bubonic plague:
The plague struck indiscriminately at towns as well as the tiniest hamlets
(some with only four houses) so we conclude that it was not density
dependent.39
When this citation and the previous citation from their monograph are
juxtaposed for comparison, it can be readily seen that the Black Death,
which Scott and Duncan fervently assert is not bubonic plague, and the
southern French epidemic of 1720–2 exhibit an identical basic pattern
or structure of spread; in the co-authors’ terminology, the Black Death
“struck indiscriminately in the countryside and in the towns”40 and the
French epidemic about 370 years later struck “indiscriminately at towns
as well as the tiniest hamlets.” According to ordinary methodological
considerations, these citations should provide good evidence to the
effect that both waves of epidemics were the same disease since they
exhibit the same basic pattern of spread. Since the last epidemic’s
microbiological nature is known and it is generally agreed upon to be
bubonic plague, also by Scott and Duncan, the Black Death should
consequently be bubonic plague.
Admittedly, it is difficult to understand what Scott and Duncan mean
by maintaining that the Black Death struck “indiscriminately” in the
countryside and in the towns, and efforts to understand are much frus-
trated by the fact that Scott and Duncan make this assertion with
respect to the Black Death’s pattern of spread without a supporting
footnote and also without clarification of the types of spread, in this
case specifically the scholarly meaning of the concept of “indiscrimi-
nate.” If the meaning is that as many people died in urban centres as in
the countryside it is clearly erroneous and without support in demo-
graphic studies; if they mean that as many urban centres were visited as
villages it is also obviously erroneous and without support in demo-
graphic studies. The point is that the overwhelming part of the English
population lived in the countryside, quite likely about 85 per cent,41
much like in India around 1900. For this reason, the Black Death in
39
40
Cf. Scott and Duncan 2001: 366: “We have little quantitative evidence concerning
exactly how the Black Death struck at the different naïve communities in the vast meta-
population of Europe but it appears that it attacked largely indiscriminately.”
41
Hatcher and Bailey 2001: 140.
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306 chapter eight
England, like the epidemics of bubonic plague in India, struck far more
villages than urban centres and killed far more rural inhabitants than
townspeople. The basic pattern of spread of Indian plague epidemics
and the Black Death are also similar or closely related: plague arrives
first in coastal urban centres and spreads out along main lines of com-
munication with goods and people along the coast and to inland urban
centres and thence into the countryside along local tracks and foot-
paths.42 In the words of P. Slack: “They [plague epidemics] began in
ports and major towns; they spread along main routes of communica-
tion to other urban centres and from there to smaller communities and
to some of the less isolated villages.”43 Indisputably, in relative terms a
much higher proportion of urban centres than villages or rural com-
munities were ravaged by the Black Death.44 This appears to have occa-
sionally dawned upon Scott and Duncan:
Each epidemic was introduced from the Continent or Ireland. Some out-
breaks were also spread by boats trading up the east coast at ports between
London and Scotland. The inhabitants were well aware of the dangers of
transmission by this means […].45
It is erroneous that the Black Death struck “indiscriminately” in a
scholarly meaning of the term. It is true that it spread efficiently in the
countryside in times when there was no real knowledge of the nature
of epidemic disease, no knowledge of the mechanisms of spread of
bubonic plague, and no effective anti-epidemic organization, in con-
trast to the situation in India around 1900.
What Scott and Duncan avoid admitting or recognizing is that the
Black Death, the last wave of epidemics in France in the early 1720s,
and the plague epidemics in India around 1900, exhibited the same
unique and defining feature of bubonic plague, namely that mortality
rates did not increase with increasing population density, but on the
contrary decreased. This is what is concealed by their assertion that the
Black Death or the last plague epidemic in France “struck indiscrimi-
nately.” The same purpose is served by their strange terminology, that
bubonic plague in France in 1720–2 was “not density dependent”
42
Above: chapter 4: 151–93, Benedictow 2004: Map xviii–ixx, 17–22, 31–4,
57–241.
43
Slack 1985: 66.
44
Benedictow 2004: 227–33, and under the spread of plague in various countries.
45
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because it did not spread according to the epidemiological pattern of

diseases that spread by cross-infection, namely that levels of mortality
increase with increasing levels of population density. The fact that the
pattern of spread of bubonic plague does not agree with this principle
but, on the contrary, exhibits increasing mortality rates with decreasing
population density, does not mean that bubonic plague is not density
dependent, but that the spread of this disease functions according to a
different structure of density dependence, namely the inverse correla-
tion. The scientific and methodological point is that there is systematic
co-variation between mortality rates and population density. This is
the reason Scott’s and Duncan’s use of the word “indiscriminate” can be
considered unscientific, since the term implies that bubonic plague
spreads in an erratic, haphazard, random or fortuitous manner and
does not spread according to systemic structures, patterns and mecha-
nisms providing regularity that can be scientifically disclosed and
applied in the form of predictions. According to the methodological
tenets of science, there is an unbridgeable abyss between asserting that
a phenomenon is systematically random, haphazard or fortuitous and
therefore cannot be understood according to rules of causation, and
the view that its character or dynamics are poorly understood or not
understood. In fact, the mechanisms of the dissemination of bubonic
plague that produce the inverse correlation are understood; I presented
the solution twenty years ago and it has not been challenged, not even
by Scott and Duncan, who have read the paper containing it, but ignore
its central topic.
As shown above, British colonial authorities in India made tremen-
dous efforts to fight the plague epidemics and under the circumstances
succeeded in reducing strongly the impact of plague. However, Scott
and Duncan go on to assert that
Major epidemics of later plagues were mostly, but not entirely, confined
to the towns. In summary, haemorrhagic plague epidemics were density
dependent whereas bubonic plague (as in the Mende area at Marseilles)
was not.46
It is not a slip of the pen when Scott and Duncan state that the Mende
area is situated “at Marseilles,” when in fact this area is situated more
than 200 km away from Marseilles as the crow flies, and much further
away on the ground. It is as misleading as asserting that Sheffield is
46
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308 chapter eight
situated at London. By stating that these two places were in proximity,

they avoid confronting the way a bubonic plague epidemic spreads by
leaps or per saltem over considerable distances as demonstrated amply
also by this wave of epidemics, and thus are able to stick to their false
assertion that bubonic plague spreads only between adjacent rat colo-
nies (see above). It is not true that bubonic plague in the last French
epidemic was not density dependent: mortality shows a very clear pat-
tern of diminishing rates with increasing population size and density
and, conversely, increasing levels of mortality with diminishing popu-
lation size and density as shown in Figure 1 above and with empirical
detail in Benedictow 1987. It has been documented above that Scott
and Duncan have read this work.47
Scott and Duncan point out that about 200 years after the Black
Death or “in the 16th and 17th centuries” plague epidemics increas-
ingly became an urban phenomenon and that this development
reflected the fact that “haemorrhagic plague” was density dependent in
their amputated meaning of the term, because it spread by cross-
infection, while this was not the case with bubonic plague which is not
spread by cross-infection:
Two hundred years later, after a succession of epidemics, the dynamics of
the epidemics were more formally established. In general, the outbreaks
were density dependent, with the major epidemics confined to towns
with some 1000 inhabitants or more. In villages or hamlets or in parishes
where the population was scattered, the epidemics rarely exploded and
the mortality was usually confined to a few dozen households and we
have given examples in Chapter 9. This is the normal pattern of infec-
tious diseases spread person-to-person (smallpox and measles are exam-
ples) where a sufficient population density is necessary to establish an
epidemic […].48
One questions why the pattern or dynamics of spread should change
from the Black Death to later plague epidemics if it was the same dis-
ease throughout the period caused by the same contagion and was
transmitted and spread by the same mechanisms, as Scott and Duncan
imply here. Why plague should need 200 years in order formally to
establish its “dynamics” is incomprehensible and indicates fallacious
reasoning. Such change in the pattern of spread of a disease must
47
Scott and Duncan 2001: 315, 377. Above: 301–02. Cf. Benedictow 1987.
48
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presumably be due to and reflect changes in people’s perception of the

disease and consequent change in their pattern of behaviour or funda-
mental changes of society and social structures or both. In their rhap-
sodic casuistic presentation of outbreaks of plague in their chapter 9,
Scott and Duncan cannot prove that outbreaks in the countryside were
usually confined to a few dozen households. Instead, one should note,
for instance, Slack’s fine study of plague epidemics c. 1500 to mid-1660s
where he concludes:
when plague did strike a village, it often raised mortality by well over 100
per cent. ‘Plague comes seldom, but then very sore’ was the saying in
rural England.49
Contrary to Scott and Duncan’s assertion, the usual pattern of mortal-
ity in villages was not confined to a few households, but took the form
of very serious outbreaks, a pattern that constitutes evidence to the
contrary of Scott and Duncan’s inference.
Also the reason that plague in England became increasingly an urban
phenomenon was very different from Scott’s and Duncan’s assertion on
this point, and in fact Scott and Duncan provide, albeit inadvertently,
elements of the explanation on the preceding page and a few other
places, namely that ordinary people discovered that plague accompa-
nied refugees from plague-stricken urban centres and therefore drove
them away by all means:
The people fleeing from the plague in London met with a poor reception
in the country towns and villages, as in 1603. Creighton described how
“They are driven back by men with bills and halberds, passing through
village after village in disgrace until they end their journey; they sleep in
stables, barns and outhouses, or even by the roadsides in ditches and in
the open fields. And that was the lot of comparatively wealthy men.” A
stranger from London arrived in Southampton on 27 August and died in
the fields […].50
Scott and Duncan’s unsatisfactory practice with regard to references
again makes for extra work: the information on popular reactions cited
in their text is not taken from Creighton’s account of the epidemic of
1603, instead it is found in his account of the epidemic of 1625.51
Creighton also provides related types of information on the epidemic
49
Slack 1985: 84, and chapter 4.
50
Scott and Duncan 2001: 204, cf. 118, 359.
51
Creighton 1891: 517–8.
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310 chapter eight
of 1603.52 At another place in their monograph, pursuing a different

line of argument, Scott and Duncan again reveal knowledge of this
topic of popular resistance in the countryside:
Some outbreaks were also spread by boats trading up the east coast at
ports between London and Scotland. The inhabitants were well aware of
the dangers of transmission by this means and, by the late 16th century,
they were prohibiting from docking boats that came from ports where
the plague was raging.53
Certainly, these comments are not exaggerated: Bell states dramatically
that
London was at open warfare with the countryside. Always there were
people seeking the safety of the country. Where the highways entered
towns and villages armed watchmen turned the travelers back […].
Suspect to all, travel-stained, tired and dispirited, the flying Londoners
were kept outside towns and forced to find refuge in the fields. A few, the
most fortunate, carried tents. Others crept for cover beneath trees and
hedges, into cow-byres and dirty hovels of the farms.54
This pattern of anti-epidemic behaviour represents a sufficient expla-
nation for the new pattern of plague epidemics that emerged in England
and elsewhere in which outbreaks were mainly limited to urban cen-
tres, from which the epidemics occasionally spread into the country-
side.55 This development is based on contemporaries’ observation and
increasing understanding that plague was spread by people and goods
and that it was desperately important to prevent persons coming from
plague-stricken urban centres or areas from entering their community.
In Slack’s words:
Villagers’ suspicions of strangers in plague-time were founded on hard
experience […]. People with houses or friends in the country fled from
infected towns, only to meet with suspicion and hostility wherever they
went.56
Thus, the reason for the development of the pattern of plague epidem-
ics as being increasingly associated with urban centres has nothing
to do with higher population density in urban centres than in the
52
Creighton 1891: 483, 492.
53
54
Bell 1951: 137, 138–44.
55
Slack 1985: chapter 4.
56
Slack 1985: 19, 87.
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countryside, and everything to do with increasing human understand-

ing of the basic mechanisms of spread in dynamic interaction with
human observation and consequent efficient anti-epidemic action
taken on this basis.
Scott’s and Duncan’s attempts to establish a case for positive correla-
tion between levels of mortality and population density in English
plague epidemics can be shown to be untenable. On the contrary, sub-
stantial evidence can be marshalled to the effect that there was an
inverse correlation from the Black Death to the last plague epidemics
in England.
Epilogue: Sweating Sickness and the Inverse Correlation
Sweating sickness suddenly appeared in England in 1485, recurred in a

few epidemics in the years 1507–8, 1517, 1528, and 1551 and then dis-
appeared. Reading Slack’s valuable account of the epidemics of sweat-
ing sickness in England, the mortality patterns seemed familiar. The
demographic effects of the epidemics of the disease appear generally to
have been quite small, “only in the smallest villages did this short-term
increase in mortality amount to a serious loss of population,” and it had
only minor effect on mortality in larger communities.”57 In reality, this
appears to be a description of a disease producing higher mortality
rates in human habitats of small population density and lower mortal-
ity rates in human habitats of high population density, in other word
the inverse correlation of mortality rates and population densities,
mortality rates increasing with decreasing population densities, and
vice versa. This suggests that sweating sickness was transmitted by
insects with a zootic background. This understanding is supported by
the fact that sweating sickness was more prevalent in the warmer sea-
sons, especially summer and autumn, much like bubonic plague. One
interesting candidate for the cause of sweating sickness could perhaps
be a virulent biovar of murine typhus.
57
Slack 1985: 70–1.
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CHAPTER NINE
DEFINING FEATURE 3: BUBOES AS A NORMAL

CLINICAL FEATURE IN EPIDEMICS
General Introduction
The great pioneers of the modern study of plague epidemiology and

medicine saw thousands of cases of bubonic plague in the field and in
hospitals. They were certain that the disease they observed had to be
the same disease as they saw described in historical sources about the
Black Death. There is a curious contradiction between their under-
standing and the opinions of the advocates of alternative theories who
have never seen a plague case in their lives and are, nonetheless, entirely
sure that historical plague could not have been bubonic plague. One
of the central arguments of the pioneers of modern plague medicine
and epidemiology for the identity of historical and modern plague was
the descriptions of buboes and their accompanying clinical features
which they met in historical sources. Advocates of alternative theories
(must) make great efforts to disprove that the usual or normal appear-
ance of buboes in diseased persons is a unique and therefore a defining
feature of bubonic plague for the simple reason that this would rule out
or invalidate their alternative theories. In these endeavours, they argue
either that
(1) buboes are not a characteristic clinical feature of historical plague
epidemics and consequently do not constitute a defining feature, or
(2) buboes are not a defining feature of bubonic plague because
buboes are more or less a characteristic clinical feature of at least
one other disease which corresponds closely to their own alterna-
tive theory, or
(3) that the incidence or locations of buboes in historical plague or the
clinical panorama within which buboes occur in historical plague
epidemics are so different from those characterizing modern epi-
demics of bubonic plague that they must be two different diseases.
Karlsson and Morris follow the first type of approach which cannot
be taken as a serious position. Nonetheless, a fresh look at Karlsson’s
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buboes as a normal clinical feature in epidemics 313
theory will be taken below in Part 4 since it has found favour with the
Journal of Medieval History as a serious publishable theory.
The term “bubonic plague” reflects the characteristic development of
buboes on persons suffering from the disease. When a person is bitten
by an infective flea, plague contagion is discharged in the bite site at a
subcutaneous level suitable for normally draining it along a lymph ves-
sel to a lymph node that consequent upon the infection swells to form
a bubo.1 Occasionally, the infection may be drained to glands, espe-
cially the parotid glands.2 The element of reservation expressed in the
choice of the word “normally” stems from the fact that one form of
bubonic plague does not exhibit buboes. In a small percentage of cases,
infective fleas bite directly into a blood vessel so that the plague bacte-
ria will be discharged directly into the blood stream and avoid the lym-
phatic system which constitutes the body’s first line of defence, and in
these cases the infection will not give rise to buboes. Since the infection
is discharged directly into the blood stream, this form is designated
primary septicaemic plague in order to differentiate it from secondary
septicaemic plague when contagion enters the blood stream secondar-
ily after having broken down the bubonic tissue by the effects of toxins.
Primary septicaemic plague is so fulminant that the diseased usually
dies the same day; the course of illness lasts an average of c. 15 hours,3
which means that the course of illness is exceptionally short. This form
accounts for the many terrified observations of dramatic brief courses
of the disease and physicians who remark that plague without buboes
is the most dangerous form.4 However, as an epidemic disease, bubonic
plague is characterized by the normal occurrence of buboes on those
who contract the disease.5
1
Historians commonly and physicians occasionally use the anatomical term
(lymphatic) gland instead of node, however, by definition glands produce something,
e.g. hormones, enzymes or saliva, but lymph nodes do not, they constitute part of the
body’s immunity apparatus.
2
Choksy 1909: 352. It is the major salivary glands that are called parotid, the sub-
mandibular and sublingual glands. The parotid glands are thus, found in association
with mouth and throat. Cf. also the preceding footnote.
3
Philip and Hirst 1917: 529–30, 534–5.
4
See, for instance, G. Block, the Swedish physician, who wrote a remarkable proto-
scientific study of a plague epidemic in his home town of Norrköping in 1710–1, Block
1711: 21, 24–5: “That plague is the most dangerous which leaves no external signs, at-
tacking directly the spirits of life in the heart itself.” My translation from the original
Swedish edition of 1711.
5
Epidemics of bubonic plague include also a tiny incidence of primary pneumon-
ic plague rising from cases of secondary pneumonic plague by cross-infection with
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314 chapter nine
Plague can affect the lymph nodes in any part of the body,6 but will
for obvious reasons tend to affect concentrations of lymph nodes, espe-
cially in the groin or nearby femoral area, in the axillas or on the neck,
in the latter case often under the jaw or ear. Since bubonic plague is
(normally) transmitted by rat fleas, this mode of transmission will
decisively affect the distribution of sites of buboes, although one must
take into account that the distribution of sites is variable as it can be
affected by various local customs of clothing and footwear.7 A typical
distribution of the sites of buboes, according to Pollitzer and two stud-
ies based on ample evidence which are cited by him, would be: in the
groin or nearby femoral area around 55 per cent (with a somewhat
higher proportion in the femoral area, about 31 per cent), in the axillas
around 24 per cent, and on the neck around 9 per cent.8
Cohn maintains that the proportion of buboes in the groin can be as
high as 75 per cent; the assertion is not supported by a footnote on page
64 where it is made, but he states thirteen pages later9 that this figure is
given by A. Yersin in a paper of six pages on the plague in Hong-Kong
from 1894. In this brief paper, Yersin reports on his discovery of the
plague bacterium which was since named after him and provides
impressionistically quantified figures on the location of buboes, figures
that are not the outcome of systematic clinical observation.10 This is
the very beginning of modern medical plague research,11 and this paper
is cited at the expense of leaving unmentioned later studies of the loca-
tions of buboes which show substantially different figures. In fact it is a
factually misleading reference which could permit raising the question
of motives (see below).
Cohn also refers to the 19th edition of 1987 of Manson’s Tropical
Diseases, the general standard work on tropical epidemic diseases,
where the proportion of inguinal-femoral buboes is estimated at 70
per cent,12 which has been a consistent piece of information at least
since the seventh edition of 1921,13 the oldest edition I have found any
plague-infected droplets which will likewise not develop buboes. Davis’s assertion to
the contrary is commented on below: 321.
6
Butler 1983: 90. See also illustration in Sticker 1910: 382–3.
7
Pollitzer 1954: 421; Chun 1936: 315.
8
9
Cohn 2002: 77.
10
Yersin 1894: 663.
11
Cohn 2002: 64.
12
Manson’s Tropical Disease 1987: 593. 1921: 267, 1982: 340.
13
Manson’s Tropical Disease 1921: 267; 1982: 340.
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reason to consult. One should keep in mind that the chapters on plague
in such general standard works on infectious disease are tiny summa-
ries of the material presented in general standard works on plague, in
this case, it constitutes, for instance, just 2.2 per cent of Pollitzer 1954.
However, since Manson’s Tropical Disease up to this edition of 1987 is
not a specialist standard work in the sense that most of the chapters on
various infectious diseases are not written by specialists on plague, and
since no supporting footnote is given in the first nineteen editions
which would allow confirmation of sources, I do not understand the
significance which Cohn attributes to it and why he avoids the stand-
ard works on plague.
However, in the 20th edition of 1996, which Cohn has also used and
refers to elsewhere in his monograph, chapters are written by special-
ists and equipped with footnotes. In the small chapter of 6.5 pages on
plague representing less than 1 per cent of Pollizer 1954, the two authors
state in a general way that 70–80 per cent of buboes are located in
the groin.14 For support of this assertion, they refer to Butler 1972:
“A Clinical Study of Bubonic Plague. Observations of the 1970 Vietnam
Epidemic with Emphasis on Coagulation Studies, Skin Histology and
Electrocardiograms.” The title reveals immediately that this must be a
very restricted paper with respect to area and number of cases. In fact,
it is based on forty Vietnamese cases who, the author explicitly states,
“were not a representative sample of the epidemic” for a number of
reasons. Also importantly, the number of cases is much too small to
warrant statistical stability and representativeness.15 Perhaps even the
authors became uneasy confronted by their figures which showed that
in 88 per cent of the thirty-five cases the buboes were located in the
inguinal-femoral area,16 since they arbitrarily reduce the percentage to
70–80 per cent. A couple of years later in 1974 Butler et al. published a
paper based on the study of twenty-two Vietnamese plague cases in
which 66 per cent (14) of the patients presented with inguinal-femoral
buboes.17 A paper relating to the study of twenty-one Vietnamese
patients presented a very different distribution of the locations of
buboes.18 Obviously, the materials are too small to provide statistical
14
Smith and Thanh 1996: 918–24.
15
Butler 1972: 274.
16
Butler 1972: 272.
17
Butler, Bell, Linh et al. 1974: S78–9.
18
Legters, Cottingham and Hunter 1970: 639–40
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316 chapter nine
stability and relate to a specific Vietnamese cultural background

that could also affect the distribution of buboes for various reasons
which the researchers under the circumstances have not studied.
Unsurprisingly, Cohn must admit that “Manson, his successors, and
Yersin have not tabulated or quantified the positions of the plague
scars,” nor have they provided the material basis for their quantifica-
tions, but the numbers involved are, as we have seen, very small.
Given this background, it is necessary to increase the level of empiri-
cal documentation and mention that Chun cites four studies on the
location of buboes according to mass materials from China and India
around 1900, but none of them show 70–5 or 70–80 in the groin plus
femoral area. Instead, they show the proportion of femoral-inguinal
buboes varies between 48 and 68 per cent; in Mumbai in 1900, two
independent studies provide figures of 55 per cent and of 68 per cent.
Chun comments on the considerable difference between these figures:
“It may be that this discrepancy is due to the difference in the style of
dress adopted by Indians and northern Chinese,” and he goes on to
address this issue in considerable detail.19
Yersin’s impressionistic guesstimate and Butler’s small study of
Vietnamese cases which is explicitly characterized as an unrepresenta-
tive sample cannot be used for generalization, as Cohn appears to
assume; these studies do not provide alternative evidence which allows
one to neglect or ignore or override the statistical materials for Mumbai
and Hong Kong provided in the special standard works on plague
which also have in common that they are meticulously annotated. The
only statistically valid material Cohn refers to on p. 74 is also from the
infancy of modern medical plague research, namely, reports from
Mumbai’s plague hospitals for the plague year 1896–7, the first plague
year in India and Mumbai. In this study 58 per cent of the patients who
developed buboes had them in the groin or nearby femoral area, a fig-
ure which agrees with the data given by Pollitzer and Chun. Cohn’s
predilection for obsolete data and disassociation between argument
and data are typical features of his monograph.
The reason that buboes arise more frequently in the groin or nearby
femoral area than anywhere else on the body is not that a flea “can bite
no higher than just above the ankles” as Cohn asserts.20 However,
19
Chun 1936: 314–5.
20
Cohn 2002: 64.
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people can be bitten by fleas not only when they walk about or sit down
but also when they lie down to rest or sleep. This is the obvious reason
that plague buboes also develop on the upper part of the body and that
persons can develop two or more buboes at various locations of the
body. Plague buboes develop most commonly in the groin or femoral
area because the legs constitute a large part of the body’s surface and
because people can be bitten in the legs both during the day when
walking about or sitting down and also when lying down to rest or
sleep: legs have a twenty-four-hour exposure to flea bites, but the rest
of the body only around one-third of this time. Not only ethnic and
historical differences of clothing and footwear can affect the distribu-
tion of the location of buboes but also sleeping arrangements. For
this reason, contrary to what Cohn may seem to assume, variation in
the statistical distribution of the location of buboes is of little or mod-
est significance for identification of the disease or at least present
some stringent demands for empirical explanation. The crucial fact
remains that buboes as a regular manifestation of an epidemic disease,
according to present medical knowledge, are associated only with
bubonic plague. The causes of this fact will now be considered more
thoroughly.
Together with its numerous other functions, the skin protects the
human body from invasion, including by infectious agents. If the skin
is broken, infection may enter, but it will encounter the body’s first line
of defence against invasion, namely the lymphatic system. Most infec-
tions can under varying circumstances and by varying mechanisms
enter through abrasions or cuts in the skin and be drained through a
lymphatic tract to a lymph node and occasionally cause a swelling and
the development of a bubo. However, this means that infection by the
cutaneous route is dependent on the presence of a cut or abrasion in
the skin before exposure to contagion and that contagion accidentally
meets the skin exactly at the point where it is punctured, cut or broken.
These circumstances produce the typical pattern of rare, occasional or
episodic occurrence of buboes. Thus Twigg is certainly correct when
he states that “buboes may occur in other bacterial and viral diseases.”
Surprisingly, he goes on to maintain that this is “notably” the case
with “anthrax and small pox.”21 For this important assertion, he does
21
Twigg 1984: 36.
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318 chapter nine
not provide a supporting reference to any scholarly study, and it there-

fore unavoidably takes on the character of an arbitrary assertion.
The reason is probably that he advocates anthrax as an alternative
microbiological theory of historical plague and is concerned about the
conspicuous role of buboes as an ordinary clinical feature of epidemic
bubonic plague, a clinical criterion of identification that anthrax can-
not satisfy. This is not accidental, it is due to a crucial difference in the
modes of infection:
(1) in the case of bubonic plague, infection is transmitted by the bite
of infective flea(s) which combines puncturing of the skin with the
depositing of contagion at a subcutaneous level suitable for being
drained from the bite site through a lymphatic tract to a lymph node,
thus, the puncturing of the skin is a part of the process of transmission;
(2) in the case of anthrax, smallpox and other infectious diseases,
in order to produce buboes the contagion must by chance meet with
an accidental portal through the skin and then be moved by some
mechanism through the broken skin to a subcutaneous level suit-
able for being drained to a lymph node. These two points explain
that buboes can be a regular feature of plague and not of other infec-
tious diseases, specifically the anthrax and smallpox mentioned by
Twigg, although buboes can be a rare contingency in these diseases. In
epidemic form, anthrax is ordinarily contracted by the eating of
contaminated un(der)cooked flesh, while smallpox is transmitted by
inhalation of contaminated droplets. Since there are no lymph nodes
in the gastro-intestinal system or in the lungs, epidemics of these dis-
eases are not associated with buboes; instead other defensive functions
of the human immune apparatus are activated. Twigg significantly
and misleadingly understates the difference in the relative incidence
of buboes when he reduces it to buboes being “more regularly pres-
ent in bubonic plague than in any other disease.”22 If Twigg wishes
to maintain that anthrax or smallpox quite often present with buboes,
he cannot neglect to explain how these infections could be often—
or usually—transported from the normal site of introduction, the
gastro-intestinal tract or the lungs, to lymph nodes. In the case he
cannot find support in the medical literature for the frequent inci-
dence of buboes in cases of anthrax or small pox or other diseases
22
Twigg 1984: 36. See also Sallares 2007: 237.
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transmitted by similar mechanisms, together with a medical explana-

tion of how this could occur in any standard work on epidemic dis-
eases, he must obviously have a very poor case. The crucial fact remains
that bubonic plague is the only epidemic disease known by medical
science which presents with buboes as a normal feature of the clinical
panorama. This fact is based on hard evidence. For this reason, it must
be addressed by all advocates of alternative theories of the microbio-
logical nature of historical plague. In order to be viable theories,
they must contain specific empirical explanations for why infected per-
sons should regularly present with buboes; if not they are ipso facto
falsified.
A generally overlooked point of considerable importance is that
another disease is characterized by the development of buboes, namely
tularaemia. Tularaemia is a bacterial disease of wild rodents, especially
of beavers, hares, muskrats, rabbits and squirrels and is mainly con-
tracted by hunters. In Europe, this disease is associated with rabbits
and hares on the Continent, in the Nordic countries with hares and
lemmings, and is also called “lemming fever” or “hare pest.” In infected
persons, this disease presents in a number of ways dependent on the
route of infection: it may occasionally infect by ingestion of contami-
nated water and also of un(der)cooked meat or by inhalation. The main
form characterized by “fever and a bubo” is transmitted by ticks or
deer-flies, but hunters can occasionally also contract infection and
develop a bubo in the process of skinning sick animals if they have cuts
or abrasions in the skin of their hands.23 Helpfully, Butler presents the
clinical and epidemiological elements of bubonic plague and tularae-
mia in a table for immediate comparison and differentiation: tularae-
mia is easily distinguishable from bubonic plague according to a
number of criteria, for instance: (1) it is restricted to wilderness
and hunters (today occasionally also campers) and, thus, ordinarily
exhibits an endemic or episodic type of occurrence; (2) the course
of illness is “usually indolent and self-limited”; (3) the buboes are
normally located on the upper part of the body in the axillas or on the
neck (reflecting the position of ticks or deer-flies in the vegetation);
(4) the level of mortality is much lower, and so on. These two diseases
cannot be confused at the epidemiological level or at the level of clinical
23
Butler 1983: 90–1; Manson’s Tropical Disease 1982: 355–9.
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320 chapter nine
analysis. Since epidemics of bubonic plague definitionally spread in

human societies in sharp contrast to tularaemia, bubonic plague is
the only epidemic disease in human habitats, rural or urban, which is
characterized by the typical formation of buboes. Therefore, this fea-
ture constitutes a defining feature of bubonic plague.
Recent genetic research has also revealed that Yersinia pestis target
“lymph tissues during infection and carry a virulence plasmid, pCD1,
which is required for infection in these tissues, as well as to overcome
the hosts’ defence mechanism.”24 This contributes to explaining why
buboes constitute a predominating and definitional clinical feature of
bubonic plague.
An important fact should now be clear, which is that the only other
case of a disease characterized by the usual development of buboes is
directly associated with insect bites and bacterial infection. The crucial
point is that the development of buboes results from insect bites which
deposit contagion at a subcutaneous level which is then normally or
usually drained through a lymphatic tract to a lymph node. In such
diseases, and according to present medical knowledge only in such dis-
eases, the appearance of buboes is an ordinary or usual clinical feature
because it is systematically related to the mode of transmission of infec-
tion by insect bites. Bubonic plague and tularaemia have in common
the fact that they do not spread by interhuman cross-infection but are
transmitted by ectoparasites conveying contagion from rodents to
human beings.
It is of crucial significance in this context that for technical reasons
associated with the mode of transmission no disease spread by inter-
human cross-infection can be characterized by ordinary epidemic
occurrence of buboes. This corresponds completely and without excep-
tion with observed fact. Conspicuously, the advocates of alternative
theories make no attempt to explain how normal manifestation of
buboes should be physically realized in persons contracting the alter-
native type of epidemic disease they advocate. The fact that they pass
by in silence this crucial problem must be taken as an indication that
they are unable to provide reasonable medical explanation. Their
silence on this point constitutes therefore crucial evidence of the unten-
ability of their assertions and the incompatibility of their alternative
theories with this basic fact. All alternative theories of historical plague
24
Dongsheng, Yanping, Yajun, et al. 2004: 1229.
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based on microbiological contagion spread by cross-infection are ipso

facto invalid; this is the case with the alternative theories of Karlsson,
Morris, Scott and Duncan and Cohn. Karlsson and Morris who advo-
cate theories of primary pneumonic plague must ignore the obvious
fact that buboes are the most usual clinical feature mentioned by con-
temporaries from the Black Death to the last plague epidemics more
than 300 years later.
Davis, who recognizes the inherent danger, makes a disquieting
attempt at doing away with this problem by asserting that
Buboes can occur in cases of pneumonic transmission and cannot be
construed as proof of transmission by fleas that infest either rats or
humans.25
In support of this statement, he refers in the accompanying footnote
to an impressive number of works on plague, among them the fol-
lowing standard works: Wu Lien-Teh 1936b: 409, Hirst 1953: 29,
Pollitzer and Li 1943: 161/212–6.26 All of these fine works on plague
have in common that they do not contain anything that supports
Davis’s assertion, neither on the indicated pages nor elsewhere—they
are spurious references (who was the journal’s consultant?). Davis
leaves out the only standard work on primary pneumonic plague,
Wu Lien-Teh 1926. The reason is clear: no such case is mentioned.27
In this footnote, Davis goes on to refer also to historical plague
works, Biraben 1975: 73, 129, and Nohl 1961: 18. These works like-
wise contain no support for this assertion on the indicated pages, and
to anyone knowing these works it will be obvious that support is not to
be found anywhere else in them, and that these references are also spu-
rious. Davis does not attempt to explain medically how plague conta-
gion could spread from the lungs to the lymph nodes nor does he
explain how a non-episodic, regular pattern of incidence could occur.
All assertions to the effect that the epidemic occurrence of buboes is
associated with any other epidemic disease than bubonic plague are
untenable.
25
Davis 1986: 461.
26
The discrepancy in number of pages is due to my use of the version published in
Chinese Medical Journal 1943: 212–6, while Davis refers to a somewhat shorter version
published at the same time in Journal of Infectious Diseases 1943: 160–2.
27
Wu Lien-Teh 1926: 241–73.
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Contemporary Notions and Observations of Buboes (and

Associated Secondary Clinical Manifestations)
Sticker’s ambitiously broad account of all historical plague epidemics in

his old but impressive two-volume work on plague28 has inevitably
become partly obsolete at least in the sense of having become increas-
ingly incomplete as new research has been published. However, some-
what disappointingly it still provides more concrete information on
clinical features than any other history of plague, and as a physician
Sticker exhibits strong interest in medical or epidemiological concepts
and terminology. Having studied plague in India at the beginning of
the twentieth century and having contracted and survived plague, he is
in a unique position to put his seemingly boundless energy into good
scholarly use. His standard work will be supplemented from later works
in the following discussion.
“There was little appreciation that individual diseases were separa-
ble entities before 1600,” Slack states,29 I would rather say before 1550.
In his diary for the years 1550–72, Absalon PederssØn, the Norwegian
humanist, identifies a number of diseases with specific terms: plague
(“pestilence”), syphilis (“pocks”), small pox (“small pocks”), tuberculo-
sis (“consumption”), exanthematic typhus (“spotted fever” or “soldiers’
disease”), dysentery (“flux”) and leprosy (“[ho]spital disease”).30 This
development appears to be closely related to a growing recognition
from about 1510–20, associated with the Renaissance, of the conta-
giousness of epidemic diseases. In Norway and Denmark this develop-
ment is noticeable from the 1520s at the latest and was apparently
influenced by the University of Rostock and presumably other institu-
tions of learning in northern Germany where students of these coun-
tries often studied at the time.31 The famous pioneering physician
J. Fracastoro systematically discerned plague from exanthematic typhus
in Italy around 1530.32
28
Sticker 1908: 42–107.
29
Slack 1985: 25.
30
Benedictow 2002: 204. The term “[ho]spital disease” for leprosy in the Nordic
languages refers to the early establishment of particular hospitals for lepers in the High
Middle Ages. In English it may have a certain parallel in the contemporary term “la-
zarhouse disease.”
31
32
Sticker 1908: 106; Ackerknecht 1963: 30.
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Against this background, it is a very noticeable fact that when the

subject is broached of how late medieval and early modern historical
plague disease presented to contemporaries, there is broad agreement
among scholars that one clinical manifestation in particular impressed
itself on their minds. From the beginning of the Black Death in the
Crimea and Constantinople, and as it spread all through Europe, con-
temporary commentators who generally had at best very confused
ideas about the nature of epidemic disease mention with conspicuous
regularity, if they present even minimal clinical detail, buboes as the
distinguishing clinical feature. This was also the case in connection
with plague epidemics in the following centuries. This clinical feature
impressed itself so strongly on contemporaries and distinguished this
disease so sharply from all other epidemic diseases ravaging contem-
porary populations that contemporaries from the very beginning con-
structed specifying designations or identifications of plague epidemics
which reflect the appearance of buboes as a conspicuous characteristic
and distinguishing clinical manifestation.33
The clinical manifestations which impressed themselves on contem-
poraries and led to the development of generalizing terminology can
be seen in Matteo Villani’s chronicle, for example, where he relates in
connection with the Black Death in Florence in 1348: “in most [of the
infected] there were growths in the groin, and with many in the pits
under the arms, under the right and the left, with others in other parts
of the body, so that almost generally some single swelling manifested
itself on the body of the infected.”34 Clearly, Villani was of the opinion
that buboes were a general and characteristic feature of the disease
which distinguished it from all other diseases known to him and his
contemporaries, and this is the basis of the generalizing terms which he
goes on to form. When he reverts to the subject in connection with the
second plague in Florence in 1362, he can avail himself of generalized
33
Cohn 2002: 63–4, 68–9, has also to some extent noted this development, but since
his aim of necessity is to reject the possibility that this proves that the disease was
bubonic plague, although he knows of no other disease characterized by this clinical
feature, his presentation becomes episodic and his discussion superficial and tenden-
tious. Of course, this development was not especially associated with Florence, it is his
narrow perspective that associates it with Florence and Italy.
34
Matteo Villani, Cronica 1995–1: 9: “e a’ piu ingrossava l’anguinaia, e a molti sotto
le ditella delle braccia a destra e a sinistra, e altari in alter parti del corpo, che quasi
generalmente alcuna enfiatura singulare nel corpo infetto si dimostrava.” My transla-
tion of the chronicle’s text. Cf. ibid.: 11.
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324 chapter nine
terms referring to buboes for identification of the disease and as the

same disease as the Black Death (see below). It is also noteworthy that
he gives main locations of buboes which are similar to those observed
in cases of modern bubonic plague.
These generalizing designations focus on buboes of the groin area
(in Latin inguen, in modern Italian “inguinàia” or “inguine”/ “inguinale,”
in contemporary northern Italian often slightly changed into
“anguinaia”/ “anguen”), or provide more generalized expressions of a
disease characterized by buboes, especially in the groin area, and great
mortality: “pestis inguinaria”35 (= inguinal pestilence, Modena 1348),36
glandular plague, “mortalité des boces”37 (= mortality of buboes,
Rheims 1349), “l’épidémie des boces” (Narbonne 1349),38 “sterffde van
den droesen” (= mortality of the buboes, Cologne 1350),39 or charac-
terized by “dolor ignitus in inguine” (= a fiery pain in the groin, France,
Paris).40
Cohn 2002: 64, cites three generalizing expressions “inguinarie,”
“pietolenzia dell’anguinaia” (= pestilence of the groin), and “mortalità
dell’anguinaia” which I have not mentioned above as associated with
“Florence after 1348.” In the accompanying footnote 51, Cohn refers to
Matteo Villani, Cronica con la continuazione di Filippo Villani 1995,
Volume 1: 273, 300, 514, 585–6, 660–1, 663. However, on these pages
nothing is said about plague or buboes—all of these page references are
erroneous. As we shall see, the second and third of the medical terms
for plague that Cohn cites are instead associated with the second vol-
ume of Matteo Villani’s chronicle and with the next plague epidemic in
Florence of 1362; the first term may be associated with the second
plague epidemic in Siena in 1363 and a different source (see below).
Cohn also asserts in this connection that the development of terms to
describe plague in connection with the Black Death which were
“derived from the boil’s position in the groin” took place “particularly
in Florence.” As we have seen this was not the case; this assertion
depends on false references to Matteo Villani’s chronicle and a narrow
35
Sticker 1908: 51, without specification of source.
36
Cohn 2002: 64.
37
Desportes 1977: 794.
38
Sticker 1908: 59. For his account of the Black Death in Narbonne, Sticker refers to
works which I have not had occasion to get hold of, namely Cayla 1906 and Martin
1859.
39
Sticker 1908: 75.
40
Littré 1840–1: 202, 232. Cf. Gasquet 1908: 40–1.
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Florentine or Tuscan perspective. Such terms arose in connection with

the Black Death elsewhere in northern Italy and also in France and
Germany and also in connection with subsequent plague epidemics
elsewhere, in Ireland, Belgium, and Russia.
In the subsequent plague epidemics, the use of generalized designa-
tions continued to be developed, strengthened and familiarized. Matteo
Villani comments on plague in Germany and Brabant in 1358 calling it
“pistolenzia dell’anguinaia” and mentions in another chapter “moria
dell’anguinaia” in Brabant which also spread to some areas in Italy, and
he refers to the second plague in England also with the characteristic
expression “pistolenzia dell’anguinaia.”41 Matteo Villani makes it clear
that the plague of 1362 was the same disease as the Black Death, calling
the first chapter on it “How the Mortality of the Groin Recommenced
in Various Parts of the World,”42 and after having used the expression
“mortality of the groin” in the chapter’s title, he goes on to state in the
first line of the text: “the mind-boggling disease of the groin recom-
menced this year, similar to that which had begun in 1348.”43 He reverts
to this plague epidemic later in his chronicle using in the chapter’s title
the expression “mortalità dell’angunaia” and in the opening text of the
chapter the expression “pistolenza dell’ anguinaia (= pestilence of the
groin area, Florence 1362).44
In the Necrology of the Dominican cemetery in Siena it is casually
written in the margin in 1363 when there is a huge increase in inter-
ments: mortalitas generalis inguinarie45 (= general inguinal mortality).
Also elsewhere in Europe such expressions or terms were developed
41
Matteo Villani Cronica 1995–2: 273, 300, 514.
42
“Come mortalitá dell’anguinaia ricominció in diverse parti del mondo,” my
translation.
43
“la moria mirabile dell’anguinaia in questo anno ricominciata, simile a quella
che prencipio ebbe nel MCCCXLVIII […],” my translation. Matteo Villani Cronica
1995–2: 448.
44
Matteo Villani Cronica 1995–2: 585–6, see also pages 660, 663. Cohn 2002: 138,
makes a free translation of the introductory passage, again showing, as pointed out by
Carmichael, a strange reluctance to use the word buboes, perhaps because of its strong
association with bubonic plague, instead translating the expression “pestilence of the
groin area,” with “pestilence of the glandular swellings” which ignores the original
text’s unambiguous association of the disease with the groin and indication that it was
characterized by clinical features associated with the groin.
45
I Necrologi di San Domenico in Camporegio 1937: 95. Written rather casually
in the margin of the necrology, which in this case is a burial register, this expression
indicates quite a widespread term and notion. Cohn erroneously includes this source
in his reference to the development of such terminology in post-Black Death Florence
(see above).
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326 chapter nine
to designate plague: disease of buboes or mortality of buboes (Russia

1360, 1387),46 pestis inguinaria (Cologne 1365),47 pestis glandium/
glancium (Ireland 1369), disease of buboes (Liège, “Belgium” 1370),48
infirmitas carbunculi et glandulae (= disease of carbuncles and glands,
Parma 1371),49 peste anguinaia (Florence 1449),50 and so on. The proc-
ess of familiarization with the specificity of bubonic plague can be
illustrated by Marchionne Stefani’s statement on the plague of 1374
which was to him the “usual pestilence of inguinal or axillary swell-
ings,” and in 1383 commented that the plague killed “in the same way
as the other mortalities, with that sign of great swelling under the arm
and over the leg at the groin.”51
Another related development is that bubonic plague was considered
such a conspicuously specific disease that a distinguishing term for this
disease was needed according to the medical notions of the time. First,
the term “epidemic” was employed for specific designation of bubonic
plague in order to distinguish it notionally and terminologically from
other contagious diseases which generally were called “pestilence” or
“pestilential.” The generalized expression “l’épidémie des boces” was
used in Narbonne to designate the Black Death in 1349,52 under the
influence, as it may seem, of the medical faculty of Montpellier. In Paris
physicians called the Black Death “épidémie,” as also was the case with
a chronicler discussing plague in the area around Trier in western
Germany (epidemia).53 This terminological development appears in
strengthened form when the plague in Hesse and Westphalia in 1371
was characterized by the term pestilentia epidemiarum54 = the epidem-
ics’ pestilence, implying that that plague was considered the essence of
epidemic disease, the highest and most dangerous refinement of mias-
matic poison, the King Death of epidemic diseases. A related term, pes-
tis epidemialis was used in Thuringia, especially in Frankfurt and
Eisenach.55 The link becomes obvious with the expression inguinaria
46
Sticker 1908: 76, 80.
47
Sticker 1908: 77.
48
Sticker 1908: 77.
49
Cohn 2002: 61.
50
Herlihy and Klapisch-Zuber 1978: 375.
51
52
Sticker 1908: 59. The Black Death was recognized as present in Narbonne around
1 March 1349, Benedictow 2004: 101.
53
Sticker 1908: 60, 67.
54
Sticker 1908: 77.
55
Sticker 1908: 81.
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pestis seu epidemiae morbus = “inguinal pestilence or disease of epi-

demic” used to designate the plague which reigned in Wittenberg in
1535.56 Thus, logically the term “epidemie van die pestilentie”57 = “epi-
demic of pestilence” was developed, showing that “pestilence” could be
used as a specific term for bubonic plague, producing, therefore, a need
for another general term for contagious diseases, a role which was
increasingly filled by epidemia or “epidemic,” which has retained this
position to this day, while the form “pest” has retained its position as a
specific word for bubonic plague. In English, the word “plague” reflects the
fact that the English found another solution to the need for specificity
in the designation of this disease, taking this term slowly into specific
use as an Anglicized form of Latin plaga with the meaning of “a blow,”
which originally was a general term for a dangerous disease, a develop-
ment that was becoming pronounced by the late sixteenth century.58 In
a document of September 1349, Magnus Eriksson, King of Norway and
Sweden, used the word plaga to designate the Black Death.59
This perception of plague as dominated by buboes did not start with
the Black Death; it has been a consistent feature of how people of the
past perceived plague and what really characterized the disease, besides
the exceptional mortality. Twigg rejects the fact that Gregory of Tours
uses the term lues inguinaria = “disease of the groin” to designate the
first plague epidemic of the Justinianic pandemic of 541–76660 which
spread over southern France and conquered Old Gaul in the years
543–4.61 However, he does not point out any alternative specific disease
which could fit this clinical descriptive term, presumably because every
specification easily could be rejected by anyone knowledgeable of epi-
demic disease or with access to a standard textbook on epidemic dis-
eases. Since small pox (variola maior) was probably not present in
Europe at the time or for a long time to come,62 the alternative Twigg
has in mind would have to be anthrax. Any reader interested in the
matter is encouraged to look up anthrax (or smallpox) in any standard
work on epidemic disease and see whether buboes are mentioned at all
or as more than episodic individual occurrences that would never give
56
Sticker 1908: 92.
57
Sticker 1908: 99.
58
Slack 1985: 64–5.
59
Benedictow 2002: 22, 96–7; Benedictow 2004: 152, 160, 171–2.
60
Twigg 1984: 35–6.
61
Simpson 1905: 15; Sticker 1908: 30: Little 2007: 11.
62
Cartwright 1977: 76–7; Greenwood 1935: 227; Copeman 1960: 127–8.
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328 chapter nine
rise to a generalized designation of the disease as involving this symp-

tom. Twigg ignores the accounts of the violent plague epidemics in
Constantinople given by the Byzantine physician Procopius which
contain quite detailed clinical information on buboes,63 for instance:
“On a sudden they became feverish […] in some cases, on the same
day, in others on the next, in others in a few days after there arose a
bubo, not merely on what is called the groin, but under the armpit; in
some cases the bubo appeared behind the ears and in other parts.”64
Also in this pandemic of plague, similar generalized terms referring
directly to the ordinary occurrence of buboes as a characteristic clini-
cal feature of the epidemics are in frequent use: inguinarium (550),
inguinarium morbum, fever with buboes, glandulae (561), morbus
inguinarius (582), clades65 inguinaria, pestis inguinaria (589), lues ingui-
naria (591), pestis inguinaria (599), clades glandolaria (600), and so
on,66 which about exhausts the potential of Latin for forming clear des-
ignations of a disease characterized by the formation of buboes, espe-
cially in the groin and nearby femoral area. Buboes in the axillas or on
the neck are also specifically noted quite often.67
Recently, M.G. Morony has supplemented and corroborated this
with information from Syriac sources on the Justianic pandemic focus-
ing on epidemics specified by the use of the clinical term “sharcūṭā”
“which refers both to the swellings or tumors and to the disease itself,”
and the term “mawtānā de sharcūṭā” meaning epidemic of tumors.68
Also the corresponding Arabic term “ṭācūn” is used in this meaning.
The terms (“mawtānā de) sharcūṭā” or “ṭācūn” were used to designate
the first plague epidemic of 541–4, next in connection with epidem-
ics of 562, 573–4, 600, 639, 686–7, 698–9, 713, 744–5.69 One should
note that a plague focus running in quite a broad territorial band from
the Persian Gulf up to eastern Syria and south-western Turkey was
established at the latest during the Justinianic pandemic and would
give rise to local outbreaks of plague.70
63
See, for instance, Simpson 1905: 6–14.
64
Cited after Simpson 1905: 7–8. Cf. Little 2007: 8–9.
65
The word clades here has the meaning of “mortality”; it usually has the related
meaning of military losses.
66
Sticker 1908: 31–4; Simpson 1905: 15–16.
67
Ibid.
68
Morony 2007: 61.
69
Morony 2007: 61, 65–6, 70, 73, 76.
70
See for instance Benedictow 2004: 37–40, 44–8.
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By now, quite a number of scholarly studies on this pandemic pro-

vide ample material for the identification of the disease as bubonic
plague.71 Importantly, new developments in paleomolecular analysis of
DNA have in recent years given rise to several papers reporting recla-
mation of DNA of Yersinia pestis from skeletal remains of the time of
the Justinianic pandemic a.d. 541–766, from the second half of the
sixth century or later, from Sens in northern France, Aschheim near
Munich in Upper Bavaria and from Vienna,72 providing independent
and substantial, even decisive evidence to the effect that Gregory of
Tours’s use of the term lues inguinaria, disease of the groin, refers to
bubonic plague.
The tendency towards generalized designation of the epidemics with
reference to buboes is reflected in numerous accounts or descriptions
of buboes from the very beginning of the Black Death to the final par-
oxysm of plague in southern France in 1720–2. When the inhabitants
of the north-eastern French city of Rheims in 1349 use the term “mor-
talité des boces” (= mortality of buboes) to designate the Black Death,
the reason must be that plague cases in this city conspicuously and
ordinarily presented with this clinical feature. This is corroborated by a
list established in order to register by name, approximate age, and social
status persons who had been miraculously healed from plague disease
by prayer to St Remi, in which list some of the entries include some
basic clinical description as proof that the disease really was plague. A
mother declared to have seen her small boy be healed from three
buboes, two buboes in the groin (area), and one in an axilla; at the time
of Ascension Day (21 May), a young girl first had a bubo under her
arm, and then a second bubo appeared on her neck; a married man had
an enormous bubo on his neck 17 July; Jehan de Blanzy, a man of some
learning, related that his wife’s disease began with strong fever, next
buboes appeared in the groin (area) and her condition began to improve
29 July after intercessory prayer to St Remi had been said. The local
canon and poet Guillaume de Machet emphasizes buboes as the distin-
guishing feature of the disease. All information about the locations of
buboes on the body is consistent with modern bubonic plague. Thus,
not only the general terminology but also all the individual pieces of
clinical information provided by contemporaries are consistent with
71
See for instance Russell 1968; Biraben and Le Goff 1969; Allen 1997; Keys 1999;
Sarris 2000.
72
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330 chapter nine
bubonic plague—only with bubonic plague and with no other disease.

This is also the case with the seasonality of the epidemic in Rheims,
arriving in the autumn of 1348, being suppressed by cold winter
weather, developing rapidly with the advent of warmer spring weather,
and fading away in the autumn.73
Correspondingly, the inhabitants of Narbonne not only used the
generalized term of an epidemic of buboes (“l’épidémie des boces”) but
also used more individualized clinical information to the effect that
plague cases started abruptly with fever and headache and then devel-
oped buboes in the groin (area) and in the axillas,74 again a description
which is entirely compatible with modern bubonic plague both with
respect to the start of illness, the typical early symptoms of high fever
and severe headache, and the development of buboes and their loca-
tion.75 In Strassbourg a local chronicler relates that all victims died
from buboes or (enlarged) glands which swelled under the arms or
high up on the legs, and when the bubo appeared, they died on the
second, third or fourth day.76 When Dubois concludes with respect to
the Black Death that “everywhere in France, the plague has taken on
the bubonic form with secondary manifestations,” he has a solid empir-
ical foundation for this summary of the evidence.77
In “Germany” it is stated in the Upper Palatinate (Ober Pfalz) that
persons developed a bubo and died on the third day, and in Cologne
there was a “great mortality from the buboes.”78 In addition to the pres-
entation of more generalized terms and expressions used by contempo-
rary Florentines, it can be mentioned that in the north-eastern Italian
provinces of Friuli and Istria the diseased generally presented with
three main clinical manifestations “in glantia (= in the glands), carbun-
cle et sputo sanguinis (= carbuncle and bloody expectoration).”79
Carbuncles are a normal part of the clinical panorama of modern
bubonic plague: they may either develop at the bite site as a local infec-
tion caused by remaining plague bacteria, often called primary plague
73
Desportes 1977: 794–9. Cf. Dubois 1988: 320.
74
Sticker 1908: 59.
75
Simpson 1905: 263; Chun 1936a: 310; Pollitzer 1954: 411; Butler 1983: 73.
76
Sticker 1908: 67.
77
Dubois 1988: 316. My translation from French. With the term secondary mani-
festations he has probably in mind bloody expectoration in cases of secondary
pneumonia.
78
Sticker 1908: 75. My translation from contemporary German: “groß sterffde van
den droesen.”
79
Sticker 1908: 50.
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carbuncles, or may, like pustules, be due to an invasion of the skin

through the blood-stream, and may, thus, be considered secondary and
consequent upon the development of septicaemia.80 Carbuncles as a
usual clinical feature of an epidemic disease cannot be associated or
explained by any of the alternative theories, although they occur epi-
sodically in relation to anthrax in cases where contagion is contracted
through abrasions in the skin. As a usual clinical feature carbuncles
could probably represent a defining feature or a very strong indication
of the nature of the disease as bubonic plague. This explains why car-
buncles are not entered as a clinical feature of any epidemic disease in
the indices of general textbooks on epidemic diseases,81 in contrast to
the standard works on (bubonic) plague where this is an ordinary
entry.82
In his historical presentation of plague, Sticker cites a great number
of historical sources in which buboes are mentioned, often with speci-
fication of locations on the body, that buboes were associated with
sharp intense pain, and other clinical manifestations that are consistent
with modern bubonic plague: severe headache, spitting of blood, rapid
course and brief duration of illness, and so on. For sceptics it can be
mentioned that, in the case of the pandemic that started with the Black
Death and petered out in the seventeenth century and ended (except
in Eastern Europe) at the beginning of the eighteenth century with a
couple of explosive outbreaks, Sticker provides such information in the
first volume for the Black Death on pages 45, 47, 49–54, 57–60, 64, 65,
67–8, covering most of Europe, from Kaffa on the Crimea and
Constantinople to Northern Germany and Poland, but misses out
England (see below). For the next wave of plague epidemics of 1361–5,
see pages 76–7, also with great geographical distribution, for the third
wave of 1368–71, see page 77, and so on through the centuries. The
total amount of evidence is massive.
80
Pollitzer 1954: 206, 425.
81
See, for instance, Manson’s Tropical Diseases 1982, Jawetz, Melnick and Adelberg
1982, with their indices.
82
Usually carbuncles are associated with boils or abscesses caused by yellow staphy-
lococci and have an individual type of occurrence. The cutaneous type of anthrax may
develop into carbuncle-like forms, but will be closely associated with a few occupations
using wool or hides where workers with abrasions on their hand will be exposed to
infection by the cutaneous route. Carbuncles with this background are for obvious
reasons unlikely to appear in epidemic form or to assume the character of a usual clini-
cal feature. See also below: 556–8.
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332 chapter nine
British chroniclers and other contemporary observers and commen-

tators provide little clinical detail on the Black Death, however, when
they do, it is consistently compatible with bubonic plague. The most
informative chronicler is the Irish friar John Clyn of the monastery of
Kilkenny:
[…] many died of boils and abscesses, and pustules on their shins [= legs]
and under their armpits; others frantic with pain in their head, and
others spitting blood […].83
As can be seen, John Clyn refers to buboes (boils), and specifies the
characteristic and usual locations on the legs and under the armpits.
However, the friar is perhaps shy when it comes to identifying the sex-
ually sensitive area of the groin and the nearby femoral area, but feels
free to specify the location in the armpits. The excruciating headache
which tends to drive people out of their minds is also a characteristic
accompanying clinical feature of bubonic plague.84 John Clyn’s obser-
vation that some died spitting blood cannot be taken as evidence to the
effect that the Black Death was an epidemic of primary pneumonic
plague as asserted by Morris (see below). The strongly restricted refer-
ence to the occurrence of cases with bloody expectoration, i.e., the fact
that only some developed this feature, indicates clearly the normal pro-
portion of plague cases which develops secondary pneumonic plague
in epidemics of bubonic plague. The friar also mentions abscesses and
carbuncles,85 and he mentions pustules which are quite a usual cutane-
ous manifestation.86 This account contains, then, a good description
(for the time) of an epidemic of bubonic plague, and is thus a good
source on the medical and epidemiological character of the Black
Death in England.
Other accounts and descriptions are compatible with John Clyn’s but
contain fewer details. Galfrid le Baker states, for instance:
Swellings suddenly breaking out in various parts of the body, racked the
sick. So hard and dry were they that, when cut, scarcely any fluid matter
83
Hirst 1953: 13.
84
Simpson 1905: 263; Chun 1936a: 310; Pollitzer 1954: 411; Butler 1983: 73;
Benedictow 2002: 208, where two cases in the epidemic in Bergen of 1565–6 are
described in Absalon Pederssøn’s diary: “A man was ill with pestilence, he raged, he
stood up in his rage and ran to L. Lundegaard where he drowned himself.” A clergyman
of one of the Hanseatic congregations in Bergen died in the plague “and raged some-
what in his head in his illness.” My translations from contemporary Norwegian.
85
86
Pollitzer 1954: 427. See below: 557.
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came from them. From this form of the plague many, through the cutting
[incision?], after much suffering, recovered. Others had small black pus-
tules distributed over the whole skin of the body, from which very few,
and indeed hardly anyone, regained life and strength.87
Le Baker mentions buboes without localization and says that they were
incised, and that many of those who underwent this treatment sur-
vived, an indication that he has his information from a barber-surgeon
or perhaps physician who apparently added some self-serving com-
ments on the efficacy of this treatment. On the other hand, the asser-
tion that buboes hardly contained any fluid appears to be incorrect and
is inconsistent with other contemporary and later accounts.88 He men-
tions also that some of those diseased from plague developed wide-
spread dark pustules, a clinical feature which is associated with
septicaemic developments and are observed also in modern observa-
tions of plague cases and discussed at length below.89
Standard works on English plague history like Creighton 1891 and
Shrewsbury 1971 must for various reasons be used with caution but
can provide additional interesting concrete clinical detail. Valuable
information is also provided in Slack 1985 and in Bell 1951 who gives
detailed and informative material for the London epidemic of 1665.90
Johan van Beverwijk, the Dutch physician, described plague as
“manifestation of buboes” (“manifestatie van bubonen”), and Jacobus
Viverius noted that buboes appeared on the neck, in the armpits and
in the groin, mentions carbuncles and that buboes suppurate (if not
incised).91 W. Swinnas, another physician, considers “pest-buylen, Pest-
koolen en peperkoorens,” i.e., buboes, carbuncles and dark-coloured
spots in the skin called peppercorns (caused by haemorrhages) as
“convincing” indications of plague, but mentions also headache and
other secondary accompanying clinical features as indicative.92
Although there is considerable variation in the clinical panorama of
bubonic plague, contemporary observers of historical plague epidem-
ics nonetheless focus on certain features, first of all on buboes and the
87
Cited after Gasquet 1908: 136.
88
Chun 1936: 316. Cohn 2002: 60, cites the account of Michael of Piazza (Michele
da Piazza) to the effect that buboes “filled with a putrid liquid,” but this must be a mis-
translation. Nohl 1961: 9; Sticker 1908: 49.
89
Below: 370, 372–8.
90
Bell 1951: 126–7.
91
Noordegraaf and Valk 1996: 25–6.
92
Dijkstra 1931: 13–7.
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334 chapter nine
great sharp pain associated with them,93 but also on carbuncles, sudden
onset of high fever, early appearance of splitting headache, purple or
black spots, pustules, and spitting of blood. All of these clinical features
noted by contemporary observers are also mentioned by modern spe-
cialists on plague on the basis of vast numbers of medical observations
in India, China, Madagascar, and elsewhere, and are described in all
standard medical works on bubonic plague.94 I cannot see that further
amassing of evidence would be of any additional use in disproving the
alternative theories about the plague: this evidence is to be found eve-
rywhere in serious scholarly work on historical plague epidemics.
Scott and Duncan: The Problem of Buboes
Scott and Duncan follow the second of the approaches mentioned

above in their attempt to reject the conclusion that buboes are a defin-
ing feature of bubonic plague, that is, they claim that buboes are a char-
acteristic clinical feature of at least one other disease. However, they do
this in a special way that deserves closer attention. They do not at the
beginning of their monograph present filoviridal contagion and the
Ebola and Marburg forms of disease caused by this pathogen and its
variants in order to test the historical material against this epidemio-
logical and clinical presentation. Instead, and at variance with normal
scholarly practice, Scott and Duncan (like Cohn) start their mono-
graph by asserting their thesis and conclusion to be true, that historical
plague epidemics were not bubonic plague but rather haemorrhagic
disease, or “haemorrhagic plague” as they arbitrarily go on to call it,
and that this was some type of Ebola or Marburg filoviridal disease.95
In consequence, they pretend that they can legitimately conclude that
any characteristic feature of historical plague epidemics must be reflec-
tions or manifestations of their phantom haemorrhagic disease. When
historical sources state that persons diseased with plague presented
with buboes, this simply proves that the normal occurrence of buboes
is a characteristic feature of “haemorrhagic plague” (see below). When
contemporary physicians or barber-surgeons incised mature buboes,
this proves that such simple surgery was a suitable treatment for
93
Below: M346–54.
94
See, for instance, Pollitzer 1954: 411–40; Chun 1936: 309–17.
95
Scott and Duncan 2001: 1, 7–10.
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haemorrhagic buboes.96 When historical plague epidemics show strong

seasonality with a very pronounced prevalence for the warmer periods
of the year, this proves that this feature is characteristic of haemor-
rhagic filoviridal disease.97 When the duration of the disease is three to
five days, this proves that this is the duration of the course of illness of
haemorrhaghic plague,98 and so on. Clearly this is an instance of the
fallacy of methodology called circular inference, and these examples
show that it is an integral part of the construction of Scott and Duncan’s
alternative theory.
Thus, in the view of Scott and Duncan the ordinary clinical occur-
rence of buboes does not prove that a disease is bubonic plague but
proves that buboes are a characteristic and defining feature of haemor-
rhagic plague.99 The two crucial parts or arguments in the following
citation are enumerated by me and will be commented on following the
citation with references to these numbers:
Indeed, apart from [1] the fact that the victims of both diseases pre-
sented with enlarged glands and subcutaneous swellings, it is difficult
to suggest a more unlikely candidate than Yersinia as the infectious agent
of haemorrhagic plague. [2] In the 1720s, 60 years after the disappear-
ance of the plague, London was swept by a series of epidemic fevers
which were characterised by buboes and carbuncles [Creighton, 1894100],
confirming that these clinical signs were not exclusively diagnostic of
bubonic plague.101
(1) The crucial assertion that buboes are an ordinary and characteris-
tic clinical feature of any or some form of Ebola or Marburg haemor-
rhagic disease is not given support in the form of reference(s) in the
text or in a footnote to studies providing such clinical evidence, not
here or anywhere else in the monograph, and this assertion is ipso
facto unfounded and arbitrary. When Scott and Duncan at the very end
of their monograph at long last finally provide some systematic, but
highly deficient clinical and epidemiological information on filoviridal
types of disease, their presentation does not contain a word about
96
97
Scott and Duncan 2001: 148, 152–4, 193, 252–3, 364–6.
98
Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1.
99
100
In 1894, the complete work of Creighton appeared, where the first volume is
a reprint of the edition of 1891 and the second volume completes Britain’s epidemic
history “to the present time.” See bibliography.
101
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336 chapter nine
buboes.102 They are completely unable to provide any support from pri-
mary medical studies on filoviridal diseases or standard works on
infectious diseases for the suggestion that any strain or variant of Ebola
or Marburg filoviridal contagion produces haemorrhagic disease which
presents with buboes. In fact, they are unable to document that any
bubo has ever been observed in any patient diseased by any known
(and therefore testable) form of filoviridal disease. The assertion in the
citation to this effect, which is at the heart of their alternative theory, is
arbitrary. This explains their choice of a methodologically fallacious
approach.
(2) The fact that Scott and Duncan are unable to adduce evidence to
the effect that buboes are associated with the clinical panorama of filo-
viridal diseases should, according to ordinary methodological consid-
erations, have settled the matter. Even if it were true that other diseases
presented with buboes, it would obviously not support the validity or
tenability of their specific alternative theory. Nonetheless, they assert
that other diseases do present with buboes and maintain that support
for this view is provided in the second volume of Creighton’s great work
on Britain’s epidemic history published in 1894 covering the period
from 1666 to “the Present Time,” which, they maintain, contains
descriptions of epidemic diseases in London in the 1720s “character-
ised by buboes and carbuncles.” No footnote with identification of page
is given. After having done my best to identify the textual source, I have
had to throw in the towel. In this volume, epidemic diseases in London
in the 1720s are discussed in a chapter called “The Epidemic Fevers of
1726–9: Evidence of Relapsing Fever.” In this chapter, the words buboes
or carbuncles are not mentioned.103 Relapsing fever is, of course, an
entirely different disease and the victims of this disease do not present
with buboes. Consequently, Creighton states nothing “confirming that
these clinical signs were not exclusively diagnostic of bubonic plague.”
This claim is taken out of thin air in order to create a false argument in
support of their theory which reveals again the untenability and arbi-
trariness of their alternative theory.
The curious reader may here become an inquisitive reader and ask
pointedly why Scott and Duncan must make this important point
for the viability of their theory on the basis of purported historical
102
103
Creighton 1894–2: 66–74.
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evidence in a proto-scientific history of epidemic diseases based on

miasmatic theory, and why they do not base their view on modern
medical or historical studies of epidemic diseases. The answer can be
given on their behalf: no such studies can be found because there are
no such studies to be made because there are no such diseases; the epi-
demic occurrence of buboes is a unique and defining feature of bubonic
plague.
In the popularized version of their book published three years later,
they revert to the problem of buboes in a related way; again the crucial
points in the citation are enumerated by me and will be commented on
following the citation with references to these numbers:
The characteristic [1] (but not specific symptom) of bubonic plague is the
appearance of the bubo. [2] Once Yersin had announced his seminal
results, [3] it was realized that victims of haemorrhagic plague also some-
times presented with swollen lymph glands.104
These assertions are presented without any evidentiary support and, as
shown above, the reason is that there is no support for any of them.
(1) It has been documented above that bubonic plague is the only epi-
demic disease that presents with buboes as an ordinary clinical
feature, the reasons for this have also been given. Scott and
Duncan’s assertion that the bubo is not a “specific symptom”
remains unsubstantiated by evidence and is as such arbitrary.
(2) Yersin’s discovery of the plague bacillus in 1894 was published the
same year and contains nothing in support of Scott and Duncan’s
position (what do they mean by “announced”?). Filoviridal haem-
orrhagic disease was discovered in 1976,105 eighty-two years later,
and it is obviously not true that “once” Yersin had published his
discovery anything “was realized” about the clinical manifesta-
tions of cases of filoviridal disease.
(3) Consequently, it cannot be true that it was recognized in 1894 or
for eighty-two years to come that “haemorrhagic plague” “also
sometimes presented with swollen lymph glands.” In the research
literature published in the three decades following the discovery
of Filoviridae not a single patient has been recorded who has
104
105
www.who.int/inf-fs/en/fact103.html 2003: 2; Manson’s Tropical Diseases 1996:
653.
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338 chapter nine
presented with a bubo or “swollen lymph glands.” This is the rea-

son Scott and Duncan are unable to present a single case in sup-
port of their assertion, despite the fact that most infectious diseases
may occasionally infect by the cutaneous route, be drained to a
lymph node and cause the development of a bubo. The three asser-
tions constituting the passage are all spurious. Throughout their
monographs, Scott and Duncan presume identity between the
incidence of buboes in cases of bubonic plague and in “haemor-
rhagic plague.” The present formulation “sometimes presented
with swollen lymph glands” approaches a notion of episodic or
individual occurrence, although as emphasized above, they are
unable to supply a reference to a single victim of filoviridal disease
who has, in fact, presented with a bubo, so this formulation is also
unfounded. But in any case, episodic or individual occurrence
would not have epidemiological significance for the present dis-
cussion, since the point is that bubonic plague is the only epidemic
disease that presents with buboes as an ordinary feature of the
clinical panorama and this feature is therefore a defining feature of
bubonic plague. For these reasons, the unnamed scholars implied
in the formulation “it was realized” are fictitious, they do not exist,
and this is the reason Scott and Duncan are unable to substantiate
their assertions to this effect in their monograph of 2001 or in the
popularized version of 2004.
Since Scott and Duncan proclaim at the opening of their monograph
that their alternative of haemorrhagic filoviridal disease is the “truth”
about the microbiological nature of historical plague, which entails as a
logical consequent the flat rejection of bubonic plague as an alternative
possibility, they can pretend that they do not need much information
on bubonic plague. They can therefore pretend that it is adequate to
rely on a chapter in a general textbook of infectious diseases by A.B.
Christie for their information on bubonic plague, a chapter consisting
of twenty-four pages of which only three pages relate directly to clinical
and medical features of human plague.106 Intriguingly, all through their
monograph Scott and Duncan consistently refer to the first edition
(1969) of this textbook which in fact does not contain a chapter on
plague. A chapter on bubonic plague does not appear until the third
edition of 1980, which attests to the author’s peripheral interest in
106
Christie 1980: 760–2. See also below: 621–8.
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bubonic plague, which according to ordinary principles of scholarly

work should be very much in focus in Scott and Duncan’s monograph.
Unsurprisingly, Christie’s account of plague has many unsatisfactory
aspects (see below) and provides a clinical description of bubonic
plague of uneven quality, though it does also contain valuable informa-
tion. Scott and Duncan cite Christie’s concluding clinical statement in
this extraordinary way:
Most importantly for our purposes, he [Christie: my insertion] contin-
ued, “The picture is non-specific: it might be any severe septicaemic illness,
or typhus, typhoid, malaria and the like [our italics]. The only distinguish-
ing feature is the bubo.”107
Astonishingly Scott and Duncan cite this statement under the assump-
tion that they can “legitimately” focus solely on the initial words in
Christie’s statement, that the “picture is non-specific,” emphasizing this
point with italics, and can infer that Christie asserts that bubonic plague
has no defining feature. This is what they consider “Most importantly
for our purposes.” This is clearly not compatible with the last sentence
of Christie’s statement where it is unequivocally stated that bubonic
plague has, in fact, one distinguishing feature, namely “the bubo,” a
crucial statement that should have been emphasized by bold type but is
left also without italics and is completely ignored. A distinguishing fea-
ture sets a phenomenon apart from all other phenomena and consti-
tutes a defining feature; for this reason the terms “distinguishing
feature” and “defining feature” are synonymous. Consequently, even
Scott and Duncan’s brief and peripheral source of modern medical
information on bubonic plague in Christie’s general textbook makes it
clear that description of buboes as an ordinary clinical feature of dis-
eased persons in an historical plague epidemic constitutes a sufficient
condition for the identification of the disease as bubonic plague. It pro-
vides also a sufficient explanation of why Scott and Duncan do not
present a model of filoviridal diseases at the beginning of their mono-
graph which would enable readers to perform continuously a critical
comparative analysis. Comparison of the clinical panorama of known
diseases with the clinical panorama of historical plague is the crucial
methodological approach for resolving the problem of the identity of
107
Scott and Duncan 2001: 68. Scott and Duncan do not provide footnotes, how-
ever, information on buboes is given in Christie 1980: 761–2. Scott and Duncan’s
italics.
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340 chapter nine
historical plague. Their failure to present (sufficient) material premises

for performing a valid comparison means that readers cannot perform
ordinary critical functions and will tend to become helpless victims of
their arguments. This is the reason why when a presentation of filo-
viridal diseases can no longer be postponed and at long last appears at
the end of their monograph in an unsatisfactory brief and cursory
form, it does not contain a word about buboes. In the end, reality can
no longer be evaded: they have invented a phantom disease.
Cohn: The Problem of Buboes
In the very first sentence of his monograph, Cohn states unreservedly

that “The Black Death in Europe, 1347–52, and its successive strikes to
the eighteenth century was any disease other than the rat-based bubonic
plague.” At the end of his monograph he lamely admits that he has no
idea what disease it could have been, except that it must have been a
viral disease that since has disappeared, which means that he ends arbi-
trarily with an untestable hypothesis (see below). Cohn’s approach
to the problem that epidemic occurrence of buboes represents to his
alternative theory is very different from Scott’s and Duncan’s: he prima-
rily seeks support in the writings of contemporary chroniclers and
physicians. He does not deny that contemporary accounts and descrip-
tions of plague disease often mention buboes as an ordinary clinical
manifestation. The pivotal point of his line of argument is that contem-
poraries provide descriptions of the localizations of buboes and the
wider clinical panorama of the disease which differ so greatly from
those of modern medical studies and textbooks that they would have to
be two different diseases. This paves the way for his own alternative
theory, a viral disease spread by cross-infection which since has disap-
peared and cannot therefore be tested.
At the heart of this line of argument, as so often in Cohn’s work,
is the notion or assertion that chroniclers and especially contempo-
rary physicians provide epidemiological, medical or clinical evidence
that was obtained by basically rational, systematic and quite scientific
observation. According to his view, this evidence is therefore suitable
as hard evidence for statistical inference, comparison with modern
medical data, and other forms of generalizing at a high or substantial
level of tenability, and as such forms the basis of strong arguments in
important or crucial matters. In a characteristic fashion, Cohn argues
seemingly effectively on the basis of the amassed evidence of chroniclers
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and physicians, but without actually presenting the material. Therefore,

his assertions must either be believed at his word, which is not some-
thing scholars usually demand from their readers, or must be rejected
as methodologically incomplete science: the point is that at the heart of
scholarly work are the concepts of testability and falsifiability, so that
scholars are obliged to present evidence in a way that makes its validity
and (level of) tenability readily testable and falsifiable.
Cohn maintains that he consulted “407 chroniclers, calendars and
‘necrologies’ covering the plague years from 1347 to 1450” and that
“I have been able to read in various libraries in Britain, France, and
Italy.”108 He is not so specific about the number of physicians’ plague
tracts that he maintains to have consulted but states that at least fifty-
five of these tracts provide information on the localization of buboes;109
in his Appendix III, he enters the titles of nearly a hundred “Plague
tracts cited from Sudhoff Archiv für Geschichte der Medizin,”110 which
presumably represent the majority of them.111 Thus, Cohn pretends
that it is an acceptable procedure of scholarly or scientific work to con-
front those of his readers who wish to perform the ordinary critical
obligation to test the material basis of his assertions with an ultimatum:
(1) that they either repeat his “work,” that they should travel to aca-
demic libraries in England, France, and Italy, in order to get access to
these works and spend great amounts of money and years of their pre-
cious scholarly lives just to test the material basis of his assertions or (2)
eat out of his hand. I will submit that this is not compatible with the
methodological requirements of scholarly or scientific work and that
his generalizing assertions on the supposed basis of chronicles or
plague tracts should also for this reason be rejected as invalid because
they have (so far) no practically testable evidentiary basis and there-
fore (so far) have a fundamentally arbitrary character. Cohn is not
averse to appendices, actually he has three of them in his monograph,
but he does not use this opportunity for presenting his primary mate-
rial, i.e. citations from chroniclers or plague tracts.112 According to the
108
Cohn 2002: 99.
109
Cohn 2002: 69.
110
Cohn 2002: 274–9, cf. 66–7. Cohn’s italics.
111
Cohn 2002: 66–7.
112
Actually, Cohn uses his Appendix I, “Miraculous Plague Cures,” to present mate-
rial according to sources, while the two other appendices are supplementary sections
of the bibliography. Appendix I demonstrates that Cohn is fully aware of the usefulness
of appendices for presenting material evidence in tabular form.
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342 chapter nine
basic methodological principles of scholarly or scientific work, no

scholar has the right to demand to be believed on his/her word, (s)he
has instead the right to try to persuade on the basis of the material evi-
dence which (s)he presents and the quality of source-criticism and the
general methodological framework of interpretation.
Cohn’s point of departure is his assertion that of the 407 chronicles,
calendars and necrologies, covering the period 1347–1450 which he
has consulted,
barely 16 per cent of them (68) identified the plague by pointing to
cutaneous signs—the bubo, gavòcciolo, biscica piena di veneno, apostem-
ata, macchie, rossorie, or even with just the adjectival phrase “pestis
inguinaria.”113
Since cutaneous manifestations other than buboes are included (mac-
chie and rossorie), the passage implies that even fewer works and a
smaller percentage actually mention buboes, which could be taken to
signify that this feature was not as important as usually assumed. This
impression is strengthened by his subsequent remark that the sixty-
eight chronicles which mention buboes include “double counting of
chroniclers.” Cohn asserts also that thirty-five of these chronicles are
Italian, that only three of forty-five English chroniclers refer to buboes
“or other skin disorders,” and that only nine of 117 German chronicles,
annals and calendars mention buboes, and so on.
This may resemble some sort of fact-finding on the basis of source-
criticism, but it is not. Central in this context is the question of what
chroniclers should be expected to mention according to their medieval
scholarly training, social status and cultural mindset. The inherent
methodological point has been demonstrated above. It was shown that
Cohn and other advocates of alternative theories commit the method-
ological fallacy called inference ex silentio when they infer from the
fact that chroniclers do not mention dead rats in connection with
plague epidemics that there were no rats around.114 In this case, Cohn
unquestioningly presumes that chroniclers should be expected to men-
tion buboes, and when only a small percentage does, he infers that
buboes cannot have been an ordinary or usual part of the clinical pano-
rama of the Black Death and subsequent plague epidemics. However, if
epidemics, including severe epidemics, were not among the subjects
113
Cohn 2002: 99.
114
See above: 85–91.
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that chroniclers, according to their prestigious classical models, con-

sidered important to record, it is, on the contrary, to be expected that
many chronicles would not mention the Black Death or subsequent
epidemics. And if they do not mention the Black Death, why should
they mention buboes? As now should be clear, Cohn’s unquestioning
assumption that chroniclers should be expected to mention (severe)
epidemics with concrete clinical detail involves again the fallacy of
methodology of inference ex silentio and makes him dependent on luck
not to be led into false conclusions. However, his luck fails him also in
this case.
It is known that the Roman Empire was swept by great waves of
severe epidemics, especially at the time of Emperor Marcus Aurelius
(161–80), Emperor Commodus (180–92), Emperors Valerianus (253–
60) and his son Gallienus (253–68) (with whom he co-ruled for some
years), and again under Emperor Diocletianus (284–305). Arguably, all
of these severe waves of epidemics could have been bubonic plague.
However, very little is known about them. Roman chroniclers generally
took little notice of epidemic disease, not only because epidemics were
common but importantly in this context because epidemics were not
considered an appropriate subject according to the humanistic ideals
of writing in which they were trained. Extraordinarily severe epidem-
ics could be briefly mentioned, but usually without any diagnostic or
epidemiological information that would allow identification of the
disease(s).115 These ideals associated with the writing of chronicles were
those taught in medieval schools with great authority and admiration
and moulded the intellectual framework within which educated medi-
eval people functioned.
However, from the end of the thirteenth century, these ideals were in
the process of being weakened in Northern Italy within the framework
of societal developments termed the Early Renaissance, a moderniza-
tion of culture and mind or mentality that apparently was arrested by
the onslaught of the Black Death and subsequent plague epidemics, but
was resumed around the mid-fifteenth century. At the cultural level,
this modernization was reflected in the increasing use of the vernacu-
lar instead of Latin by the educated classes, even in the case of such a
high-brow, high-social-status work as Dante’s La Divina Commedia
(1307–21). At the time of the Black Death Italian chroniclers usually
115
See for instance Gilliam 1961: 225–51; Russell 1958: 37; McNeill 1979: 112–3.
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344 chapter nine
wrote, like the Villani brothers, in the vernacular and this was also the
case with the novels written by the learned humanist Boccaccio, includ-
ing his novel Il Decamerone, a frame story set in Florentine environ-
ments at the time of the Black Death. There were also corresponding
pioneering developments of substance with respect to both literature
and chronicles (Giovanni Villani’s chronicle is truly remarkable for its
empirical orientation).
These developments had hardly started in many other parts of
Europe, and this is reflected both in the fact that most chronicles in
those regions were still written in Latin and also in the fact that many
chroniclers do not mention the Black Death at all. This is especially the
case with German and Dutch chroniclers, which makes it difficult to
produce even a general outline of the spread of the Black Death in these
countries. In fact, in the case of the Low Countries
the total lack of notices on the Black Death in chronicles and other
narrative sources is conspicuous. Despite the fact that these areas were
characterized by high standards of education and literacy for their time
[…] no source is produced with the objective of handing down informa-
tion on this exceptionally grisly event to posterity.
This central source-critical and historical point regarding the subjects
that chroniclers would like to include and which they would tend to
leave out whatever their significance has been made by several histori-
ans.116 This topic demonstrates again the fallacy of methodology inher-
ent in argumentum e silentio or inference from silence in the sources to
assumptions that a phenomenon did not occur or exist.
So far the discussion has focused on the conditions that would
affect the chances of whether or not chroniclers would mention the
Black Death at all. It is an obvious corollary that if chroniclers do not
mention the Black Death nothing will be said about buboes, but it is
also an obvious corollary that if the Black Death’s ravages of the cit-
ies or localities in which chroniclers lived tended to be a peripheral
subject for them, it is rather unlikely that a terse statement to the effect
that the Black Death ravaged the local population would be accompa-
nied by descriptions of clinical details like buboes. This historical con-
text explains why, according to Cohn, thirty-five, or slightly over half
of the chronicles in which buboes are mentioned are Italian. Even if
Cohn’s figures are reasonably correct, it must be emphasized that this
116
See my discussion in Benedictow 2004: 192–3 and fn. 9, 206–7, cf. 114–6.
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does not at all signify that buboes were not a usual feature of the
disease.
At the heart of the matter is also an implicit comparative perspec-
tive with important methodological implications which Cohn ignores:
if it was the case that chroniclers should be expected to comment on
epidemics with clinical detail, this view must have an empirical basis
documented by studies of contemporary chroniclers. Thus, Cohn is
obliged to demonstrate that he has found such a material in a specified
and testable manner. His readers are entitled to know the answers to
the following two questions: (1) what other type(s) of epidemic
disease(s) did chroniclers tend to mention and (2) for what other epi-
demic disease(s) did they provide clinical details? If these central ques-
tions cannot be answered positively with good empirical evidence, the
view will stand corroborated that, under the historical circumstances,
the Black Death is mentioned by surprisingly many chroniclers and
with surprisingly frequent additions of clinical detail.
Unfortunately, Cohn’s attitude to source-criticism is so deficient that
problems abound, especially since he uses his data for direct or implied
comparative statistical inferences. He neglects to ask a number of
important critical questions and clarify their implications.
(1) If the vast majority of chroniclers did not mention the Black
Death and buboes, around 90 per cent of them as it seems according to
Cohn’s figures, why does this not represent a serious problem of repre-
sentativeness? The inherent source-critical implication indicates that
the relatively small proportion of chroniclers who (against the odds)
actually mentioned the Black Death and buboes did so because they
were different persons socially, educationally, economically, culturally,
and so on, and different personalities from the great majority of chron-
iclers who did not mention the Black Death and buboes. In order to
make use of this material on chroniclers Cohn should have satisfied a
number of methodological demands for clarification of the problem of
representativeness, a problem that can be potentially resolved only by
source-critical means, i.e. individualized study of these chroniclers.
Since Cohn specifies the number of Italian chronicles that mention
“cutaneous signs” but not the number of Italian chronicles he con-
sulted, the same problem also looms large in this case. In short, he
must relate the number of chroniclers who mentions a certain phe-
nomenon to the total number of chroniclers, indirectly indicating also
the number and proportion that does not mention it. Since Cohn pur-
portedly sums up chronicles from all over Europe in order to produce
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346 chapter nine
his quasi-statistics on the matter, he must also methodologically clarify

on what grounds he can lump together Italian chroniclers with Ger-
man or English or Polish or Dalmatian chroniclers, demonstrating that
he satisfies the methodological condition that he lumps together only
similar chronicles, and not similar and dissimilar or like and unlike.
(2) How can Cohn attribute importance to the information given by
chroniclers and other literary sources on clinical manifestations of
plague when he does not ask the crucial question: What is the basis of
this information, how was this information obtained? Is it based on
observation? Is it based on statistically valid samples or numbers of
cases? Is it based on physical examination of a statistically valid sample
of the diseased? Or is it based on hearsay, rumours and flimsy impres-
sions? Did the chroniclers who mention specific clinical detail really
attempt to provide a realistic and medically satisfactory clinical descrip-
tion of plague disease as Cohn implies, or did they provide some
graphic detail in order to impress their readers according to the rhe-
torical classical tradition in which they had been educated? Cohn
relates that the chronicler Giovanni da Parma called the plague of 1371
an “illness of spots and glandular swellings” which seems trustworthy.
However, when he goes on to state that that he had observed with his
“own eyes” a peculiar difference between the effects of buboes that
formed on the right as opposed to the left side of the body, “claiming
that none survived with them on the right, whereas some, even if only
a few, recovered with them on the left,” it becomes clear that his state-
ments are not based on systematic observations of plague cases as he
maintains, but on rumours or hearsay, and that the assertion that he
has seen this with his own eyes is only classical rhetorical technique
applied for the purpose of literary dramatization.117 Conspicuously,
Giovanni da Parma freely makes clinical and medical assertions on the
basis of purported personal observation which to modern scholars are
obviously fictitious. This is not because he is a liar, but because, as dem-
onstrated above, medieval man had a much weaker empirical orienta-
tion and much weaker requirements for repeating assertions of fact
and because they liked to form their assertions and accounts according
to prestigious classical Greek and Roman models.118 When even a
chronicler who insists that he had seen clinical and medical facts with
117
Cohn 2002: 61.
118
See above: 78–84.
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his own eyes freely and unembarrassed presents fantasy data, why
should any other chronicler be trusted and taken at his word? This
illustrates the important point which also has been made above in other
connections that chroniclers are not trustworthy even when they claim
to have observed something with their own eyes. Chroniclers’ state-
ments must be generally and unrelentingly tested by source-critical
and empirical means in order to be usable and useful.
Thus, when Cohn points out that a few chroniclers mention only
buboes in the groin, “and no chronicler, not even the statistically
minded Florentines, ever suggested that the vast majority of plague
boils appeared there,” and that some chroniclers mention two locations
of buboes, namely in the groin and axillas, and others mention three
locations, including also the neck, and others do not mention any loca-
tions of buboes,119 why is this significant for any scholarly discussion of
the microbiological nature of the Black Death? The assumption that the
“vast majority” of buboes should have appeared in the groin, is as
shown above not based on the mass of evidence gathered in connection
with modern plague epidemics and provided in the standard medical
works on plague, where it is indicated that around or more usually
somewhat above half of the cases normally have inguinal-femoral loca-
tion of bubo(es). Cohn’s comparatively based assertion on this point is
therefore a misleading piece of quasi-statistics. It is also a misleading
piece of quasi-statistics because Cohn does not address the question of
the circumstances to which these statements refer. Were they based on
personal clinical inspection of plague cases? If they were, were they
based on a statistically tenable sample? Were they affected by the sexual
connotations of the groin and mostly based on what could be observed
in sexually less sensitive parts of the body? Were they based on hear-
say? And so on. Also the spectre of a fallacy of distribution looms large
over Cohn’s argument.
The assertion that the Florentines were generally “statistically
minded” is not supported by any evidence and is as such arbitrary.
Certainly this was the case with Giovanni Villani, but he died in the
Black Death and did not provide posterity with a word on the disaster
in Florence. Real statistical orientation can only be said to be weakly
discernable in a couple of other Florentine chroniclers, for instance
Giovanni di Pagnolo Morelli. Crucially, Cohn maintains without any
119
Cohn 2002: 65–6.
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348 chapter nine
justification that Florentine chroniclers should have been expected to

provide empirically based scientifically tenable statistics on the loca-
tion of buboes when he is completely unable to document that contem-
porary Florentines implemented a systematic medical examination of a
valid sample of plague cases in order to determine (inter alia?) the dis-
tribution and localization of buboes. Instead, the only significant infor-
mation that can be obtained from chroniclers is that contemporaries
noted according to various pieces of hearsay or incidental observation
that the single most conspicuous clinical feature of the disease was
buboes and that these buboes strongly tended to be localized in the
same parts of the body as buboes of bubonic plague.
Does Cohn possess the scholarly qualifications necessary to evaluate
evidence statistally and to make demographic analyses? Cohn main-
tains that “at least four chroniclers saw the first plague killing more
women than men”120 and assumes throughout his monograph that this
is tenable information. Next, he goes on to claim that for “the next
plague, however, several chroniclers saw the sex bias swing in the oppo-
site direction.” But what about all the other chroniclers, in both cases
the vast majority of them, who did not make such comments, do they
not count? Why? The assertions that the Black Death killed more
women than men or the other way around are demographic and statis-
tical in nature. How did these chroniclers observe or obtain tenable
demographic information of a statistical nature? How were their mate-
rials gathered or constituted? Were the chroniclers’ statements based
on anything of real substance, does they constitute real demographic
data? Were these materials representative and valid samples suitable
for forming statistical valid statements about reality? Or was it all just
flimsy impressions or hearsay affected by prejudice, preconceived
assumptions and superstition and without evidentiary or scholarly
value? If the scientific validity and tenability and representativeness of
their materials and the premises on which their assertions or state-
ments are made cannot be ascertained, how can it be possible to use
these opinions for a demographic purpose? Is it not in fact possible to
find four chroniclers who hold much the same opinion about any con-
temporary matter, even the most outrageous and fantastic nonsense?
According to the tenets of historical demography, Cohn’s approach is
invalid and his estimates on these matters are quasi-statistics. Maybe
120
Cohn 2002: 129.
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painstaking hard work on the individual chronicles with intensive

application of source-criticism might provide tenable material, but this
work has not been performed by Cohn. He has no real material basis
for his assertions and his demographic qualifications may be called
into question. It seems that Cohn’s ambition to present a revolutionary
theory of the nature of historical plague forced him into variance with
the tenets of the methodology of historical and social science.
All of Cohn’s premises and arguments are arbitrarily chosen and are
presented in a way so as to produce the resemblances of statistical evi-
dence. As mentioned above, in English historiography the term “bas-
tard feudalism” is used to mean what resembles feudalism but is not,
for instance, enlistment in royal armies of gentlemen warriors for
longer periods of service than the forty days associated with feudal
obligations. In this sense, Cohn’s various estimates are bastard statis-
tics: they resemble statistics but are not. And this is only the beginning
of bastard statistics in this context.
Attempting to pave the ground for more seemingly supporting
quasi-statistics, Cohn goes on to argue that the plague tracts of con-
temporary physicians are more useful than the chronicles, because
(footnote in brackets)
(1) these fourteenth- and early fifteenth-century plague tracts turned on
practical experience of treating plague patients. [fn. 77] [.…]
(2) Doctors, by contrast [to chroniclers: my insertion], because of their
attempts to cure the plague by addressing its surface manifestations,
focused consistently on these cutaneous signs.121
Cohn indicates the relevant period for his material by the formulation
“fourteenth- and early fifteenth-century,” which I will take to mean the
early plague period 1347–c. 1410 or about the first sixty-five years of it.
Cohn provides a supporting footnote only for the first of these crucial
but also surprising two assertions, so the second assertion may imme-
diately be judged arbitrary. In support of the first assertion, he refers in
the accompanying footnote 77 to a single brief paper and states: “For
this impression, see Andreina Zitelli and Richard J. Palmer, ‘Le teorie
mediche sulla peste e il contesto veneziano’ [= The Medical Theory of
Plague and the Venetian Context], Venezia e la peste 1348–1797 (Venice,
1979), pp. 21–8, esp. 24.” Recognizing uneasily that this reference could
appear suspiciously tiny and unimpressive for the evidentiary demands
121
Cohn 2002: 68.
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350 chapter nine
put on it and that some of his readers might be puzzled and ask why
he does not refer to the central standard works on Italian medical his-
tory, he adds: “For these doctors’ emphasis on practical experience,
see chapter 9.”122 This means that these two references must be com-
mented on.
Anyone familiar with Italian and contemporary medical history will
immediately recognize that this tiny paper by the outstanding scholars
Zitelli and Palmer, a 6.5-page summary of medical history 1348–1631,
i.e. almost three centuries, contains nothing that would faintly corrob-
orate Cohn’s assertion. On pages 21–4 the two scholars summarily but
excellently present the miasmatic theory of epidemic disease in which
physicians of the time generally believed and which they generally used
to explain epidemic disease, and specifically plague, from the advent of
the Black Death to the end of the fifteenth century. The key words,
opening a new theme on page 24, are “A partire dal tardo secolo xv” =
“From the end of the fifteenth century,” there were some new develop-
ments inspired by the “humanistic intention of returning to the pure
sources of classical knowledge,”123 reflecting the development of the
culture and mentality of the Renaissance. In this context, two impor-
tant late medieval physicians are mentioned, first Marsilio Ficino whose
plague tract Consilio contra la pestilenzia from c. 1480124 reflected the
“spirit of the Renaissance” and contains a discernable increased ele-
ment of empirical observation,125 and Alessandro Benedetti who pub-
lished a plague tract in 1493 titled De observatione in pestilentia.
However, these pioneering physicians represented only the start of a
long-term slowly developing trend towards more empirical observa-
tion of epidemic disease throughout the Renaissance and the Early
Modern Period. According to Zitelli and Palmer, Benedetti asserted
that plague was introduced through the skin, since persons diseased
with scab were immune, a view which is certainly not based on empiri-
cal observation. The remaining 2.5 pages of their paper relate to this
long line of development through the sixteenth century with a clear
emphasis on the second half of the century and the decades up to the
city’s last plague epidemic of 1630–1. It has long been recognized that
122
Cohn 2002: 68, fn. 77.
123
My translation from Italian.
124
According to Zitelli and Palmer it was written 1478; according to the editor of
this plague tract, it was written c. 1480, see Ficino 1983: 6.
125
Cf. above: 209, 343.
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the Renaissance from the end of the fifteenth century brought an

increasing tendency towards empirical orientation based on real obser-
vation, as has been repeatedly stated also in this monograph, but this is
not the issue here. Instead, it is Cohn’s assertion that Zitelli’s and
Palmer’s paper supports his view that physicians contemporary with
the Black Death and subsequent plague epidemics examined their
patients physically in order to cure them: this assertion has now been
shown not to be correct, which means that the assertion is unfounded
and spurious.
In Chapter 9, Cohn is not able to present empirical support for his
two assertions. He maintains that
Perhaps the most incisive and detailed of such attempts to understand
the rise of plague in human terms was that of the Gatari chroniclers of
Padua for the plague of 1405. Their reasoning is closer to the nineteenth-
century understanding of crowd diseases than it is to the Black Death
mindset of floods of frogs.126
It is interesting to note the way Cohn now disparages the medieval
mindset—the very mindset of the chroniclers and physicians whom he
held in such high esteem when the subject was buboes 175 pages earlier
(see above). However, Cohn’s subsequent lengthy citation of the text
does not confirm his view as to the increased empirical orientation
and scientific epidemiological understanding of epidemic disease.
The Gatari chroniclers underline the importance of the overcrowding
in Padua caused by the on-going war which made the peasantry of
the surrounding rural districts flee into the city with their domestic
animals. This caused extreme overcrowding and unhygienic condi-
tions, and meant that many of the domestic animals died and began
decomposing:
Manure and mud beyond measure filled the city outside as well as within
houses, and the stench was so great that it putrefied the air, corrupting
the entire city. And there was a dearth of basic necessities beyond meas-
ure, […]. And these conditions combined with other forces of darkness
sparked a ferocious plague in the city of Padua with little nuts forming on
some around the throat, on others, on the arms, and on some, on the
thighs, along with an intolerable and burning fever with discharges of
blood. With this illness the victims lived two or three days at the most
and died.127
126
Cohn 2002: 230.
127
Cohn 2002: 230.
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352 chapter nine
Clearly, the Gatari chroniclers interpret events according to the ordi-

nary miasmatic theory of plague and are in this respect representa-
tive of chroniclers and physicians of the late medieval period up to the
end of the fifteenth century. Their description of buboes and plague
disease is quite inaccurate and does not reveal any personally acquired
clinical knowledge, as was the case with some other chroniclers who
commented on the Black Death and the following plague epidemics
for almost 150 years. Parts of this clinical description of bubonic
plague cases are compatible with inaccurate, flimsy or casual observa-
tion of diseased reaching the writers’ ears in the form of rumours or
hearsay.
Next, Cohn mentions Marsilio Ficino’s plague tract,128 written around
1480, which for temporal reasons has no relevance for his two asser-
tions that are under discussion here. Chapter 9 is the last chapter of
Cohn’s monograph and is oriented towards concluding and synthetic
inferences; it is therefore permitted to wonder why new material that
relates to earlier chapters and discussions is introduced there.
It is a conspicuous feature of Cohn’s discussion of this topic that he
gives the impression that the history of Italian medicine has not been
written. Actually, there are several fine monographs on this subject. We
must particularly emphasize G. Cosmacini’s fine history of medicine
and hygiene in Italy from the Black Death to 1918 which appeared in
1987.129 I. Naso has published a fine monograph on physicians and
sanitary structures in late medieval society in the Piedmont. Cohn
refers to two papers by A. Castiglioni (1874–1953), the leading Italian
medical historian of the first half of the twentieth century, but he has
avoided Castiglioni’s highly admired history of Italian medicine of
1927, so excellent that it was published in French in 1931 and in English
in 1941 and reprinted as late as 1975. Thus, Cohn consistently avoids
the fine standard works on Italian medical history which summarize
the endeavours of generations of Italian scholars in the field. The rea-
son, perhaps, is that they are incompatible with his assertions on this
subject and provide collectively a broad and solid basis for rejecting
them.
This puts in perspective another of the misleading accusations that
Cohn levels against Cipolla:
128
Cohn 2002: 231.
129
I was lucky and acquired a copy of the sixth edition in Milan in 1994.
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Others such as Carlo Cipolla in glancing at them [the plague tracts] have
judged that it was not until the seventeenth century that doctors would
tear themselves free from the “scientia” of ancient authorities.130
In fact, Cipolla, the Grand Old Man of Italian historical plague research,
did not take this subject lightly with a quick glance at these sources;
it was consistently a central topic in his numerous books. Let me
mention Cristofano and the Plague. A Study in the History of Public
Health in the Age of Galileo (1973), Public Health and the Medical
Profession in the Renaissance (1976a), Faith, Reason, and the Plague in
Seventeenth-Century Tuscany (1979), Fighting the Plague in Seventeenth-
Century Italy (1981), Contro un nemico invisibile. Epidemie e strutture
sanitarie nell’Italia del Rinascimento (= Against an Invisible Enemy.
Epidemics and Sanitary Structures in Renaissance Italy) (1986), and
finally Miasmas and Disease. Public Health and the Environment in the
Pre-industrial Age (1992) containing chapters titled “The Health Boards
in Italy and Epidemiological Concepts” (pp. 1–9), “Medical Reports
and the Florentine Health Magistrates” (pp. 27–65), and “Doctors,
Diseases and the People” (pp. 66–73). Cipolla has formed his opinions
on the matter on a truly extraordinary broad basis of his own research
and also on other available research and the standard works of
Italian medical history. It will easily be seen that Cipolla’s studies of
these subjects are in accordance with those of the standard Italian
works on medical history which Cohn has avoided. It is Cohn’s view
that deviates sharply from the established scholarly knowledge on the
subject. His disparaging comments on the works of Cipolla and other
fine historians all the way through his monograph131 should be seen
with this background.
Elsewhere in his monograph, when Cohn focuses on other subjects,
material contrary to his theory with clear power of falsification slips
through. We are informed, for example, that
The famous doctor Giovanni da Santa Sofia, professor of medicine at the
University of Padua, advised that a plaster of pig fat be applied to the
larger plague boils but a plaster made from pigeon dung (de stercore
columbino) be put on the smaller anthrax and carbuncles because of their
more “vehement heat.”132
130
Cohn 2002: 234.
131
See above: 54–69, in the case of Cipolla, see 60–1, 211, 226, 293–4, 352–3.
132
Cohn 2002: 62.
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354 chapter nine
Obviously, Giovanni da Santa Sofia (†1389), who was a professor of

medicine at the University of Padua, freely makes medical assertions
which are flatly untrue and simply fictitious, not because he is a fraud,
but because, as demonstrated above, medieval man had a much weaker
empirical orientation and much weaker requirements for repeating
assertions on reality or fact.133 Although Professor Giovanni da Santa
Sofia was a prestigious medical figure of his time, here is not a trace of
the empirical orientation which Cohn attributes to physicians of that
period.
Since Cohn’s assertion with respect to the increased empirical orien-
tation of contemporary physicians of the second half of the fourteenth
century and early fifteenth century has now been analyzed and shown
to be untenable, the original discussion of the contemporary material
on buboes can again be addressed. It now appears reasonable to assume
that Cohn’s two assertions to the effect that physicians’ plague tracts
show significant or substantial empirical orientation in the aftermath
of the Black Death were formulated to serve as the basis of more bas-
tard statistics on buboes. The following citation illustrates this point
(I place Cohn’s footnote in brackets):
The positions of the buboes pinpointed in these texts [physicians’ plague
tracts] are at variance with those give by the chroniclers. Only one plague
tract, and that one not by a doctor but by a German schoolteacher,
located the plague boils in a single bodily spot. Furthermore, it was in the
armpit, as opposed to the most usual place with modern plague, the
groin.[fn. 80134] Even more curious, the pairing of boils in the groin and
under the armpits, which the chronicles to some extent and modern his-
torians more often have seen as the late-medieval plague’s unmistakable
signs, is almost wholly missing from the tracts.135
This citation should be seen in the source-critical light of Cohn’s admis-
sion three pages later that “the plague texts rarely described individual
patients with the exact locations of their boil or boils” and that they are
“generally prescriptive rather than descriptive.”136 In the cited text,
Cohn sees his case served by not addressing the question of whether
the purported high incidence of more than one bubo reflects the fact
that physicians “rarely” described individual cases but “generally” made
133
See above: M50–4.
134
“Konrad von Megenberg, ‘Tractatus de mortalitate in Alamannina [sic],’ in Sabina
Krüger, ‘Krise der Zeit als Ursache der Pest?,’ p. 865.”
135
Cohn 2002: 68.
136
Cohn 2002: 71.
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prescriptive or generalizing comments on the locations of buboes,

which would strongly tend to imply plurality. In the final sentence,
Cohn asserts that some chroniclers and modern historians, in contrast
to contemporary physicians, quite often have seen the pairing of buboes
in the groin area or under the armpits as “the late medieval plague’s
unmistakeable signs.” But this assertion is unaccompanied by a sup-
porting footnote, which means that it is arbitrary and fictitious. One
would have liked to know which chroniclers and which modern histo-
rians held or hold this view. Until tenable facts are presented in sup-
port, these are all bastard statistics.
As can be seen from Cohn’s footnote, the only contemporary scholar
identified by name in support of this citation in Cohn’s footnote 80 is
Konrad von Megenberg who was not a physician but a natural scientist,
best known for his Book of Nature. Surprisingly, Cohn calls him a
schoolteacher, although he earned a Master degree at the University of
Paris, lectured at the university for a number of years and died as a
canon of the Cathedral of Regensburg. According to the principles of
the methodology of social science, the works of just one natural scien-
tist cannot provide empirically tenable insights or knowledge about the
scholarly attitudes of contemporary physicians. The works of a natural
scientist, including just one book, could function as a basis for estab-
lishing a working hypothesis about the attitudes or works of contempo-
rary physicians, which, according to the methodological principles of
scholarly work, should lead to an active search among physicians’ med-
ical writings for confirmation.
Konrad von Megenberg did produce two small plague-related works:
in 1349 he wrote Causa terre motus on the association between earth-
quakes, which let out miasmatic poisonous gases from the ground, and
plague epidemics, which, according to his profound religious views,
had God’s anger over men’s sinfulness as their final cause, the causa
remota. It does not contain traces of empirical attitudes or approaches
but represents a combination of intense personal religiousness with
speculative scholastic reasoning which was so typical of scholars at the
time. Later he wrote Tractatus de mortalitate in Alemannia (= Tract on
mortality in Germany). Cohn cites a paper by S. Krüger for support of
his claims about Megenberg’s medical and epidemiological views.
However, Krüger clearly argues that Megenberg’s views were exactly
the opposite of those Cohn ascribes to him: she shows how Megenberg
attempts to align the notions of God’s wrath as the cause of severe epi-
demic disease and the Black Death with miasmatic theory, arguing that
God used earthquakes to let out miasmatic poisonous gases from the
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356 chapter nine
ground into the human sphere. Krüger describes Megenberg’s views as

based on “simple, tradition-based, tradition-burdened/tradition-
loaded piety” which understood “the plague as God’s punishment.”137
Thus, Megenberg does not discuss plague in an empirically oriented
way, but as a pious scholastic. The idea that persons diseased from
plague should be physically examined is entirely alien to him, and there
is no indication that he ever did so, or that he ever thought that a statis-
tically valid sample should be studied in a scientifically valid way. This
is, consequently, also a fictitious reference. In short, the cited text con-
sists of bastard statistics.
Cohn goes on to mention that physicians in their plague tracts linked
the locations of buboes to “Galen’s three emunctoria” and that this was
the reason that buboes formed on the thighs or in the groin, in the axil-
las or on the neck (I indicate Cohn’s footnote in brackets):
Except for the two tracts mentioned above, every other one that pointed
to plague boils (at least 55 tracts) said they formed in these three zones.
[fn. 84] According to the position of the boils, the doctors would then
advise where to place their plasters and of what materials they should
be composed, and more often, which veins were to be tapped for
bloodletting.138
The supporting footnote 84 contains references to forty-three plague
tracts in Appendix III enumerated according to Sudhoff ’s enumeration
in his edition in Archiv für Geschichte der Medizin;139 in addition there
are references to three other works by named physicians. Thus, Cohn
provides forty-six references, not (at least) fifty-five, as should be
expected. Of the forty-three enumerated plague tracts, two refer to the
same work, namely nos. 27 and 28, which reduces the number of tracts
to forty-two. Of these forty-two plague tracts, two refer to numbers not
entered in Appendix III, which are therefore irrelevant;140 eight are,
according to the temporal information given by Cohn in the Appendix,
later than the early fifteenth century141 and are therefore also irrelevant
137
Krüger 1972: 839–83. My translation from German: “Seine einfache, traditions-
gebundene, traditionsbeladene Frömmigkeit deutet diese Entwicklung als schuldhaftes
Verhalten der Menschen, die Pest als Strafe Gottes.” In an appendix to this paper Krüger
publishes the full text of Tractatus de mortalitate in Alemannia, Krüger 1972: 862–3.
138
Cohn 2002: 69.
139
Vols. 4–9, 11, 14, 16, 1910–25.
140
Nos. 99, 111.
141
Nos. 26, 58, 75, 182, 192, 193, 265, 285.
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as support for the assertion under discussion; eleven are not dated142
and their relevance is therefore uncertain and as such they are not usa-
ble. Thus, over half of these references are invalid. Cohn also refers, as
mentioned, to three other works by physicians: Marsilio Ficino’s plague
tract of 1480, Antonio Guaineri’s rare Practica (Antonii Guainerii) from
1517,143 which is not a plague tract but a more general medical work;
and a work written in 1382 by Chalin de Vinario who worked as a phy-
sician at the papal court in Avignon.144 Thus, two of these three works
are anachronistic in relation to the topic under discussion and must be
grouped with the other eight works outside the temporal parameter of
the issue. Taken together, ten of Cohn’s references contain nothing on
physicians’ empirical practices and cures in the second half of the four-
teenth century or early fifteenth century, and thirteen other references
are invalid, so in all twenty-three out of forty-five, or over half, are
irrelevant or invalid. This means that only twenty-two methodologi-
cally valid references remain which shall cover for at least fifty-five
plague tracts; this is obviously fallacious and must be rejected.
Materially, Cohn’s readers are left to eat out of his hand, since the evi-
dentiary material is not gathered and presented for ready testability
(for instance in an appendix) as is the scholarly norm. This material is
for several obvious reasons flawed and unusable as the basis for valid
and tenable statistics.
However, it is not difficult to give Cohn a helping hand by provid-
ing the necessary additional information from Sudhoff ’s edition of
late medieval plague tracts: the two tracts with numbers not entered in
his Appendix, nos. 99 and 111, are temporally acceptable since they
appear to have originated at the beginning of the fifteenth century,
and among the eleven tracts without dating nos. 19, 27, 50, 61, 97,113
are temporally acceptable, while nos. 9, 49, 116, 117, 184 must be
rejected as anachronistic. This means that of the forty-five references145
thirty are formally relevant and fifteen are irrelevant and misleading.
Methodologically, it is a very serious matter that thirty references
142
Nos. 9, 19, 27, 28, 49, 61, 97, 113, 116, 117, 184.
143
Practica Antonii Guainerii Papiensis doctoris clarissimi et omnia opera. (Impressum
Venetijs: mandato and expensis nobilis viri Luceantonij de Giunta, 1517. die 13 mensis
Julij). As can be seen, it was published in Venice, not in Florence as Cohn claims.
144
Hoeniger 1882: 171.
145
42 plague tracts + 3 other works by the physicians Ficino, Guaineri, and de
Vinario = 45.
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358 chapter nine
should cover for at least fifty-five plague tracts that Cohn claims consti-
tute his evidential basis, and that fifteen plague tracts which are intro-
duced and mixed up among them are irrelevant and distort his
remaining relevant material. Inevitably, this undermines the validity of
his discussion or rather leaves it invalid for formal methodological and
material reasons.
I have read through the thirty relevant plague tracts; many of them
are quite brief. They do not provide any support for Cohn’s assertions
as to the clear empirical orientation of post-Black-Death physicians, on
the contrary, the established view in the history of medicine on this
matter stands vindicated. Cohn appears unwilling to recognize that the
condition for making valid and tenable assertions on this matter is to
present sufficient evidence from the plague tracts which can, taken
together, demonstrate that physicians at the time (c. 1347–1410) actu-
ally examined their patients bodies reasonably thoroughly and noted
down their findings in a sufficiently systematic way in order to be usa-
ble for producing (valid and) tenable statistics on clinical manifesta-
tions. On the contrary, physicians’ tracts provide hardly any evidence
of such empirical attitudes. This explains or accords with Cohn’s later
admission that “the plague texts rarely described individual patients
with the exact locations of their boil or boils” and that they are “gener-
ally prescriptive rather than descriptive.”146
On the contrary, the little evidence there is on such matters from
this period (c. 1347–1410) points rather in the opposite direction, as do
much later plague tracts. A plague tract written shortly before 1450
advises physicians who visit plague patients to stay at a good dis-
tance from patients and turn their faces towards the [open] door or the
window, an attitude that would of course exclude real physical exami-
nation of patients for identification of clinical features, but makes
good sense according to miasmatic reasoning. The author also states
that indications of a patient’s chance of survival can be obtained by
dripping breast milk in one’s own hair.147 This accords with Cohn’s cita-
tion of a chronicler elsewhere in his monograph to the effect that “no
one dared use or even touch the clothes of the plague-stricken” and his
statement that “Chroniclers of later plagues continued to see touching
the infected and their belongings as a sure means of catching the
146
Cohn 2002: 71.
147
Archiv für Geschichte der Medizin, 11, no. 117: 132, 135.
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plague.”148 This material makes it hard to understand how anyone would

dare to physically examine plague patients. For the same reason
Carmichael, a leading scholar on the medical plague history of the
period (although not according to Cohn’s disparaging remarks149),
concludes: “This kind of medical commentary, characteristic of late-
medieval plague treatises, was formulated with good Galenic univer-
salism. It is difficult to deduce physicians’ first-hand experience from
the information included.”150 This confirms that Cohn’s various statis-
tics are misleading bastard statistics without evidentiary power, but not
without power for misleading readers.
In my opinion, the preceding citation from Cohn’s text on the great
influence of the Galenic concept of “emunctoria” as a contemporary
medical explanation of the location of buboes can be read very differ-
ently from Cohn’s intentions. Cohn admits that, with only a couple of
exceptions, late medieval physicians state that in plague epidemics
buboes formed in these three areas of the human body, in the inguinal-
femoral area, in the axillas and on the neck.151 These are the same main
areas for the formation of plague buboes registered by modern physi-
cians.152 Thus, if the quasi-statistics and unrealistic claims for empirical
orientation at the time are dispensed with, contemporary evidence
provides in a general fashion support for the identity of historical and
modern plague.
Cohn and Boccaccio: Buboes, Pustules and Spots
Although chroniclers’ and physicians’ various writings seemingly con-

stitute the central evidence for Cohn’s argument on buboes and some
other clinical manifestations, he places great emphasis on the eviden-
tiary value of Boccaccio’s account of the Black Death in Florence in the
introduction to his amorous novel and frame story Il Decamerone,
written c. 1350.153 In order to claim that Boccaccio’s literary account
148
Cohn 2002: 113.
149
Above: 54–5, 84.
150
Carmichael 1998: 158. See below.
151
Cohn 2002: 69. The use of the term “late medieval” reflects the fact that most of
these plague tracts are from the fifteenth century.
152
153
According to the editor C.S. Singleton, nothing more precise can be said about
the date this work was written than that “a few years have elapsed” since the Black
Death. Boccaccio 1982–3: 804–5.
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has this value he must dispense with source-criticism (as he also does
with other types of sources): “Boccaccio’s description cannot be simply
dismissed as poetic license to heighten the plague’s horror,”154 he states.
This urging can be accepted, but The Decameron is, indisputably, a lit-
erary work, and thus the central source-critical point remains and gives
Cohn a task, namely to identify the author’s literary intentions and to
separate the literary functions of dramatization from the reality-
oriented parts. Instead, Cohn invites his readers to swallow Boccaccio’s
text hook, line and sinker (see below).
This point relating to the functions of literary technique and poet’s
license which Cohn should have addressed can be put more concretely.
Clearly, some of the frequently cited contemporary accounts and des-
criptions of the Black Death were quite likely not written by persons
who lived through the epidemic.155 Much like the young persons in
Boccaccio’s frame story these authors seem to have fled from its ravages
and returned after it had subsided; according to Matteo Villani, this was
quite a usual strategy employed by Florentines, at least by those who
had the means or opportunity to do so.156 There are, in fact, clear indica-
tions in Boccaccio’s text that this was also the case with him. Boccaccio’s
use of the narrator’s I-form, which provides the impression of personal
experience and observation and hence increases the credibility of what
is being told, is a usual literary technique for dramatization. Boccaccio
employs it not only in the introduction but also in connection with the
constituent stories, particularly in their openings. He insists, for
instance, that the disease spread as easily from plague cases to animals
as to other human beings, and with the same deadly effects. This claim
is highly suspect to put it mildly; what disease could that be?
A marvellous thing to hear is that which I have to tell and one which, had
it not been seen by many men’s eyes and by my own, I should scarcely
have dared credit, much less set down in writing, even though I had
heard it from one worthy of belief, I say, then, that of such virulence was
the pestilence […] a thing which had pertained to a man sick or dead of
the aforesaid sickness, being touched by an animal foreign to the human
species, not only infected this latter with the malady, but in a very brief
space of time killed it. Of this my own eyes […].157
154
Cohn 2002: 59.
155
This seems to be the case, for instance, with Michael of Piazza (see below).
156
Villani 1979: 297–8.
157
Boccaccio 1982–1: 9–10.
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Boccaccio’s ample use of the narrative I-form his references to

personal observations are conspicuous in the introduction to this
incredible story, but he also records some information from hearsay. Is
not deep scepticism of Boccaccio’s assertion that he has seen this with
his own eyes the correct scholarly attitude? Fortunately, Boccaccio
dramatizes this point by going on to give a concrete example, the
account of the two hogs which rooted with their snouts in rags of
clothes that had belonged to a pauper dead from plague, and almost
immediately “fell down dead upon the rags.”158 There is no disease pre-
senting with buboes in human beings, as described by Boccaccio, which
is hyper-dangerous to pigs; pigs are refractory both to plague and
tularaemia. Such a disease is unknown both to medical and veterinary
sciences, Boccaccio’s anecdote must be rejected as empirical evidence.
The overwhelming probability is that he relates in I-form an anecdote
which in fact is based on hearsay; as such it becomes evidence not of
reality but of his literary technique and medieval humanist mindset.
On the other hand, this anecdote is compatible with the miasmatic
theory of contagious disease which for quite some time now has been
out of fashion for extremely good reasons, but was fashionable in
Boccaccio’s time.
There are overwhelming reasons for considering this an anecdotal
story made up or repeated by Boccaccio and related in the I-form in
order to dramatize the introduction to his novel. It serves a literary
purpose and would be perfectly acceptable to his audience according to
their miasmatic epidemiological notions, but it should not be accepta-
ble to modern scholars. Boccaccio’s account of the Black Death in
Florence is compatible with conveyance of second-hand information
or hearsay on the disease and is moulded to serve his (legitimate) liter-
ary purpose of dramatization. Boccaccio must be understood on his
own terms. He was a humanist writer of his time and a pioneer of this
form of the art of literary entertainment, not a modern scientist, and he
had no intention of including a study of the Black Death with medical
information of scholarly value for posterity.
For these reasons, it is clearly fallacious when Cohn fails to fulfil the
scholarly imperative for adequate source-criticism and neglects to con-
sider elementary critical questions with regard to Boccaccio’s account:
Did Boccaccio recognize the importance of empirical observation?
158
Boccaccio 1982–1: 10.
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362 chapter nine
Did he have the methodological knowledge or understanding to carry

out observations of plague cases according to scholarly principles? Did
Boccaccio base his clinical description of plague cases on observation?
How can we know that he has seen plague cases at all and did not prac-
tise the strategy of his novel’s characters, i.e. that he did not flee the
city and avoid the plague by strict isolation from the surrounding
world? If he has seen plague patients, did he perform a physical exami-
nation? Did he perform physical examinations of a valid sample of
patients? If this can be shown to be the case, what was his frame of
medical reference for understanding what he observed? If he did not
base his description on personal observation, did he base it on observa-
tions made by others? If that was the case, who were those others and
how did they perform and pass on their observations?
As Cohn does not ask these basic source-critical questions, he does
not know that Boccaccio’s description is not based on rumours, hear-
say and a poet’s license for producing literary effects. In short, it is
Cohn’s scholarly task to prove that Boccaccio’s clinical description rep-
resents valid source material for modern historians. If he should suc-
ceed in making this point, it would be his task to clarify at what level of
tenability it would be usable and to identify and specify which parts are
usable as evidence. Only such identified valid and tenable parts of the
text will be usable for empirical comparison with modern medical
materials on the clinical manifestations of bubonic plague obtained by
scientific means. However, Cohn does not ask a single one of these
elementary and indispensable source-critical questions, which means
that his use of this account as hard evidence on the clinical panorama
of plague disease is fallacious for two independent reasons. Firstly, it is
fallacious to accept as hard evidence historical sources which have not
been source-critically scrutinized and had their potential evidentiary
value ascertained. Secondly, it is fallacious to use it for comparison
with modern medical clinical descriptions because he cannot demon-
strate or ascertain that the two sides of the comparison have similar
scientific and scholarly status, and are thus in pari materia, in other
words are comparable and as such valid and usable for the comparative
methodology of analysis.
Since chroniclers and physicians cannot be seen to have significant
or pronounced empirical orientation on the matter, and certainly were
too scared of being miasmatically contaminated by contact with the
diseased or their belongings, or even by look, to examine patients, why
on earth should Boccaccio, a literary artist, examine patients? In fact,
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Boccaccio asserts demonstratively for every scholarly supporter of

source-criticism to see that
this pestilence was the more virulent in that, by communication with
those who were sick thereof, it got hold upon the sound […] for not only
did converse and consortion with the sick give to the sound infection or
cause of common death, but the mere touching of the clothes or of what-
soever other thing had been touched or used by the sick appeared of itself
to communicate the malady to the toucher […].
Obviously, Cohn should have underlined this evidence and asked the
crucial question of how Boccaccio, holding these beliefs about the dan-
gers of talking with or touching persons diseased or dead from plague,
would have dared to approach such persons, to converse and consort
with them, and to touch their clothing and examine them physically.
Clearly, to take Boccaccio on his word is methodologically flawed
and fallacious but to dismiss his text, in the meaning of ignoring essen-
tial pathways to the understanding of it, can cause neglect of valua-
ble knowledge and also be reprehensible. It is the challenge of
source-critical scholars to sail their ships safely through the strait
between (the whirlpool of) Charybdis and the (sea-monster) Scylla
and like Odysseus put wax in the ears to avoid the Sirens’ lovely but
dangerous song of the revolutionary new theory.
This does not mean that Boccaccio’s informants could not have
picked up factual clinical elements and that his account cannot contain
valuable or tenable information, only that source-criticism will have to
be applied in quantum satis. Boccaccio states that
In men and women alike there appeared, at the beginning of the malady,
certain swellings, either on the groin or under the armpits, whereof some
waxed to the bigness of a common apple, others to the size of an egg,
some more and some less, and these the vulgar [ordinary people] named
plague-boils [gavocciolo].159
These pieces of clinical information are mostly credible and acceptable:
the early appearance of buboes corresponds to many other descrip-
tions of the initial phase of bubonic plague, and the locations are those
usual in bubonic plague, although the neck is left out. These basic ele-
ments are compatible with the disease being bubonic plague. Buboes
as large as apples or even bigger, if they existed, must be quite or even
159
Boccaccio 1982–1: 8–9. As for the vernacular term “gavòcciolo,” see also Sticker
1908: 84.
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364 chapter nine
very rare in bubonic plague, but this is legitimately explicable as liter-

ary exaggeration and also as a reflection of the sensational augmenting
tendencies of information transmitted by hearsay.
This prepares the ground for taking a closer look at Cohn’s con-
cluding assertions on the matter of buboes and other clinical
manifestations:
Boccaccio recorded buboes and then their spread along with black pus-
tules over the entire body. Nor was his description unique, or the Black
Death’s first appearance a radical departure from the “normal” signs of
the disease once it became established. Other contemporary texts—
chronicles, plague tracts, saints’ lives, and poetry—attest to the persist-
ence of these pustules’ spread […]. Further, the medieval plague boil was
neither singular, as in 94 per cent of the cases with modern plague, nor
located predominantly in the groin as happens with the flea-conveyed
modern plague. Instead, they often formed under the breasts, on the
shin, the face and even up the nose—places not mentioned in the 3000-
plus cases reported from hospitals around Bombay City during the plague
years 1896–7. Mostly, these late-medieval sores formed higher up the
body than those that characterise modern bubonic plague, in the cervical
region, higher than a flea can possibly jump. To keep the paradigm,
should we hypothesise that medieval men and women were more supine
than modern Indians or Glaswegians?160
The cutaneous signs of the two [late-medieval and modern plague] hardly
match in their positions on the body, number, or character. The Bombay
plague report at the end of the nineteenth century showed that in 94 per
cent of cases, the victims had only a single boil, that 57 per cent of them
were in the groin and in not a single case of over 3000 clinical studies did
the boils spread from the lymph nodes, bursting into tiny black, green,
and red pustules across the body. By contrast, for the medieval plague
two-thirds of the cases showed multiple boils; the neck, not the groin was
the boils’ pride of place, and one chronicler after another from Wales to
Novgorod, Sicily to Uzbekistan described the invasion of small pustules
preceding, accompanying, or following the formation of boils.
In place of Yersinia pestis I offer no alternatives […].161
Cohn has not furnished these numerous assertions with support-
ing footnotes that would allow evidential testing, which means they
are arbitrary according to the basic tenets of methodology. The only
160
Cohn 2002: 81.
161
Cohn 2002: 247.
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references are those given in the text to Boccacccio and to “The Bombay
plague report at the end of the nineteenth century,” a surprising refer-
ence to the report on plague in Mumbai of 1896–7, only one of several
reports on plague written at the end of the nineteenth century, a fact
that will be considered more closely below.162 The juxtaposition of these
two sets of information in a formal comparison of important clinical
manifestations of late medieval and modern plague is clearly fallacious.
The late medieval side of the comparison consists of pre-scientific types
of information which in not a single case can be shown to be based on
physical examination of a valid sample of plague cases and must
therefore be assumed to have an impressionistic and unsystematic
character, constituting on the whole quasi-empirical material. This
quasi-empirical material cannot be compared with a scientifically valid
sample of scientifically studied modern plague cases for the purpose of
demonstrating valid differences between the two clinical panoramas.
These two materials can only be legitimately juxtaposed for compara-
tive purposes in order to reveal the unscientific aspects of medieval
accounts or presentations of the matter.
For the same reason, the other juxtapositions of materials on the
distribution of buboes on the body are further instances of quasi-
statistics. Importantly, one should note that Cohn has not presented
the evidence for his statistical assertions as to the location of buboes
according to late medieval sources; his statistics have no empirical
basis, they are taken out thin air, which means that they are invalid and
untenable. His citation of Boccaccio does not corroborate or support
his assertion with respect to the distribution of buboes on the body. If
it was really the case that late medieval buboes formed more often on
the upper part of the body than in modern bubonic plague, why does
Boccaccio not mention buboes on the neck? At variance with normal
methodological considerations Cohn does not think that this has any
source-critical significance and does not affect the reliability of this
source.
On the contrary, Cohn goes on to cite Boccaccio’s account as the
very truth, his assertion that the original buboes “would begin to
spread, and within a short time would appear at random on every
part of the body” is taken as cast-iron scientifically acquired evi-
dence, although he is not able to cite any chronicler or physician who
162
Below: 371–4.
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366 chapter nine
has made a similar observation. Thus, in essence Cohn asserts that

Boccaccio’s account on this point overrides the significance of all
other medieval comments on the matter—but without affecting the
value or tenability of this evidence when that evidence is useful for his
argument. It now becomes clear why Cohn must reject or ignore the
fact that Boccaccio’s account was affected by literary intentions and
functions, since this could undermine his use of the dramatic account
of how buboes spread all over the body as hard evidence with crucial
significance. For the same reason, Cohn must refrain from asking the
obvious anatomical question: Can buboes really spread all over the
body, can buboes arise where there are not lymph nodes or glands? He
has also dropped his own argument that late medieval physicians with
only a couple of exceptions located buboes in relation to the Galenic
concept of emunctories163 which means that they would predominantly
form in relation to the inguinal-femoral area, the axillas and the neck.
However, it is not correct that in India buboes only arose in those
parts of the body, as Cohn asserts; there was also a significant incidence
of other locations. Choksy sums up the medical experience on this
point in India around 1900, using the term “gland” both for glands and
lymph nodes:164
Such glands may be situated in different parts of the body, the order of
frequency being the femoral, inguinal, and iliac165 glands, separately but
more often in continuation, the axillary, and the brachial166 chain with
epitrochlear,167 the cervical, parotid168 and submaxillary169 glands, and
but rarely also in other positions, such as the femoral chain, the pop-
liteal,170 in the calf, at the ankle, at the bend of the elbow, pre-auricular or
even occipital.171
Many of these locations of buboes are illustrated with photographs
from the Indian plague epidemics in Simpson 1905: 275–83, 285–6,
163
Above: 356, 359.
164
Choksy 1909: 352.
165
Iliac artery = each of the two arteries, right and left, into which the abdominal
aorta divides. The common iliac lymph nodes, four to six in number, are grouped be-
hind and on the sides of the common iliac artery, one or two being placed below the
bifurcation of the aorta.
166
Brachial = belonging to the arm.
167
Epitrochlear gland, situated just above the elbow.
168
Gland situated besides or near the ear, producing saliva.
169
Situated under the jaw.
170
Pertaining to the ham or the hollow at the back of the knee.
171
Belonging to or situated in or on the occiput or back of the head.
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which is a standard work Cohn refers to three times and must be

assumed to be acquainted with. True, nothing is said about an instance
of a bubo up the nose that Cohn refers to, but is this statement true?
Was the existence of this bubo ascertained by adequate anatomical
means? Which lymph node or gland is implied? Could this not reflect
an observation of a patient with septicaemia where bursting blood
vessels in the nose due to vascular damage by plague toxin had occa-
sioned epistaxis, “bleeding from the nose,” as observed also in modern
plague epidemics and described in the standard works of plague?172
Bleeding from the nose is repeatedly mentioned in the historical
sources, and why could it not lead to the notion with people who did
not perform anatomical dissection and analysis that this was caused by
a bubo in the nose? No doubt because it would put another critical
question mark on Cohn’s assertions about the empirical orientation of
late medieval physicians.
It now becomes clear why Cohn cannot exercise source-criticism
and ask the crucial question: How were the clinical elements of
Boccaccio’s account obtained, did he or anyone else examine plague
cases physically? If they did not, how would this affect the clinical opin-
ions that would come into circulation? Are there not very good reasons
for assuming that the very bashful or shy attitudes towards sexual
matters of these times would affect how often buboes in the groin
would be mentioned? If plague cases were not physically examined,
would not more easily observable buboes on the upper part of the
body, in the axillas, on the neck, and so on, be relatively more often
noted than buboes in the groin area, and would that not skew the rela-
tive incidence of the locations of buboes as mentioned in the writings
of the time? Thus, again the conclusion must be drawn that Cohn
argues his case on the basis of bastard statistics. The application of ele-
mentary source-criticism also reveals that Cohn’s sarcastic question
whether one should assume that medieval persons “were more supine
than modern Indians or Glaswegians” simply reflects his neglect of
source-criticism and the pervasive methodological weaknesses of his
discussion.
Cohn has not furnished these concluding and crucial extractions of
his text cited above with supporting footnotes. However, there are
clearly two clinical features at the centre of Cohn’s line of argument,
172
Simpson 1905: 265; Chun 1936: 313. Cf. Manson’s Tropical Diseases 1921: 268.
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368 chapter nine
namely the location and number of buboes, and the appearance of

pustules,
Boccaccio recorded buboes and then their spread along with black pus-
tules over the entire body […].
not a single case of over 3000 clinical studies [in the Bombay report of
1896–7] did the boils spread from the lymph nodes, bursting into tiny
black, green, and red pustules across the body […].173
Pustules appear to be the single most important criterion, since accord-
ing to Cohn, this type of clinical manifestation was unknown or unreg-
istered in studies of plague in India or elsewhere:
with no modern plague have black pustules spreading randomly all over
the body been reported […].174
For historical documentation he refers in identifiable and testable form
only to Boccaccio’s description of plague cases in Il Decamerone and he
adds in order to strengthen its significance:
“Boccaccio’s description cannot be simply dismissed as poetic license
to heighten the plague’s horror […].”175 However, this reference to pus-
tules can be revealed to be fictitious, even when compared with Cohn’s
own citation of Boccaccio’s text on this point176 twenty-two and 206
pages later:
From the two areas already mentioned [the groin and the armpit],
the aforementioned deadly gavòcciolo would begin to spread, and within
a short time would appear at random on every part of the body.
Afterwards, the illness would change with the appearance of black or
blue spots (macchie nere o livide) forming on their arms, thighs, and
other parts of the body, sometimes large and few in number, at other
times tiny and closely spaced.177
Clearly, nothing is said about pustules, only about (buboes and) darkly
coloured spots and, as shall be expanded on below, pustules and spots
are different categories of clinical manifestations. This shows that
Cohn’s assertion to the effect that Boccaccio emphasized the impor-
tance of black pustules as a clinical feature is spurious (and that he
173
Extracted from the citations above on page 364.
174
Cohn 2002: 59.
175
Cohn 2002: 59.
176
Cohn refers to an edition which I have not succeeded in getting hold of, namely
V. Branca, Boccaccio 1976: 10–1.
177
Cohn 2002: 58–9. Gavòcciolo = bubo.
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probably knows better). Nonetheless, it is in connection with the text

just cited that he for the first time links Boccaccio to the topic of “black
pustules.”178 This assertion is based on a false translation of the infa-
mous “petechiae” as “pustules.” In the case of bubonic plague, the
appearance of petechiae reflects the fact that bacteria have reached the
small subcutaneous blood vessels and by toxic effects on the walls of
the vessels (and a tendency of clotting) caused them to burst, letting
out drops of blood that through the skin take on the form of black, blu-
ish or livid spots. These are the indications of imminent death that
made early modern Englishmen call them “the tokens,” “God’s Token”
or “God’s Mark.”179 This demonstrates again the means Cohn must
resort to in order to form a seeming evidential basis for his grand the-
ory. Thus, Cohn has constructed an important or even crucial argu-
ment for rejecting the identity of late medieval and modern plague by
making a false translation of words meaning “darkly coloured spots” as
“pustules” which is at variance with all scholarly translations and edi-
tions of Boccaccio’s text,180 including the one that he himself used.
178
Cohn 2002: 59.
179
See, for instance, Bell 1951: 127; Slack 1985: 65.
180
Boccaccio 1982: 8–9: “but in men and women alike there appeared at the begin-
ning of the malady, certain swellings, either in the groin or under the armpits […] and
these the vulgar named plague-boils [gavòccioli]. From these two parts of the aforesaid
death-bearing plague-boils proceeded, in brief space, to appear and come in every part
of the body; wherefrom, after awhile, the fashion of the contagion began to change into
black or livid blotches, which showed themselves in many on the arms and about the
thighs and (after spread to) every other part of the person, in some large and sparse and
in others small and thick-sown; […] a very certain token of coming death […].”
Nohl 1961: 10–11: “it began with young children, male and female, either under the
armpits, or in the groin, by certain swellings […] which (in their vulgar Language) they
termed to be a Botch or Boil. In very short time after, those two infected parts were
grown mortiferous, and would disperse abroad indifferently to all parts of the body;
whereupon, such was the quality of the disease, to shew itself by black or blue spots,
which would appear on the arms of many, others on their thighs, and every part else of
the body, in some great and few, in others small and thick. Now as the boil (at the be-
ginning) was an assured sign of near approaching death, so proved the spots likewise
to such as had them.” Sticker 1908: 54, strictly, this is not an exact translation but an
almost verbatim rendering of Boccaccio’s text: “es entstanden, als sie begann, bei
Männern wie bei Frauen entweder in der Weiche oder unter der Achsel Geschwülste
[…] Das Volk nannte sie gavoccioli, Drüsenbeulen. Von jenen Körperstellen aus ver-
breitete sich das tödliche Pestgift rasch in alle Teile. Später nahm di Krankheit eine
andere Gestalt an; es kamen schwarze oder bläuliche Flecke an den Armen und an den
Beinen und weiterhin über den Leib hervor; bei dem Einen groß und spärlich; bei dem
Anderen klein und dichtgedrängt. Und wie anfangs die Pestbeule das sichere Zeichen
des herannahenden Todes war, so wurden es jetzt die Flecken für Jeden, an dem sie
sich zeigten.”
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370 chapter nine
However, Cohn has actually collected material purportedly showing

an incidence of pustules which is described in Appendix I, “Miraculous
Plague Cures.”181 I have not checked this material, but it purportedly
shows that out of fifty-six instances of miraculous plague cures, seven,
or 12.5 per cent, mention pustules as a clinical feature. However, can
this material be taken seriously and be allotted any significance or ten-
ability when Cohn does not present his material in the form of texts
that allow readers to check out whether pustules are really mentioned
or whether these statistics are based on false translations of words
meaning “spots” or “blotches” as “pustules,” as he demonstrably has
done with Boccaccio’s text? Even if it is assumed that the translations
are correct or acceptable, the source-critical problems attached to any
attempt at using this material for any other purpose than to show that
pustules occurred within the broader pattern of late-medieval plague
disease is formidable for several elementary source-critical and meth-
odological reasons. Firstly and devastatingly, they do not represent a
physically systematically examined sample of cases. Next, the elemen-
tary source-critical questions which Cohn has neglected to ask queue
up, for instance: Are the reports of miraculous cures real? Were mirac-
ulously cured plague cases systematically physically examined and
their clinical panorama ascertained in a scientifically tenable manner?
Were reports of pustules relatively over-reported as a grisly feature that
made the cures even more miraculous? And so on. Nonetheless, it can
be accepted that this material shows that pustules were observed by
contemporaries, but the significance of this material for Cohn’s argu-
ments depends heavily on the following question: Is it true that pus-
tules are not normal part also of modern plague cases, that this clinical
feature was not observed in studies of plague in India or elsewhere?
As can be seen especially clearly from the second and concluding
citation above on page 364, Cohn denies that pustules were a feature of
plague in India and of modern plague more generally, referring indi-
rectly to the report Brigadier-General Gatacre compiled from evidence
collected at plague hospitals in and around Mumbai in the plague year
1896–7 to this effect. I understand that Carmichael is puzzled by Cohn’s
insistence of sticking uncritically to this report alone which he cannot
praise enough182 while ignoring all other reports and studies, also con-
temporary and also based on the Indian experience around the turn of
181
Cohn 2002: 253–4.
182
Cohn 2002: 16, 26.
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the previous century. One should note that Gatacre was a military man,
not an army medical officer, and most renowned for his leadership of
the 3rd Brigade of the Chitral relief force, and was honoured with the
publication of his biography.183 In this context one may legitimately
wonder whether it is accidental that Gatacre’s report is extremely
difficult to get hold of for critical examination. After having ordered
this work at the University Library of Oslo I got the following excep-
tional e-mail from the librarian handling the order: “We have not
found that this work (it appears to consist of three volumes) is in the
possession of any library in the Nordic countries, Germany, Austria,
Switzerland or several other countries. It is found in several libraries in
Great Britain, but none of them permits loan. Neither is the copy in
Bibliothèque Nationale (Paris, France) available for loan. The National
Library of Medicine (NLM), Bethesda, Maryland has a microfilm edi-
tion of it? Do you wish that we attempt to have it loaned in for you?”184
I responded affirmatively to this question, but a couple of weeks later
I received the following notice from the librarian: “This library does
not lend this copy outside the U.S.A.”185 All the other more extensive,
thorough and more mature studies published in the following decades
are far easier to get hold of and provide enormous amounts of new and
valuable information. Much of it is also found in compressed form in
the standard works on plague. Why do these standard works on plague
not mention Gatacre’s report? Is not the probable answer to this ques-
tion that the material contained in Gatcre’s report lost its significance
in the light of the great volume of outstanding research produced in the
subsequent years? Is it unreasonable to consider the possibility that
Cohn has chosen this work because it makes it so difficult to check out
his assertions with references to this work to which he attributes such
great importance? However, whatever his motives, the great volume of
subsequent research based on a wealth of new experience and insights
will have great precedence over such material from the earliest phase of
modern research on plague.
As pointed out by Carmichael, the outbreaks of bubonic plague epi-
demics in India in 1896 put extreme strains on medical facilities which
were entirely unprepared for such an enormous epidemic onslaught on
the population. In February 1897, when there were 900–1000 weekly
183
Develin 1896; B. Gatacre 1910.
184
Librarian Eli Fjeld in e-mail of 1 August 2007. My translation into English.
185
My translation into English.
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372 chapter nine
deaths from plague in Mumbai, at the most 300 hospital beds were
available. Many diseased persons resisted hospitalization because caste
and ethnic groups were insufficiently separated. In short, there was a
plethora of grave problems. The desperate endeavours of the English
colonial authorities to build a great anti-plague organization which
could cope with the tremendous tragedy unfolding before their eyes
absorbed much of the available resources. The production and gather-
ing of material for Gatacre’s report concomitantly with the unfolding
epidemic catastrophe was unavoidably also adversely affected by lack
of competent personnel, deficient understanding of bubonic plague as
a disease, the relevant questions to be asked and which types of infor-
mation should be gathered, and it was prepared for publication in great
haste in the autumn of 1897.186 It must also be relevant to ask the ques-
tion why Cohn only uses this report which obviously represents the
earliest phase of the combat of plague in India, the scientific study of
the disease and the collection of evidence? In critical minds, this should
raise the question of why Cohn avoids later information based on much
larger and more composite material, far better medical understanding
of plague disease and far better resources for making research into the
disease. Is it because black pustules are mentioned as a normal clinical
feature of bubonic plague?
It comes therefore as no surprise that Carmichael can cite another
contemporary report to the same effect based on the medical study of
939 plague cases at the “Municipal Hospital for Infectious Disease at
Arthur Road Bombay” in the period 24 September 1896 to February 28
1897. The study of these cases was thus produced concomitantly with
Gatacre’s:
The so-called black boils were observed in a large number of cases, and
they seem to bear a distinct causative relation to the buboes in their
neighbourhood. They differed from ordinary boils in that no inflamma-
tory areola surrounded them. They consisted essentially of a blister in
which the cuticle had become raised sharply and evenly from the skin,
without any redness or signs of inflammation. In fact it appeared as if a
glass circle had been fixed over the skin and its top tied with transparent
tissue paper.187
Indisputably, here the clinical phenomenon of black pustules is identi-
fied in great detail and it is explicitly stated that it was observed in a
186
187
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large number of cases. This confirms the assumption of why Cohn

sticks to a report compiled by a military officer and impossible to get
hold of for most scholars, and why he passes in silence by or ignores all
other important evidence on the matter produced by physicians in
much the same circumstances.
In 1905 there appeared the first standard work synthesizing the
medical and clinical knowledge won by the British medical service in
India authored by W.J. Simpson, Professor of Hygiene at King’s
College in London, and Lecturer on Tropical Hygiene at the London
School of Tropical Medicine and “formerly Health Officer, Calcutta.”
These qualifications may usefully be compared with Gatacre’s creden-
tials in relation to the matter at hand. Simpson’s standard work
appeared shortly before the IPRC started late the same year, and it pro-
vides the following presentation of some clinical features central to the
present discussion:
petechiae and ecchymotic patches188 are generally over buboes or on the
abdomen, but they may be found in other parts of the body, such as the
face, neck, breast, and extremities […] the petechiae and ecchymotic
patches probably correspond to the tokens in the Great Plague of London
which appear to have been a common feature in fatal cases.
In addition to patches of dark-coloured petechiae or ecchymoses there
has been occasionally an eruption of pustules. The pustules on the skin
may be of a variable nature, and in some cases they have been so numer-
ous as to raise a doubt as to whether it was not a case of small-pox that
was being dealt with. […] the pustules usually commence as ecchymotic
or petechial spots […] these ecchymotic patches rapidly increase in size
and then rise in the form of blisters […].189
Carbuncles, boils, vesicles, or pustules may be present on any part of the
body.190
In connection with a post-mortem examination of a Chinese plague
victim in Hong Kong:
On superficial examination the case looked like one of small-pox, vesicles
and pustules being scattered over the face, shoulders, arms, body, and leg.
188
Ecchymosis designates the passage of blood from ruptured blood vessels into
subcutaneous tissue, marked by a purple discoloration of the skin. An ecchymotic
patch in the skin is typically larger than a petechia, forming a non-elevated, rounded or
irregular blue or purplish patch.
189
Simpson 2005: 284.
190
Simpson 2005: 227.
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374 chapter nine
The caretaker of the mortuary, who has had a large experience, pointed
out the case as one of small-pox. An eruption covered the skin. Papules,
vesicles, and pustules were present side by side. They were numerous
over the neck, back, shoulders, back of arms, ventral surface of the abdo-
men, the extensor surfaces of the thigh and the buttocks […].
The pustules were the most numerous […]. There was no question of
small-pox.191
The first citation makes it clear that petechiae and ecchymoses corre-
sponding to Boccaccio’s account on this point are usual clinical features
of bubonic plague in India and of modern bubonic plague more gener-
ally. Simpson’s view that they probably correspond to the tokens in the
Great Plague of London of 1665 is confirmed by Bell’s monograph of
1951, who cites contemporary sources on this clinical feature which
show great similarity to the descriptions just cited in reports from
India.
“The tokens” were spots upon the skin. Breaking out in large numbers,
varying in colour, figure, and size […]. The colour might be red, with a
surrounding circle inclining towards blue; in others a faint blue, the circle
being blackish; others again took a dusky brown tone […] no part was
immune from these round spots, though the neck, breast, back, and
thighs were the most common places for them, “the tokens” sometimes
were so numerous as to cover all the body. It was “the tokens,” so univer-
sally dreaded, that gave to the Plague the name of “the spotted death.”192
The citations from Simpson’s standard work on plague make it clear
that that Indian plague patients presented with pustules and that this
was observed from the beginning of plague in India and was well rec-
ognized before the IPRC began its work. A severe case of pustules in a
plague patient had also been observed and described clinically in Hong
Kong a few years earlier. Simpson makes it clear that the darkly col-
oured spots of petechiae and ecchymoses are distinctly different clini-
cal feature from pustules, the confusion on this matter being entirely of
Cohn’s own construction and, unfortunately, may appear to serve an
argumentative objective. It also becomes clear that historical plague
cases presented with buboes, pustules and darkly coloured spots which
correspond to similar clinical features in modern bubonic plague and
that this fact constitutes a strong argument to the effect that they were
the same disease. Cohn’s use of Gatacre’s report can now be seen to be
191
Simpson 1905: 246.
192
Bell 1951: 127–8.
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misleading and is so throughout his monograph. One should note

that Simpson’s work is entered in Cohn’s bibliography and referred to
three times in his text, so arguably he is not unacquainted with this
information.
Pustules and petechial or ecchymotic spots as quite usual clinical
features of bubonic plague are not confined, of course, to India, but are
general clinical features of this disease. Summarizing the observations
of bubonic plague in China, Chun states:
Vesicles appearing on the hands, feet and pectoral193 region may be con-
verted into pustules which were described by old writers during the
Plague of London in 1665 as “blains.” The pustules may coalesce and
form areas of necrosis, the so-called carbuncles. […]
In some plague cases, the vesicles and pustules may resemble those of
chicken pox or smallpox. […]
There are often haemorrhages in the skin and elsewhere. […]
Haemorrhages may occur in different parts of the body, so that we find
petechiae, or ecchymoses […].194
Cohn has used this outstanding standard work on plague,195 which is a
composite work written by a number of distinguished plague research-
ers, but he has evidently failed not only to consult the section on clini-
cal features but even to look up the terms “pustule” and “petechiae” in
the index, as he has generally failed to consult the sections on
“Immunology,” “Hosts and Carriers,” “Insect Vectors,” “Clinical
Features,” and “Epidemiological Factors.” Chun’s identification of the
“blains” described by “old writers during the Plague of London in 1665”
with pustules is confirmed by Bell: “The ‘blains’, so-called, were like
blisters on the skin, obscurely ringed about.”196
Descriptions of pustules and petechiae in modern bubonic plague
are ordinary information of the standard works on plague. Hirst men-
tions, albeit briefly, that the “vesicular variety of plague may simulate
smallpox, but the pustules contain plague bacilli” and that “before
death dusky stains or blotches appeared on the skin of the body.”197
In his standard work, Pollitzer cites Simpon’s description of the “for-
mation of ecchymotic or petechial spots” which develop into the form
of blisters and underlines that the “appearance of numerous petechiae
193
Of the chest or breast.
194
Chun 1936: 311, 313, 316, 329.
195
Cohn 2002: 301.
196
Bell 1951: 126.
197
Hirst 1953: 30, 32.
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376 chapter nine
or ecchymoses, particularly early in the disease, is an ominous sign.”198

This shows that Simpson’s presentation of these clinical features of
bubonic plague displayed knowledge and competence that were fully
adequate fifty years later to an outstanding scholar who had lived his
professional life in the first line of combat of plague in the field and the
laboratory. Next, Pollitzer provides the following relevant clinical com-
ment on the present topic:
The appearance of generalized pustular eruptions (“plague pox” or
“plague variola”) has been recorded by several observers. According to
Macchiavello, instances of this kind were frequent in South America.199
This comment reflects the fact that pustules may be so widespread and
numerous on the body that the disease may resemble small pox, a point
also made by Simpson and Chun. Cohn has entered Pollizer’s impres-
sive standard work on plague in his bibliography and refers to it nine
times in the text according to the index (in one case the reference is
erroneous).200 Purportedly, Cohn has not used the opportunity to find
out whether Pollitzer had something to contribute on such a vital point
for his theory as the clinical feature of pustules and petechiae; he could
have done so by consulting the index under the entries “Plague pus-
tules” and “Skin plague.”
Machiavello’s statement that plague pox or plague variola was
quite usual in South America can be independently confirmed.
C.R. Eskey states in his report on this in his study of bubonic plague in
Ecuador:
Viruela pestosa begins as the ordinary bubonic disease, but the skin
eruption that follows is likely to obscure the buboes. Vesicles develop
which pass through stages very similar to those of varicella. The vesicles
may be few in number or present to the extent that they are found in a
severe case of chicken pox. The mortality of viruela pestosa is relatively
high. Doctor Martinez states that when the vesicles exceed 50 the result
is nearly always fatal.201
198
Pollitzer 1954: 425, 426.
199
Pollitzer 1954: 425–7, see also p. 206.
200
Cohn 2002: 314 (the reference to page 189 should be 188 n). The erroneous
reference is given on page 215: “the ones called iuvenis or young adults between
around 20 and 30 years old—the ones most susceptible to new diseases in general and
to modern bubonic plague in particular[fn. 100].” In the accompanying footnote 100,
Cohn refers to Pollitzer 1954: 516, where statistics on the distribution of victims of
primary pneumonic plague according to age is given, not in relation to bubonic
plague.
201
Eskey 1930: 2082.
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The frequent occurrence of plague pox in South America is also inter-

esting because it may give a clue or key to the medical understanding
of the cause of this phenomenon, whether it could, for instance, be due
to peculiarities of food or drink or variants of malnutrition or under-
nutrition. According to my knowledge, the cause of widespread erup-
tion of pustules in plague cases has so far not been studied; all knowledge
appears to be descriptive or statistical.
In the most recent standard work Butler, as a matter of course, makes
the following description of usual cutaneous manifestations or skin
lesions in cases of bubonic plague, mostly based on his experience and
observations in Vietnam:
The most common were pustules, vesicles, eschars,202 or papules near the
bubo […].203
Cohn has entered also this work in his bibliography and refers to it four
times in his text. Of particular interest is a passage where he insists
that
with no modern plague have black pustules spreading randomly over the
body been reported. At most, a few points might form around the flea-
bite, but such marks are rare and usually occur with pneumonic or septi-
caemic plague, when buboes do not have time to form at all.[fn. 9]204
In the accompanying footnote 9, Cohn refers to page 17 in Butler’s
monograph where nothing to this effect is stated. This is a spurious
reference. Cohn has avoided page 79 where the chapter on “Cutaneous
manifestations” starts and the information on pustules is given. All of
Cohn’s assertions with respect to pustules and plague are erroneous
and misleading.
Puzzlingly, in view of all of these standard works on plague which
Cohn has purportedly held in his hands, he refers for support of his
assertion that pustules did not occur or only rarely occurred in modern
plague to the short chapters on plague in three editions of Manson’s
Tropical Diseases, the 10th edition of 1935: 254, the 19th edition of
1987: 591, and the 20th edition of 1996: 920, hoping, as it would seem,
that none would make the effort to check them all.205 One should again
202
In the case of plague, a slough produced by gangrene.
203
Butler 1983: 79.
204
Cohn 2002: 59.
205
It is not easy to get hold of so many editions, it actually requires some effort and
I only managed to get hold of the American edition of the 10th edition published in
1936, but the contents should be identical with the British edition.
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378 chapter nine
keep in mind that the chapters on plague in such general standard

works on infectious diseases are very brief summaries of the material
presented in general standard works on plague; in the case of the two
last editions, of 1987 and 1996, they constitute 2.2 per cent and 0.97 per
cent of Pollitzer 1954. This also means that the information they include
on clinical matters vary considerably according to their assessment of
what is sufficiently important to warrant inclusion in consideration of
the medical circumstances of the contemporary world. However, since
the editions of Manson’s Tropical Diseases up to the 19th of 1987 are not
furnished with footnotes which allow basic checking out of the infor-
mation, the significance which Cohn attributes to them and the schol-
arly argument(s) for not using the standard works on plague are quite
intriguing.
Nonetheless, in the 19th edition of 1987 of Manson’s Tropical
Diseases’s section on “Skin affections” it is stated:
A generalized popular rash on the hands, feet and pectoral region has
been described. Should life be continued sufficiently long, the vesicles
become converted into pustules resembling smallpox. These observa-
tions confirm in a remarkable manner the old writers who described
manifestations, in the Plague of London of 1665, as “blains.”206
In the general introduction to the section “Human plague” it is also
stated that the clinical panorama is very frequently characterized by
ecchymotic spots or patches […]. Occasionally there are also furuncles,
pustules and abscesses […] ecchymoses are common in all serous
surfaces.207
Is it really possible that Cohn who claims to have held in his hand the
19th edition of 1987 and refers specifically to page 591 in the chapter
on plague has not seen the relevant information in the general intro-
duction to human plague on page 591, or the even more relevant sec-
tion on clinical manifestations on the skin on page 593?
Is it really credible that Cohn can have used all the modern standard
works on bubonic plague from Simpson 1905 to Butler 1983 without
having taken interest what they state about cutaneous manifestations?
Is it really credible that he even by accident could have missed all refer-
ences in them to pustules? But then Cohn’s reference to pustules in
206
Manson’s Tropical Diseases: 1987: 593. Cf. 1982: 340; 1996: 920.
207
Manson’s Tropical Diseases: 1987: 591. Cf. 1982: 339.
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Boccaccio’s Il Decamerone is also, as shown above, spurious in the sense

that it is based on a mistranslation.
In place of Yersinia pestis I offer no alternative […],208 Cohn admits.
Crucially, Cohn does not take interest in the problem of why he is
unable to present a single viral disease spread by interhuman cross-
infection which is known to modern medical science in which patients
present with buboes as an ordinary clinical manifestation. Viral dis-
eases that spread by cross-infection are not rare. On the contrary, cross-
infection is the usual way viral diseases are disseminated, and there
must be hundreds of them. In epidemic or endemic form of spread,
they have in common that diseased persons do not present with buboes
as an ordinary clinical feature. According to ordinary methodological
considerations, this elementary test of Cohn’s alternative theory which
now has been performed for him provides abundant empirical evi-
dence—without exception or loophole—for asserting that whatever
disease historical plague could have been or whatever microbiological
contagion could have caused it, it could not have been a viral disease
spread by cross-infection. According to ordinary methodological con-
siderations, this is a sufficient condition for rejecting Cohn’s theory
that he should have recognized early in the process of planning his
alternative theory. According to the elementary principles of method-
ology and social and medical science, the complete absence of a viral
disease which presents with buboes provides maximum evidentiary
powers to the fact. This invalidates Cohn’s alternative theory.
This fact implies that there must be a very strong systematic cause or
combination of causes which excludes any exception, i.e. which excludes
the possibility that the disease could have been a viral disease spread by
cross-infection. This systematic cause is probably identified since the
only two diseases which regularly present with buboes, namely bubonic
plague and tularaemia, are transmitted by ectoparasites which system-
atically deposit bacillary contagion at a subcutaneous level suitable for
being drained through lymphatic vessels to lymph nodes (see above).
This distinguishes these diseases from all diseases spread by cross-
infection in which the contagion is normally inhaled into the lungs
in droplets, landing the infection in an anatomical location without
contact with lymph nodes, which is the reason no scholar has inti-
mated the occurrence of pneumonic buboes. This clarifies the question
208
Cohn 2002: 247.
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380 chapter nine
of crucial importance which Cohn has ignored, which is: How, by

which physical routes or mechanisms or properties, should his pur-
ported viral disease spread by cross-infection have been regularly
transported to lymph nodes? What Cohn is trying to make his readers
believe is that he in confused and unscientific medieval texts has found
tenable evidence of the only viral disease which regularly produce(d)
buboes in diseased persons and that this (miraculously) is his pur-
ported alternative microbiological theory of historical plague. Cohn is
unable even to make an attempt at explaining the medical or epidemio-
logical process of causation. What was so unique about this viral dis-
ease that buboes should be expected to be an ordinary manifestation of
the infection in contrast to all other viral diseases known by medical
science? Cohn simply maintains that it was spread like hundreds of
other viral diseases, namely by cross-infection, but in an obvious breach
of elementary methodology pretends that he is not obliged to explain
why this mode of (viral) transmission of infection should uniquely
produce buboes only in the case of his purported disease without a
unique and specific mechanism of transmission which leads to the
regular infection of lymph nodes. As now should be clear, what Cohn
has constructed is not an alternative theory, it is an alternative specula-
tive flight of the imagination, a phantom disease which has not the
slightest resemblance with any viral disease known to medical science.
It is overwhelmingly probable that such a disease has never existed and
never disappeared because it never appeared in the real world but lived
its entire short life as a brainchild in an academic ivory tower.
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CHAPTER TEN
DEFINING FEATURE 4: DNA OF YERSINIA PESTIS FROM

PLAGUE GRAVES
The advocates of alternative theories of the microbiological identity of

historical plague find themselves dramatically confronted by modern
microbiological and genetic sciences which have now reached a level of
sophistication which provides entirely new opportunities for historical
studies of biological material of the past and the development of the
new science of paleomicrobiology. Identification of the microbiologi-
cal agent of historical plague epidemics can be achieved by reclamation
of genetic material or specific proteins of plague contagion taken from
human remains in historical plague graves. Reclamation and study of
such biological material will provide certain evidence of the microbio-
logical identity of historical plague if the results from a significant
number of excavated plague graves with significant geographical spread
are consistent. Since the development of the scientific discipline of
paleomicrobiology is quite recent, starting in 1993,1 the following pres-
entation will give a brief outline of the research history and the results
up to the present be summarized in Table 6.
In 1998 a team of French scholars, M. Drancourt, G. Aboudharam,
M. Signoli, O. Dutour and D. Raoult, published a study of DNA recov-
ered in dental pulp2 taken from unerupted teeth extracted from indi-
vidualized skeletal remains excavated from two mass graves of plague
victims in Provence. This material was taken from a mass grave con-
taining the skeletal remains of 133 plague victims buried after a plague
epidemic in Lambesc3 in 1590 and from a mass grave in Marseilles con-
taining skeletal remains of 200 plague victims buried in May 1722. The
scholars extracted dental pulp from the teeth of two individualized
skeletal remains in Lambesc and from the remains of three individuals
1
Drancourt and Raoult 2008a 55.
2
See La, Aboudharam, Drancourt 2008: 175–96.
3
Lambesc is a town situated c. 45 km north of Marseilles. Cf. Les saison d’une peste
(avril–septembre 1590): Le cimetière des Fédons à Lambesc. B. Bizot (ed.). 2005. Rouen:
CNRS Editions.
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382 chapter ten
in Marseilles. In seven of the eight cases,4 the scholars found DNA of

ordinary strains of the plague bacterium Yersinia pestis which causes
bubonic plague (and the variants and modalities of plague disease that
can develop from such cases).5
In 2000, another group of French researchers (including three of the
scholars who participated in the 1998 study) published a similar study
performed with improved techniques aimed at molecular identifica-
tion by so-called “suicide PCR” which should exclude any possibility of
contamination of the material. The study was nonetheless carried out
under the observance of draconian precautions to exclude contamina-
tion; it was, among other things, performed in a building where plague
contagion never had been introduced before, and the dental pulp was
extracted with techniques which were specifically designed to exclude
any form of contamination with extraneous DNA. The material was
dental pulp, in this case extracted from twenty-three teeth of three
skeletons, two adults and a child, buried hastily and without shroud in
the same grave in a cemetery in the city of Montpellier some time in
the period 1348–1400, probably in the Black Death (1348). As a nega-
tive control, four unerupted teeth were collected from ancient skeletal
remains excavated from a medieval grave in Toulon, France. In this
period, Montpellier was ravaged by plague in 1348, 1374–5, 1385 and
1397, and the number of registered households fell from c. 9500 in
1348 to c. 1000 in 1397. This means that a large majority of the buried
persons must have died in these plague epidemics, indicating that the
recovered genetic material is probably connected with the Black Death.
In one of the four teeth taken from the child and in all nineteen teeth
taken from the adults, the researchers found Yersinia pestis-specific
DNA fragments representing the genetic code of ordinary strains of
this contagion. None of the four negative control teeth tested positive
for plague contagion.6
It must be highly improbable that a few episodic cases of deaths from
bubonic plague in the historical past should be found by chance. The
consistent identification of Yersinia pestis constitutes therefore substan-
tial evidence to the effect that bubonic plague spread in epidemic form
in southern France in the period 1347–1722 covering the whole second
4
Drancourt, Aboudharam, Signoli et al. 1998: 12638.
5
Drancourt, Aboudharam, Signoli et al. 1998: 12637–40.
6
Raoult, Aboudharam, Crubézy et al. 2000: 12800–3. Cf. Drancourt and Raoult
2002: 5–6.
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dna of yersinia pestis from plague graves 383
plague pandemic from the Black Death to the last great epidemic. Since
these epidemics have the same characteristics as historical plague epi-
demics elsewhere in Europe, this genetic evidence constitutes signifi-
cant evidence that the plague epidemics in the second pandemic were
generally epidemics of bubonic plague. The scholars conclude trium-
phantly (but arguably prematurely): “We believe that we can end the
controversy: Medieval Black Death was plague.” In later papers, pre-
senting the further development of this type of research, they have had
occasion to repeat this conclusion on an even more certain basis, last
time in 2008: “Our results enabled us to resolve the long dispute over
the aetiology of the Black Death by showing that the disease was in fact
plague caused by Y. pestis.”7
In 2002, a comprehensive study appeared of genetic material taken
from individualized skeletal remains in mass graves in seven localities,
namely Aubagne, Cassis, Puy-Sainte-Réparade, Marseilles, Martigues,
Salon, and Vitrolles relating to the plague epidemic in Provence in
1720–2. This genetic material was studied by use of improved molecu-
lar biology techniques on dental pulp which determined the infectious
agent with even greater certainty. Yersinia pestis was identified in all
cases.8
Now microbiologists from other countries have begun to make simi-
lar studies and make similar findings. The same year, two Australian
scholars published a study in which they had succeeded in identifying
the DNA of Yersinia pestis in skeletal material taken from a putative
plague grave from the Black Death in London (1348–9) using the PCR-
technique (see below, Table 6 and fn. 28, no. 3).
Frequent, usual or consistent identification of Yersinia pestis in
plague victims of the past without concomitant identification of any
other alternative mortal pathogen should put and end to all microbio-
logical alternatives argued by the revisionists. For this good reason,
a team of scholars set out to test the almost sensational results obtained
by the French scholars by carrying out an independent study with
microbiological techniques of other samples of dental pulp taken
from skeletal remains in presumed plague graves in various countries.
A preliminary negative communication was published in Science by
7
Drancourt and Raoult 2002: 105–9; Drancourt and Raoult 2008b: 153. Drancourt
and Raoult 2008c: 182.
8
Signoli, Séguy, Biraben et al. 2002a: 838–9, 841; Signoli, Séguy, Biraben et al.
2000b: 846, 849.
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384 chapter ten
A. Cooper and H. Poinar in 2000 to the effect that it had not been pos-
sible to reproduce the results of the first French study,9 the final study,
also negative, was published by Gilbert and al. in 2004. They had stud-
ied dental material taken from putative plague victims in five burial
sites from the late thirteenth century to the seventeenth century with
wide territorial distribution in Europe using a sample of 108 teeth taken
from sixty-one individuals, however, without succeeding in finding the
DNA of Yersinia pestis.10 Unimpressed by the French scholars’ descrip-
tions of the impressive pre-cautions taken to avoid contamination and
their insistence in the first paper that “Contamination of the samples
during handling is highly improbable”11 and in the second paper that
the researchers had used a special technique that would “avoid any pos-
sibility of molecular contamination of the ancient DNA,” Gilbert et al.
suggested that “the DNA-sequences […] derive from the contamina-
tion of DNA extracts with formerly amplified or extracted Y. pestis
DNA.”12 However, Gilbert et al. do not attempt to explain concretely
how contamination could have occurred in view of the French research-
ers’ descriptions of their techniques and anti-contamination measures
and they did not test the French researchers’ more specific techniques
and the use of “suicide PCR.” Gilbert et al. overlook the fact that the
French scholars also tested control samples taken from non-plague
sites, and that they tested negatively,13 which constitutes strong evi-
dence against contamination in the laboratories. Gilbert et al. did not
comment on the positive findings presented in the paper of 2002 which
was produced by another team of French scholars attached to other
institutions using other laboratory facilities and who insisted on the
“absence of contamination of the research workers.”14 Also, they did
not comment on the positive identification of DNA of Yersinia pestis
relating to the Black Death in London performed by entirely independ-
ent scholars, despite the troubling fact that they had not succeeded in
identifying such DNA from two sites with plague burials in London.
9
Cooper and Polnar 2000: 1139.
10
Gilbert, Cuccui, White et al. 2004a: 342–9. Cf. Prentice, Gilbert and Cooper
2004: 72.
11
Drancourt, Aboudharam, Signoli et al. 1998: 12637, 12640.
12
Gilbert, Cuccui, White et al. 2004a: 352.
13
Drancourt, Aboudharam, Signoli et al. 1998: 12637–8.
14
Signoli, Séguy, Biraben et al. 2002a: 838–9; Signoli, Séguy, Biraben et al. 2000b:
846.
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Gilbert et al. argue also that it is suspect that the French scholars
found Yersinia pestis-specific DNA in all cases, since “during an epi-
demic, not all deaths can be expected to arise due to the specific patho-
gen […]. Therefore, it seems unlikely that, among the eight individuals
sampled in these two studies, only one negative for Y. pestis was
observed.”15 However, this argument does not bear the significance
allotted to it, since the mortality caused in historical plague epidemics
was so enormous that normal mortality from other causes would be
strongly affected by the fact that many of those who in normal circum-
stances would have died from other caused died from plague instead.
This greatly affects the numerical relationship and the statistical prob-
abilities. Although it is true that persons died from other causes during
plague epidemics, it is also true that the probability of selecting by
chance the remains of such persons in mass graves with plague victims
would be small, even tiny. I have had the opportunity of approaching
the problem in my Norwegian plague history on the basis of continu-
ous information on the number of corpses brought to the Cathedral in
Bergen during the plague epidemic of 1565–6 in its capacity as parish
church. This is material which provides the opportunity for deleting all
persons dying outside the plague season and a number of persons about
whom it was specifically stated did not die from plague. This process
would be much the same in a plague year, when people dying outside
the plague season would receive normal burials and the mass graves of
plague victims would tend to contain very few non-plague deaths.
About 40 per cent of Bergen’s population perished in the epidemic, and
I could conclude: “the material on the deaths in the plague epidemic
was probably affected by slightly below 0.5 percentage point of normal
mortality for each of the two years in which the epidemic took
place.”16
In their monograph of 2004, Scott and Duncan refer to a talk given
by one of the members of the team, A. Cooper of the University of
Oxford, at a meeting of the British Society of Microbiology in
Manchester in September 2003 in which he apparently suggested that
the DNA analysis technique used by Drancourt and Raoult was flawed.
He also purportedly maintained that “splitting the teeth and scraping
out the inside, as the French team did, contaminated them with
15
Gilbert, Cuccui, White et al. 2004a: 351.
16
Benedictow 2002: 201. My translation into English.
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386 chapter ten
bacteria.” In the opinion of Scott and Duncan, this justified calling the
findings of the French scientists “A Red Herring.”17
However, later in 2004, Drancourt and Raoult responded briefly to
Gilbert et al.’s paper and pointed out a serious flaw in the critics’ work:
Gilbert et al. did not test systematically “our dental technique” and that
they had only tested dental pulp in seven suspected specimens. This
included five teeth from a cemetery in Verdun: in their work they had
tested three teeth from this cemetery which also had tested negative for
Yersinia pestis. “Therefore this result did not surprise us.”
Moreover, we found that the recovery of dental pulp via the tooth apex,
as described by M.T.P. Gilbert, is almost ineffective. In our work, we
always recovered dental pulp after complete opening of the dental pulp
cavity. This approach is more difficult to perform and a dentist is proba-
bly necessary here. This allowed the recovery of all the pulp remnants.
When this technique was applied, only two dental pulps, recovered by a
different technique, from patients sampled in Copenhagen gave results
different from ours. The use of the less satisfactory technique makes a
very weak basis to contest our data.18
Drancourt and Raoult also point out that another strategy of genetic
research, PRC techniques (“suicide PCR”), as practiced by Gilbert et al.
was open to substantial criticism and was “very different from what we
reported […]. We therefore believe that our test conditions were not
reproduced.” “We therefore disagree with the authors’ conclusion that
they failed to reproduce our results since they did not use our tech-
niques to obtain material of our PCR testing techniques.”19 The defen-
sive response from Gilbert et al. shows that the serious flaw Drancourt
and Raoult had pointed out was justified and tenable.20 The tenability of
17
18
Drancourt and Raoult 2004: 263–4.
19
Drancourt and Raoult 2004 : 263–4. Cf. Drancourt and Raoult 2008: 153.
20
Gilbert, Cuccui, White et al. 2004b: 264–5. Gilbert, Cuccui, White et al. 2004a,
has also other weaknesses. For their information on the Black Death they refer only to
Cohn 2002 and Scott and Duncan 2001 without taking interest in the fact that these
monographs are not devoted to the general study of the Black Death, and without tak-
ing any interest in the fact that their alternative theories on the microbiological nature
of historical plague are entirely incompatible, so that at least one of them must be mas-
sively erroneous, which may be taken to indicate a certain element of preconception.
Surprisingly, they argue that since the mortality rates were 40–50 per cent, this can be
taken as a serious argument in favour of Scott and Duncan’s filoviridal virus theory, a
type of disease that for transmission and dissemination requires direct physical contact
involving transmission of cellular material. This is compatible with the fact that these
diseases produce only small or tiny outbreaks, and are, furthermore, dependent on a
highly local African animal reservoir (see below). One would also like to have seen a
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the important points made by Drancourt and Raoult have since been
confirmed by the continuous stream of new positive studies (Table 6)
and the fact that apparently no other microbiologists have failed to
identify Yersinia pestis in biological material taken from plague graves
since 1998.
Revisionists are also rejecters and have consistently continued to
refer to the preliminary negative communication by Cooper and Poinar
from 2000 and Gilbert et al.’s paper from 2004 in order to reject the
significance of the French scholars’ research.21 This is what Cohn does
briefly and superficially in his monograph of 2002 and in his paper in
The American Historical Review the same year.22 This attitude requires
that subsequent studies exhibiting positive identification of bubonic
plague DNA, also by other scholars associated with other research
institutions in other countries, must also be overlooked. This is what
Cohn still does in 2008 (see below).23
In 2007, Drancourt, Roux, Dang et al. published a study designed to
resolve another controversy and enlarged in the process the pool of
examinations of dental pulp taken from plague graves of the past. They
took up again a central team of the paper of Drancourt, Roux, Dang
et al. of 2004 (above) concerning the historical role of various types of
Yersinsia pestis. In 1951 R. Devignat published a very interesting paper
where he identified three biovars of plague characterized by special
properties, namely ability to convert nitrate to nitrite, or to ferment
glycerol, or both, and he assumed that each were responsible for an
independent pandemic, namely Antiqua, Medievalis and Orientalis.24
reference to at least a single modern case of filoviridal haemorrhagic disease that has
presented with a bubo. It is also surprising that they evidently have a positive view of
Cohn’s theory involving an unknown virus that long ago has become extinct. Is this a
testable theory? Why do they not take interest in the crucial fact that Cohn does not
underpin his alternative theory with a single example of a viral epidemic disease that
ordinarily presents with buboes in the diseased? Would it not be reasonable that they
at least attempt to identify a viral epidemic disease which ordinarily presents with
buboes in the diseased, and if this proves impossible, to establish a rule of regularity
that would include untestable assertions with respect to viral theories of the nature of
bubonic plague? These and other relevant issues or topics have partly been discussed
above in relation, for instance, to buboes; other points will be discussed and clarified
below. Here, it is the lack of questioning and critical attitudes in these scholars’ paper
that have attracted attention.
21
See, for instance, Christensen 2003: 417, fn. 16; Knudsen 2005: 25.
22
Cohn 2002a: 248–9; Cohn 2002b: 735–6.
23
Cohn 2008: 88–9, 100.
24
Devignat 1951: 247–63; Devignat 1953: 509–14. Cf. Pollitzer 1954: 103.
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388 chapter ten
Drancourt, Roux, Dang et al. confirmed by molecular analyses that

these three biovars existed, but found also that the biovar Orientalis
was involved in all three pandemics and probably was the main biovar
also in the two first pandemics. They also found that isolates of biovar
Antiqua are more distantly related to other isolates than biovars
Orientalis and Medievalis, and that one Y. pestis Antiqua isolate formed
a fourth branch, which “suggests that Y. pestis may comprise four dif-
ferent lineages instead of the three that have been recognized so far.” In
the new paper, the French team of researchers expanded their territo-
rial search for biological material to include teeth taken from twelve
skeletal remains including five children buried within the ruins of a
Roman temple from 7th–9th centuries in Vienna, in addition teeth
were taken from five skeletal remains found in mass graves in Martigues
about twenty-five km west of Marseilles which had been dated to
1720–1, and five teeth from three skeletal remains in a mass grave in
Marseilles containing 216 victims who had been buried in May 1722,
a mass grave that had been used also earlier and given positive identi-
fication of Yersinia pestis. Usual strict precautions were implemented in
order to prevent contamination, material was also collected for nega-
tive testing, and the usual paleomicrobiological techniques were
applied. All eleven negative controls proved negative, but five of thirty-
six teeth yielded positive identification of Yersinia pestis in “2 of 4 per-
sons’ remains from Vienna, 2 of 5 from Martigues, and 1 of 3 from
Marseilles.” They exhibited total similarity with the genetic structures
of Yersinia pestis Orientalis. The French scholars concluded that these
results confirm the earlier detection of Yersinia pestis-specific DNA in
the skeletal remains of plague victims from the first and second pan-
demics. After having demonstrated the presence of Yersinia pestis-type
genetic material in Justinianic and medieval specimens, “we now have
cumulative evidence using 2 different molecular approaches that
Yersinia pestis closely related to the Orientalis biotype was responsible
for the 3 historical plague pandemics.”25
Considering the comprehensive evidence available after ten years of
paleomicrobiological research, there can hardly be any doubt that the
three identified historical pandemics of plague were caused by Yersinia
pestis, principally the Orientalis biovar. This constitutes also independ-
ent defining evidence based on identification of the microbiological
nature of the contagion.
25
Drancourt, Signoli, Dang et al. 2007: 1–3.
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This emphasizes the importance of presenting a complete survey of

the most recent literature in studies which present positive identifica-
tion of Yersinia pestis in biological material taken from historical plague
graves with the objective of making them an indispensable part of
future discussions of this subject. After 2002, new studies were pub-
lished by scholars from quite a number of countries who reported the
identification of Yersinia pestis in various localities at various times, all
of them overlooked or ignored by all revisionists. Dental pulp, bones
and other biological remains from plague graves were studied with
improved or new molecular techniques which increased the range of
usable biological material and determined the infectious agent with
great certainty, even complete certainty since the spectre of laboratory
contamination was eliminated.26 Soon, studies also provided identifica-
tion of Yersinia pestis from plague graves dating back to the first pan-
demic/the Justinianic pandemic, from Sens about ninety km south-east
of Paris, from Aschheim near Munich in Bavaria and from Vienna in
Austria, thus, with great territorial spread.27
All studies providing identification of DNA or specific proteins of
Yersinia pestis in material from historical burial sites are synoptically
displayed in Table 6; the two first columns indicating the chronology
of the papers and the development of this discipline as presented in
fn. 28.28
26
Excepting the negative control samples which all were negative.
27
See fn. 28, (5), (7), (8), and fns. 29–31.
28
(1) Drancourt, Aboudharam, Signoli et al. 1998: 12637–40; Castex 2008: 29–34.
(2) Raoult, Aboudharam, Crubézy et al. 2000: 12800–03;
(3) McKeough and Loy 2002: 145;
(4) Signoli, Séguy, Biraben et al 2002a: 821–47; (English ed.) Signoli, Séguy,
Biraben et al. 2002b: 829–54. The material relating to Marseilles is taken from
the same mass grave as no. 1, and as in nos. 8 and 9–10; the material relating
to Martigues is taken from the mass grave at Le Delos, same as in no. 9–10.
(5) Drancourt, Roux, Dang et al. 2004: 1585–92; Castex 2008: 25–34.
(6) Pusch, Rahalison, Blin, et al. August 2004: 484–5. Cohn claims that this paper
supports the revisionists’ rejection of the significance of the plague-related
genetic research. Cohn 2008: 88. However, Pusch et al. maintain that they
have succeeded in identifying both DNA and proteins specific to Yersinia pes-
tis in skeletal material taken from a charnel house associated with the church
of St Germanus in Stuttgart which can be dated to the seventeenth century
but not to a specific plague epidemic among the several which ravaged the
city in that century. True, in the opening statement they apparently disagree
with the view that plague in the past was caused by Yersinia pestis which is
clearly at variance with the substance of their paper. In a personal communi-
cation responding to me by e-mail of 30 December 2009 Professor Pusch
states that the “confusion is due to the final editing process […] unfortunately,
I had no influence on it.”
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390 chapter ten
Table 6. Microbiologcal identifications of Yersinia pestis, year of publi-

cation, time of epidemic(s), and localities
Paper 1. Pandemic 2. Pandemic Locality
541–766 1346–1722
No. Year
1 1998 1590 Lambesc: Provence
1722 Marseilles: Provence
2 2000 1348(–1400) Montpellier: Languedoc
3 2002 1348–9 London
4 2002 1720–2 Aubagne, Cassis, Puy-
Sainte-Réparade,
Marseilles, Martigues,
Salon, Vitrolles: Provence
5 2004 57129 Sens: 90 km south-east of
Paris
1348 Dreux: 70 km north-west
of Paris
1348 Montpellier: Languedoc
6 2004 1626–78 Stuttgart: Germany,
south-west
7 2005 544/c. 56030 Aschheim: Bavaria (near
Munich)
8 2007 600–76631 Vienna: Austria
(7) Wiechmann and Grupe 2005: 48–55;

(8) Drancourt, Signoli, Dang et al. February 2007: 332–3;
(9–10) Bianucci, Rahalison, Ferroglio, et al. October 2007: 747–54; Bianucci,
L. Rahalison, E. Massa et al. March 2008: 361–7. These two papers are closely
related, but the teams of scholars are not identical and the second paper
appears to be an improved and expanded version of the first; I have therefore
chosen to consider them together.
29
According to the sources and maps in J.-N. Biraben and J. Le Goff, “La Peste dans
le Haut Moyen Age.” Annales Économies Sociétés Civilisations. 24; 1969: 1493–4, 1500–
07, bubonic plague epidemics could have reached Sens twice in the first pandemic,
both times in epidemics occurring in the sixth century which is also the latest time
limit of the radiocarbon dating: in 543 when the first epidemic of the Justinianic pan-
demic spread in France and next in 571 in the third epidemic. Castex 2008: 28. See also
Little 2007: 20.
30
544 and c. 560 are the two years in the two first epidemics of the Justinianic pan-
demic when plague came geographically closest to Munich, Biraben and Goff 1969,
1493–4, 1500–07. This demonstrates that knowledge of the spread of plague epidemics
can be increased or extended by paleomicrobiological studies.
31
The graves in Vienna are dated in two ways, by a 5th century coin, which allows
dating to the sixth century, but dating by C14 indicates seventh or eight centuries.
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Table 6 Cont.
Paper 1. Pandemic 2. Pandemic Locality
541–766 1346–1722
No. Year
1720–1 Martigues: Couvent de
Capucins32
1722 Marseilles
9–10 2007/8 1590 Lambesc
1628–32 Puy-St.-Pierre:
Dauphiné,33 east
1649–50 Draguignan: Provence
1720–1 Martigues, Le Delos34
1720–1 Martigues, Couvent des
Capucins
1720–1 Berres L’Etang, near
Martigues
1722 Marseilles
Table 6 shows that by March 2008, after mere ten years, ten studies
had been published with twenty-six independent identifications of the
DNA of Yersinia pestis relating to twenty different historical burial sites
of plague victims. Among them were three geographically widespread
graves from the Justinianic pandemic (near Paris, near Munich, in
Vienna), twenty-three localities in the second pandemic comprising
three relating to the Black Death 1348–9, i.e. Montpellier, Dreux and
London, and also in widespread localities across southern, western and
north-western Europe. Since French scholars pioneered this new disci-
pline of paleomicrobiology developing techniques suitable for the
identification of Yersinia pestis in biological material from historical
graves and enthusiastically exploited the new opportunities, fifteen
different sites of plague graves in France have so far yielded positive
findings, one from the Justinianic pandemic in Sens, three from the
The two first epidemics of the Justinianic pandemic came closest to Vienna according
to the sources and maps in Biraben and Goff 1969, 1493–4, 1500–07.
32
Le Couvent de Capucins de Ferrières; Ferrières is a section of the town Martigues
in Provence west of Marseilles. See also Tzortzis and Signoli 2009: 749–60.
33
Region north of Provence; Briançon is situated in the north-eastern corner on the
border with Italy.
34
Le Delos is another section of Martigues.
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392 chapter ten
Black Death (two of them in Montpellier), one from 1590, two from
seventeenth-century south-eastern France, and nine from the last epi-
demic in southern France in the years 1720–2. In addition, there has
been one positive finding in biological material from seventeenth-cen-
tury Stuttgart in south-western Germany situated at about the same
latitude as Paris but in Central Europe. Consistently, the genetic char-
acteristics of the same mortal pathogen have been identified, specifi-
cally the DNA fragments or specific proteins of Yersinia pestis of the
biovar Orientalis, excepting in Stuttgart where the technique did not
lend itself to identification of biovar. This demonstrates that bubonic
plague spread in a dynamic broad epidemic form over large parts of
Europe both in the first and second pandemic.
It appears that Gilbert et al. are the only scholars in the field who
have not succeeded in identifying DNA or proteins of Yersinia pestis in
sites of plague burials. Is it true that this study is still valid in the face of
so many and varied positive identifications by so many scholars from
so many different academic institutions in so many countries?
This puts in perspective the fact that Cohn in 2008 had only found
more negative comments made by scholars associated with Gilbert
et al., and claims to have found no new positive studies, i.e., finds of
Yersinia pestis DNA in plague graves.35 He does however cite a study by
Pusch et al. as supporting the negative stance of the rejecters,36 although
they actually report positive findings of genetic material and proteins
35
In Cohn 2008: 100, footnote132, Cohn maintains that “Few have in fact, corrobo-
rated the findings of the Marseilles team; for the latest of these scientists’ results, see
G. Aboudharam, M. Drancourt, O. Dutour, H. Martin, D. Raoult, and M. Signoli,
“Validation de la saisonnalité des décés et authenticité biologique de la nature de
l’épidémie,” in Bizot, et al. (eds.), op. cit., note 56 above, pp. 63–7 [= La Saison d’une
peste].” This brief statement arguably contains five incorrect or misleading assertions:
(1) it is not true that by 2008 “few have corroborated the findings of the Marseilles
team, as can readily be seen from Table 6 (it would, nonetheless, have been useful if
Cohn had specified the “few”; (2) that in 2008, the paper referred to by Aboudharam,
Drancourt, Dutour, et al. 2005: 63–7, is the last which corroborates the findings of
the “Marseilles team, as can be seen from Table 6, studies nos. 7–10, all published in
the years 2005–07/8; (3) one must also add nos. 3–6 which Cohn has also overlooked;
(4) this study cannot be said to corroborate earlier findings, since it does not include a
new microbiological study of biological material taken from the cemetery at Lambesc,
in this paper, the scholars present early research, microbiological techniques, and find-
ings; (5) however, such microbiological studies performed on biological material taken
from this cemetery are published in nos. 9 and 10 in Table 6.
36
Cohn 2008: 88–9, 100. He appears to suggest in fn. 122 that Aboudharam,
Drancourt, Dutour et al. 2005: 63–7, have corroborated the DNA findings, this is not
the case, since they have not made any attempt.
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of Yersinia pestis in skeletal material from seventeenth-century Stuttgart

(see above Table 6 and comments in footnote 28, no. 6).
In a line of argument that at least comes close to the methodological
fallacy of not fulfilling the principle of invalidatability, Cohn asserts in
his monograph and paper of 2002 that the identification of Yersinia
pestis in the two first studies cannot be correct because it is at variance
with what he designates two “enigmas for biological evolution” based
on central conclusions in his monograph, i.e.: “Why did a disease that
once passed rapidly person-to-person become a rat disease dependent
on a flea vector? Why did the human species once possess an ability to
acquire immunity to this microbe and then lose it?” Cohn reiterates
this stance in his paper of 2008.37 Although Cohn presents these pur-
ported enigmas as based on historical truth or fact established by his
research, they are in my opinion due to combination of seriously flawed
selections of material and misinterpretations which I believe have been
brought to light in this monograph.
The identification of the DNA of the ordinary biovar of bubonic plague

in dental pulp from a plague grave in London dating back to the Black
Death holds important implications. The spread of geographical loca-
tions of such finds were thus greatly expanded, roughly by 1000 km
from south-eastern France to London in north-western Europe at
51° 30' North. Furthermore, the bubonic-plague contagion arrived in
southern England from Bordeaux after having spread via Montpellier
from the first French outbreak in Marseilles whence it arrived by ship
from Kaffa in the Crimea via Messina or possibly via Constantinople.
Thus, the contagion which reached England was in all likelihood the
same that has been identified twice in Montpellier, Yersinia pestis
Orientalis which in all likelihood must have been the original contagion
which was shipped out of Kaffa with Italian galleys in the spring of
1347 and reached Marseilles at the latest in mid-September with subse-
quent epidemic outbreak around 1. November.38 The Black Death was
spread from a port in south-eastern England (possibly London) to Oslo
in south-eastern Norway late in 1348, and probably from King’s Lynn
on the Wash (about 140 km north of London) to Bergen in western
Norway with a(n identified) shipment of grain in the summer of 1349.
37
Cohn 2002a: 248–9; Cohn 2002b: 735–6: Cohn 2008: 88–9.
38
Benedictow 2004: 72–3, 96–104, 123–37.
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394 chapter ten
This makes it highly probable that the Black Death in Norway was also
ordinary bubonic plague caused by the Yersinia pestis Orientalis. The
Black Death spread from Norway into western Sweden and parts of
Denmark in late 1349, and Denmark was also contaminated from
northern Germany in 1350 but quite likely from the same original
“source:”39 the Black Death was probably shipped from Oslo to Elbing/
Elblag in the south-eastern corner of the Baltic Sea in the early autumn
of 1349 from whence it spread into Poland and northern Germany,
northwards into the Baltic area and thence eastwards across Russia.40
This expands greatly the probable extent of the spread of the Black
Death in the form of ordinary bubonic plague in the northerly and
eastern parts of Europe and predicts similar identifications of Yersinia
pestis Orientalis in biological material taken from putative plague
graves relating to the Black Death in these parts of Europe.
Considering the comprehensive evidence available after only ten years

of paleomicrobiological research, there can hardly be any doubt that
the three identified historical pandemics of plague were caused by
Yersinia pestis, principally the Orientalis biovar/pathovar. This also
constitutes independent defining evidence based on identification of
the microbiological nature of the contagion.
This means that the alternative microbiological theories can be con-
sidered invalidated on the basis of these paleomicrobiological studies
on plague, according to usual criteria or tenets of methodology for
invalidation. This means that the French paleomicrobiologists’ trium-
phant conclusion can be accepted: “Our results enabled us to resolve
the long dispute over the aetiology of the Black Death by showing that
the disease was in fact plague caused by Y. pestis.”41
These genetic studies also demonstrate, on the basis of an entirely
independent platform, that Karlsson’s entirely speculative alternative
theory from 1996 to the effect that the contagion of medieval plague
was a mutant of Yersinia pestis which caused pure epidemics of primary
39
In English: Benedictow 2004: 146–78, 196–7, see also an earlier version in
Benedictow 1993/1996: 75–94. The most detailed presentation and discussion of the
arrival and spread of the Black Death in Norway are unfortunately or regrettably rather
written in Norwegian, see Benedictow 2002: 44–57, 67–77; Benedictow 2006: 86–131,
English summary pages. 161–2.
40
Benedictow 2004: see Map 1 between page xvi and I, and 161, 194–202, 209–15.
41
Drancourt and Raoult 2002: 105–09; Drancourt and Raoult 2008b: 153. Drancourt
and Raoult 2008c: 182.
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pneumonic plague can be discarded. The biovars of Yersinia pestis have

now been genetically identified but no such mutant has been discov-
ered in any of the samples, and Yersinia pestis orirentalis has proved to
be the common pathovar of all three pandemics.
Can it be accepted that all advocates of alternative microbiological
theories have collectively failed to discover this development, especially
since they must have known at least the two first genetic studies of this
kind? Would it not be natural for serious scholars to look eagerly out
for further developments and studies? Would it not be natural accord-
ing to this material alone to take a strong renewed interest in how the
alternative theories are argued, their material basis and use of the meth-
odology of history and medical science?
The triumph of the emerging new scientific discipline of paleom-
icrobiology is concordant with the triumph of another emerging scien-
tific discipline, namely zoo-osteoarchaeology which, as shown above,
by now has documented the broad existence of the black rat all over
Europe, also Northern Europe and in the Nordic countries, in Sweden
up to almost the 61st parallel and back to the Viking Period, in Norway
almost up to the 63rd parallel and dating back to at least the early
twelfth century (see above). Even if zoo-osteoarchaeology had not been
established as a scientific discipline, the success of paleomicrobiology
would have indicated that this was the case. Now, the triumphs of these
two new scientific disciplines can be seen to be complementary and
have a synergetic interrelationship or pattern of interaction which pro-
duce decisive evidence to the effect that historical plague epidemics
were bubonic plague.42
Finally, the huge contribution these French paleomicrobiologists
have made to historical science by the development of their techniques
and to historical plague research by their very important findings must
be emphasized.
42
A few years ago, Drancourt, Houhamdi, and Rault 2006: 234–41, presented a
research project which could be misinterpreted as indicating that they considered the
human flea a serious candidate as an important or the important vector of historical
plague epidemics. As mentioned above, in a personal communication in an e-mail of
30 April 2009 Professor Michel Drancourt made it clear that this was not the case, and
that any such notion had been abandoned, but that they still were looking into a
possible role for the human louse. Drancourt, Houhamdi, and Rault 2006: 234–41.
See above: 12, fn. 28.
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CHAPTER ELEVEN
DEFINING FEATURE 5: SEASONALITY OF

BUBONIC PLAGUE
Introduction: Bubonic Plague’s Association with Moderately

Warm Temperatures and Seasons
Bubonic plague has a distinctive seasonal pattern. According to obser-

vations and studies performed in India and other developing countries
with a more or less tropical climate, when humidity is reasonably
favourable, favourable temperatures for plague epidemics are generally
around 20 °C, while temperatures much above or below this range,
generally above about 30 °C and below 10 °C, will weaken or suppress
them. I have pointed out above that it is a fallacy of methodology to
assume that these precise climatic limits apply in more northerly coun-
tries with the implication that bubonic plague is not possible in the
north, since one must take into account the ability of rats and fleas to
evolutionarily adapt to various climates and ecological niches.1 In the
words of G. Lamb, Senior Member of the IPRC: “While plague can
exist and spread under a great range of climatic conditions, it exhibits a
marked seasonal prevalence, which is the most striking feature of the
epidemiology of the disease.”2 Lamb considers the seasonality of
bubonic plague in terms approaching the concept of defining feature;
he also emphasizes that it can spread efficiently under “a great range of
climatic variation.”
This defining feature is mainly due to two central structural aspects
of the epidemiology of bubonic plague springing from its basis in
(black) rats and their fleas:
(1) The natural mortality rate of fleas is high. Levels of temperature
and humidity affect the reproduction of fleas, the rates of egg-laying
and development of fertilized eggs, and the rates of survival and devel-
opment of larvae and cocoons on the ground. This means that in
adverse temperatures and conditions of humidity, the population of
1
See above: 116–22.
2
Lamb 1908: 1, 85.
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seasonality of bubonic plague 397
fleas will not be replenished by reproductive processes and their

number will fall. This will affect the intensity with which a rat-flea pop-
ulation can transmit and disseminate plague and therefore the dynam-
ics of the epidemic process.
(2) Plague septicaemia in rats falls strongly at temperatures below
10 °C. Consequently, in chilly and cold circumstances rat fleas which
draw blood from plague-diseased rats will become much less infected
and will, therefore, develop blockage far more slowly and at much lower
rates. Protraction of this process also implies higher death rates of fleas
from other causes which will contribute to a corresponding reduction
of infected fleas and the further weakening of the disseminative powers
of the flea population.3
This means that the plague season will vary with temperature and
humidity in various countries or within the same country if it covers
two or more climate zones.4 In India and other countries with very
warm summers bubonic plague epidemics will subside and disappear
with the advent of the warm season. In India, for instance,
epidemics normally attain their maximum severity in Bombay in
October; in the Central Provinces in February; in the United Provinces
and Bihar in March; and in the Punjab in April. In the remaining prov-
inces, taken together, March is the month of maximum mortality.5
In Egypt, the plague seasons were March to May in Upper Egypt, April
to June in Middle Egypt, April to July in the Nile Delta and Suez, and
May to October in Mediterranean ports. In Peru, “as elsewhere the plague
seasons fell into an earlier period in areas where the winter months
were warm than in localities with a colder climate.”6
The same two basic factors also explain why historical plague epi-
demics in Europe are strongly associated with the warmer seasons and
falter, subside or disappear with the advent of chilly autumn weather
and cold winter weather. The use of words like “falter” and “subside” is
not fortuitous. One should note that rat fleas are typical fur fleas (and
not nest fleas),7 which means that they spend much of their adult lives
3
IPRC 1908c: 285–8; Lamb 1908: 88–90; Hirst 1953: 270–82, 340–5; Seal 1969:
288–9; Benedictow 1993/1996: 156–70, 227–64.
4
See, for instance, Pollitzer 1954: 20, 22, 24–5, 28, 33, 37, 43, 46, 48–50, 58, 60, 63,
65, 487–90.
5
Pollitzer 1954: 28, 487–90.
6
Pollitzer 1954: 33, 63.
7
IPRC 1908b: 245–6, 258; Liston 1924: 997; Pollitzer 1953: 321; Pollitzer and Meyer
1961: 461; Busvine 1976: 37.
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398 chapter eleven
in the fur of their hosts, enjoying there a relatively warm microclimate

even in chilly or cold weather and ample feeding opportunities. This
explains why plague epidemics can produce cases in chilly or cold
autumnal weather, although at a rapidly diminishing rate. The notion
that plague epidemics stop abruptly with the advent of chilly or cold
weather is erroneous. The notion of Shrewsbury (and some other schol-
ars who have apparently picked up this notion from his monograph)
that the usual flea of the black rat, Xenopsylla cheopis, hibernates in the
winter is a misunderstanding. It is also a misunderstanding that it is a
typical nest flea, although this is the case for most species of fleas.8
Consequently it is a double misunderstanding that this flea normally
hibernates in the host’s nest.9
The same two basic factors explain also why historical plague epi-
demics tended to start earlier and to last longer in Southern Europe
than in Northern Europe.
Seasonality of Historical Bubonic-Plague Epidemics with

Emphasis on the Transseasonal Form
For the same basic two reasons, epidemics in the northerly parts of
Europe will often not have taken their full course through the rat colo-
nies when they are suppressed by cold weather. In many cases, plague
contagion transported by rat fleas or (less often) by infected rats will
arrive late in the plague season, often on merchant ships returning
from abroad at the end of the sailing season, which will have the same
effect. At the end of the plague season, there will therefore quite often
remain a murine epidemic potential that can permit the epidemic to
recrudesce with the advent of warmer spring weather (see below). As
shown in my monograph on the Black Death, this pattern is very evi-
dent in the Black Death in central and northerly parts of Europe (see
below).10 This alternative transseasonal pattern of bubonic plague asso-
ciated with late arrival in the plague season, withdrawal with cold
weather and recrudescence with warmer spring weather was also
8
Shrewsbury 1971: 3, 21, 62, 117; Scott and Duncan 2001: 26.
9
It is another matter that when extra-mural rat colonies die out from plague, fleas
from rats dying in the nest will be forced to stay in the nest, dependent on re-occupation
by new rats for their survival.
10
See Benedictow 2004: 233–5, which contains a summary of these data and the
page references in the index under “seasonality” (418).
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studied in India at the beginning of the twentieth century, especially in

the Punjab where this pattern was quite frequent:
This recrudescence was not due to importation but apparently to an epi-
zootic continuing below ground, progressing slowly during the off-season
on account of a scarcity of fleas, or at least highly infective fleas, but
quickening up with a return of conditions suitable for flea transmission.
The study of seventeen villages in the Pune (Poona) region roughly
100 km south-east of Mumbai revealed the following pattern:
If infection of a village occurred early in the plague season the epidemic
died out before the arrival of the off-season, but when a village was
infected late in the season the disease was apt to linger through the off-
season and to reappear the next season […] the important fact was estab-
lished that all the 17 villages had been infected late in the preceding
plague season.
On this background, a practical scheme was developed for “predicting
the carrying over of epidemics, based upon (1) the size of the commu-
nity and (2) the month in which it was primarily infected.”11
It is correct that bubonic plague in full epidemic form (in contrast to
the endemic or sporadic occurrence) requires a certain minimum level
of temperature in Europe and is dependent on the temperatures of the
warmer seasons. But it is erroneous or fallacious, as has been empha-
sized several times, to assume that this level was exactly the same in
Europe (and across Europe) as in India and to deny or ignore the pos-
sibility of evolutionary adaptation by natural selection of rats and fleas
to various European biotopes or climatic zones. Also in the winter, the
temperatures would in many areas in the southerly parts of Europe
quite often allow a certain low-scale, lingering epidemic or endemic
activity at least temporally, and this could also have overarching sea-
sonal effects. One should also take into account the effects of ocean-
regulated and Gulf-Stream-affected coastal climates in western and
north-western Europe that tend to produce relatively mild winters,
which would no doubt dampen or restrain epidemic activities but not
necessarily suppress them into an enzootic existence among rats or
complete extinction. This is the case even along the coasts of Norway
since the Gulf Stream raises average temperatures by 10 °C.12
11
Wu Lien-Teh 1936c: 397–9.
12
See above: 139.
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400 chapter eleven
With this background we may consider H. Dubois’s summary of the

seasonal pattern of the Black Death in France: “Almost everywhere in
France, the plague has taken on the bubonic form with secondary
manifestations, and most often it has been inhibited or slowed down by
the winter, staying away to re-emerge in the spring.”13 In Rheims, for
instance, the Black Death arrived in the autumn of 1348, too late to
develop an epidemic form, but after the disease had smouldered in the
rat colonies during the winter the outbreak started in April at the latest,
was raging in the summer and reached its “paroxysm” in August.14
Biraben generalizes this information from a historical perspective,
pointing out that the epidemics of bubonic plague which dominate the
scene in France “are arrested or diminished by the cold season.”15
Carmichael states: “Also characteristic was the season of the plague:
throughout the fourteenth century, chroniclers reported a faithful
May-to-September course of plague in each city epidemic.”16
In Northern Europe the plague took on a somewhat different but
predictable version of this pattern. In my doctoral thesis I found no
instance of a winter epidemic in late medieval Norway, and after having
finished my history of Norwegian plague epidemics in 2002, ten years
later, I could conclude that in the 300 years of Norwegian plague his-
tory, from the Black Death to the last epidemics in 1654, i.e., in the
course of more than 30 (waves of) epidemics, there never was a case of
a winter epidemic of plague.17 In his 2008 paper, Cohn maintains,
nonetheless, that “the seasonality of the late medieval plagues does not
resemble that of modern plague […] could occur at any time of year,
including January in places as inhospitable to the subtropical rat flea
[…] as Norway.” He refers for support to my doctoral thesis and to
Walløe 1982, the English translation of “199518 pp. 25 passim” main-
taining that
For the Black Death in Bergen, Norway, in January, see Ole Jørgen
Benedictow, Plague in the Late Medieval Nordic Countries: Epidemiological
Studies, Oslo, Middelalderforlaget, 1992, p. 44. For plague in Trondheim,
13
Dubois 1988: 316. My translation from French.
14
Desportes 1977–2: 795–6.
15
Biraben 1975–1: 86. My translation from French.
16
17
18
Walløe mentions in the preface that it was mostly finished by 1977, Walløe
1995: 4.
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Norway, that peaked in February 1566 and many other examples of win-
ter outbreaks in Scandinavia, see Lars Walløe, Plague and Population:
Norway 1350–750.19
Neither on page 44 in my doctoral thesis nor elsewhere in it, is it stated
that the Black Death raged in Bergen in January 1350 simply because
there is no evidential basis for it. The few dated or datable sources relat-
ing to the Black Death in Bergen are from September 1349, the earliest
from briefly after 8 September and the last from 26 September. On page
44, the account in the Icelandic Lawman’s Annal is cited on the circum-
stances leading to the contamination of Bergen by a ship from England.
In my Norwegian plague history, I have quite likely identified this ship
together with the merchants from King’s Lynn who in early May, while
the Black Death raged in the areas on the Wash, received royal permis-
sion to sail to Norway with 1000 quarters of grain,20 the most danger-
ous of all goods with respect to metastatic spread of rat-flea-borne
plague. The time perspective fits nicely to a scenario where a ship sail-
ing from King’s Lynn in the early summer of 1349 and putting into the
harbour of Bergen in the first half of July with a cargo of grain infested
with infective rat fleas which first unleashed a rat-epizootic. According
to the usual development pattern of rat-flea-borne plague, it would
produce an early epidemic phase among the human population about
six weeks later and develop into a full-blown epidemic in September,
when it would start to take its toll among the upper classes and scare
them into making their wills. According to the mortality pattern of
Table 7 showing the development of mortality in the plague epidemic
in Bergen 1565–6, the Black Death would be expected to begin to
diminish abruptly in November or perhaps in late October since it
apparently arrived earlier in the season than the 1565–6 epidemic, and
it would disappear around the turn of the year. Cohn refers also to
Walløe 1995: 25 passim for support of the assertion that a plague epi-
demic peaked in Trondheim in February 1566. This assertion is also
without basis in the text referred to. The historical source on plague in
Trondheim on this occasion is a notice in the Diary of Absalon Pederssøn
(Beyer),21 the highly regarded Norwegian humanist and ecclesiastic in
Bergen, where it is stated in his entry for February 1566 that he had
19
Cohn 2008: 78 and 92, fn. 38.
20
Benedictow 2004: 137–40, 149, 154–6.
21
Absalon Pederssøn 1963. My translation of the title into English.
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402 chapter eleven
received a letter from a priest in Trondheim informing him that “600

persons had died from plague in this town.” Walløe cites the source
correctly, and there is no way it can be understood to the effect that the
epidemic peaked in Trondheim in February or that it took the form of
a winter epidemic.22 On the contrary, it is implied by the use of the past
tense and by the rough estimate of the number of victims that the epi-
demic had been over in this small town for some unspecified time.
Clearly, this indicates the normal seasonal pattern, the epidemic hav-
ing broken in the early autumn, quite likely after importation from
Bergen, and declined and disappeared with the arrival of cold weather.
Moreover, during the plague epidemic in Bergen 1565–6, Absalon
Pederssøn indicates in his diary the number of dead persons brought
each day to the Cathedral in Bergen for burial in its function as a parish
church. This information provides the opportunity to follow closely the
development of the plague epidemic in detail, particularly as he speci-
fies the few cases which were not caused by plague and because he pro-
vides increasing information on the number of plague victims being
brought to the other three parish churches in the city. This information
is summarized in Table 7 and Figure 2 below, which shows that the
epidemic broke out in early September 1565, peaked predictably in
November and then was rapidly diminishing until it disappeared, a
pattern that was repeated the next autumn. The number of victims in
February 1566 was only a small fraction of the number of victims in
November. This seasonal pattern is, of course, inexplicable with respect
to diseases spread by cross-infection and must almost inevitably reflect
a disease transmitted and disseminated by insects on which chilly and
cold weather have strong deleterious effects (above). Cohn’s further
reference to “many other examples of winter outbreaks in Scandinavia”
according to Walløe’s account is also not correct. Since Walløe men-
tions only Norwegian epidemics, this can be confirmed in my history
of Norwegian plague where all epidemics are identified and all sources
are presented and discussed extensively. In his Diary, Absalon Pederssøn
provides information on the introduction of the contagion and the first
cases which lends itself to epidemiological analysis and makes it pos-
sible to identify a period of latency which is a defining feature of rat-
flea-borne plague (see above).23
22
23
Benedictow 2002: 190–4. Above, Chapter 7.
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In the period 1348–1599 plague was mainly imported into Norway

from England, occasionally also from the Netherlands, probably from
England:24 the microbiological basis would have to be the same. In
Norway, the Black Death evidently arrived in Oslo in the autumn of
1348 with ship(s) returning from south-eastern England, was sup-
pressed by cold weather, and broke out again in April, as it seems; a
new introduction of plague from England took place in Bergen in the
summer of 1349. From these two bridgeheads or epicentres the epi-
demic spread across Norway in 1349 and petered out and became
extinguished at the end of the year with the advent of winter weather;
there is no evidence of epidemic activity in the winter of 1350. Only
one person is known to have died from the Black Death in Norway in
1350, namely the bishop of Stavanger who died 7 January, which con-
firms the seasonal pattern and the Black Death’s rapid disappearance
with cold winter weather.25
In Sweden the Black Death was introduced into a few localities across
the border in late 1349, from Halland (Denmark) whence the Black
Death had presumably come by ship from Oslo to Halmstad, into
Småland, from south-eastern Norway into Västergötland, and to Visby
in Gotland Island in the Baltic Sea late in 1349 by a Hanseatic ship. In
all three cases, the epidemic was suppressed by cold weather and broke
out again in the spring to spread all over the country in 1350 from the
bridgeheads in the west and disappeared at the end of that year. In
Denmark, the Black Death was introduced in Halland in the summer
whence it spread southwards along the coast to the cathedral city of
Lund which it reached at the end of 1349, and was also introduced in
the town of Ribe in the south-western corner of the country (Jutland)
at the end of 1349. Also in these cases, the epidemic developments were
arrested by cold winter weather and recrudesced with warmer spring
weather, and from these bridgeheads spread all over Denmark in 1350,
again to disappear with cold weather at the end of the year.26
This means that in the case of Oslo in Norway, and the points of
introduction in Sweden and Denmark, the Black Death developed
according to the transseasonal model or pattern. Probably in all these
cases plague was introduced in Sweden and Denmark from Norway
24
Benedictow 2002: 103–8, 131, 139–43.
25
Benedictow 2002: 47–82; Benedictow 2004: 149–58; Benedictow 2006: 86–123,
128–31.
26
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404 chapter eleven
which had received the contagion from England, and one should there-
fore expect that the disease was the same with the same basic epide-
miological properties and that the seasonal pattern should be broadly
similar when it is taken into account that England is situated south of
Scandinavia and enjoys a milder Atlantic climate and the effects of the
Gulf Stream.
Predictably some subsequent plague epidemics took on this trans-
seasonal form, being suppressed by chilly and cold weather but break-
ing out again in the spring, producing a bimodal curve of mortality
showing two peaks. Some examples may be useful. At the end of August
1547 plague broke out in Oslo; around 20 September the epidemic had
developed such a severe form that the commander of Akershus Castle
in Oslo left the castle for his manor in a nearby island where he could
isolate himself and his family. With the advent of cold(er) weather the
plague declined and disappeared. However, 24 April the commander
wrote to the Chancellor of the Realm Eske Bille that “the plague had
broken out again and raged severely.”27
Importantly, this pattern does not manifest itself only in Northern
Europe but also in the Alpine areas much further to the south where it
is high altitude that makes for cold winter climate. Spreading north-
wards from its original epicentre in Venice, the Black Death crossed the
Tyrolese Alps at the Brenner Pass in July 1348, reaching deep into
Austria in some areas in the autumn of 1348, ravaging the inner moun-
tain areas of the province of the Tyrol in September, and breaking out
in areas west of Innsbruck, among other places. The distance from
Innsbruck to the present-day German border is roughly twenty-five
km which distance the disease should have been able to cover in (less
than) a month. However, the Black Death did not advance further into
the Alpine areas and did not break out in southern Germany until the
following (late) spring. At lower altitudes the epidemic could continue
its spread, although at a moderate pace: spreading westwards the Black
Death reached Pfäfers about 200 km from the Brenner Pass in eastern
present-day Switzerland in May 1349. Presumably the onset of cold
winter weather is the reason that the Black Death did not proceed
directly from its outbreak in November in Constance on the central
Swiss-German border into Germany’s south-western province of
Baden-Würtemberg. The Black Death was forced to postpone its
27
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invasion of south-western Germany from this advanced position until

the arrival of spring brought warmer weather. Much the same appears
to have happened with the Black Death’s spread out of the Swiss city of
Basle on southern Germany’s south-western corner in the spring. Many
German Hanseatic cities on the North Sea and the Baltic Sea were
infected in the late autumn of 1349 with the return of the ships.
However, except for a few recognized outbreaks that soon were sup-
pressed by the advent of cold winter weather, it was not until the fol-
lowing spring that the Black Death broke out in force and formed a
northern plague front spreading southwards which met the southern
plague front which was moving northwards somewhere in central
Germany.28 Thus, clearly the transseasonal pattern was an important
feature of the Black Death in Austria, Switzerland and Germany.
Since the plague contagion of the Black Death was introduced into
England from France where, as underlined by Dubois and Biraben, the
transseasonal form of the epidemic was usual, it is difficult to imagine
why the Black Death should not tend to take on the same pattern in
England when differences in climate are taken into account. Twigg takes
another view: “high mortality in late spring and early summer would
not be typical of bubonic plague and illustrates the point that the disease
produced heavy loss of life when it first made contact in a new area, no
matter what time of year that was.”29 This means that he has overlooked
or ignored the transseasonal form of plague. Twigg uses as evidential
support the sequence of plague events at the manor of Fingrith in
south-western Essex where the outbreak manifested itself in an abrupt
increase in the registered deaths among the tenants at the court of 23
March and raged during the following months.30 Interpretation of the
events at this manor requires a much broader perspective. The Black
Death broke out in London at the end of September and had by the end
of 1348 broken out in various localities along the south-eastern coast
up to the R. Stour, the border river between Essex and Suffolk/ East
Anglia. Since Fingrith is situated only about twenty-five km from London,
it appears quite likely that the manor was infected from London some
time in the late autumn of 1348, and that the epidemic processes had
been suppressed by cold weather but re-emerged with the advent of
mild spring weather, according to a usual pattern of bubonic plague.
28
Benedictow 2004: 120, 181–2, 186–7, 194–201.
29
Twigg 1984: 69.
30
Fisher 1943: 13–4, 19–20.
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406 chapter eleven
Table 7. Plague in Bergen 1565–6. Mortality in the Cathedral’s parish

Year Month Deaths
1565 September 33
October 66
November 113
December 66
1566 January 27
February 14
March 7
April 0
May 1
June 2
July 0
August 70
September 229
October 133
November 35
December 4
1567 January 0
Schofield comments sensibly on such matters in his study of plague

in Colyton in 1645–6 where plague first struck in the autumn but was
soon wholly or mainly suppressed by cold autumn and winter weather,
so that the level of mortality was quite modest until late spring or the
early summer, when the plague epidemic took on a dramatic character.
Schofield points out that there are “few examples of plague persisting as
a human epidemic through the inhospitable north European winter
months.” The ability of plague to carry episodically on through adverse
climatic circumstances reflects that “the micro-climates of rodents’
habitats continue to provide favourable conditions regardless of sea-
sonal changes outside,” which was, as shown above, also true for black
rats in the Nordic countries. One should in this context keep in mind
that the black rat’s fleas are fur fleas riding in the fur of their hosts,
there enjoying a relatively warm micro-climate even in cold weather
and easy access to nutriment, and that the black rat with its fondness
for human habitats, including the housing of domestic farm animals
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(where maids or farm-hands often slept), would tend to live in consid-

erably higher temperatures than prevailed outside during Nordic win-
ters. It is the reproduction of fleas that is seriously affected by chilly or
cold weather and, thus, the size of the flea population and its collective
vector capacity and also the level of septicaemia in rats (see above).
Another point is that “if the winter were warm and wet, the persistence
of plague through an English winter must be entertained as a serious
possibility.”31 Thus, the view that Twigg and Scott and Duncan present
as an absolute truth, that plague epidemics could never take place in
the winters in England, is not warranted, and does not constitute proof
that these epidemics could not have been bubonic plague. Episodically,
higher temperatures and other circumstances could allow plague epi-
demics to continue through the mild English winter months, albeit at a
relatively low level of intensity.
Schofield emphasizes that the transseasonal pattern (without using
the term) with bimodal mortality curve is typical of plague, referring to
a number of later outbreaks of bubonic plague epidemics in England
and Sweden as evidence.32 A beautiful instance of an epidemic with this
transseasonal form is provided by Shrewsbury, namely the epidemic
at Colchester 1665–6.33 This pattern is, of course, inexplicable for
diseases spread by cross-infection, but easily explicable for rat-flea-
based epidemics of bubonic plague. Other aspects of the seasonality of
the Black Death in England will be discussed at quite some length
below.
The information Absalon Pederssøn gives on a daily basis in his
diary on the number of dead persons brought to the Cathedral in the
plague epidemic 1565–6 indicates an interesting alternative, the two-
seasonal plague epidemic. In Table 7 and Figure 2 the development of
mortality in the Cathedral’s parish is organized according to month
and shows a very distinctive seasonal pattern. The surge in mortality
was clearly checked by chilly autumn weather followed by moderately
wintry weather typical of this south-western coastal town on the North
Sea, which first produced a rapid fall which developed into a slower
final phase of decline ending in no plague cases in April and insignifi-
cant or no plague mortality the following months. However, the plague
31
Schofield 1977: 101 and footnotes 33–4.
32
Schofield 1977: 101.
33
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408 chapter eleven
250
200 1565 1566 1567
150
100
50
0
O er
o v er
Ja er
Fe ary
M ry
ch
il
ay
ne
A ly
pt st
O er
ov er
em r
Ja er
y
ec e r
D be
ar
pr
Se ugu
Ju
b
b
N ob
b
b
N ob
ua
ar
Ju
M
em
em
nu
em
em
nu
em
A
br
ct
ct
pt
ec
D
Se
Figure 2. Plague in Bergen 1565–6. Mortality in the cathedral’s parish.
broke dramatically out again in August and developed explosively until

chilly autumn weather and increasingly wintry weather again caused a
rapid decline; in December only four cases of plague mortality were
registered, in January there was no case and the epidemic was finally
over. Late autumn and wintry temperatures hit at the heart of the epi-
demic’s dynamic powers and set it on a more or less rapidly declining
course that reflected the degree of chilliness or coldness of prevailing
temperatures, in both cases ending with the complete disappearance of
plague cases. The long interval of four months (April to July) with no
cases or with one or two cases respectively, and no case in July at the
height of warm summer temperatures, is conspicuous and indicates
that the epidemic was extinguished by the winter weather of 1566 with-
out having exhausted the murine epidemic potential and that the out-
break in August 1566 was due to re-importation. The epidemic clearly
took up its course where it had ended and died out in the same order as
it had broken out in the parishes. The two-seasonal pattern based on
re-introduction draws support from the fact that there was one plague
death in August and one in October 1567, eight to nine months after
the last plague death in December 1566. These cases must also reflect
independent re-introduction, however, at a time when the murine basis
was exhausted in a city of 5000–6000 inhabitants,34 but suggest that in
big urban centres a multi-seasonal pattern could occur.
34
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These epidemic case histories illustrate the deleterious effects of

chilly and cold weather on plague epidemics: cold weather could either
lead to the extinction of the epidemic or diminish it to the point that it
would go underground and disappear from the human scene, smoul-
dering in the rat colonies in a process that could be revealed by the
occasional case. In order to understand the developments more fully,
one should take into account the fact that there would be a delay of a
couple of weeks from when chilly weather sets in and when the nega-
tive effects on the reproduction of fleas and the reduction in the levels
of septicaemia in rats would start to affect the development of the epi-
demic, since the number of heavily infected and infective fleas will not
fall instantaneously but in a gradual process.
This characteristic temperature-dependent feature of plague epi-
demics was recognized by contemporaries. In November 1545, the
Danish Chancellor of the Exchequer Joakim Beck wrote from Roskilde,
Zealand Island’s cathedral city situated about thirty km north of
Copenhagen, to the soon-to-be Chancellor of the Realm Eske Bille:
“I will not advise you to go to Copenhagen before it begins to freeze
and the plague stops to reign there in the city. I intend to pass the
waiting time here in Roskilde.”35 In 1641, a Londoner claimed that a
proposed day for religious humiliation to ward off plague was unneces-
sary, because “winter was coming on, and then the plague would be
stayed.”36
The peculiar pattern of seasonality in historical plague epidemics
can, as shown above, be explained by the properties of rats and rat fleas
and their roles or functions when contaminated by plague contagion.
All alternative theories of the microbiological nature of historical
plague epidemics which cannot on empirical grounds explain why the
mechanisms of transmission and dissemination would produce such a
seasonal pattern and be compatible with this feature are ipso facto falsi-
fied. The central argument of this chapter has three main parts:
(1) this seasonal pattern can only be explained by the epidemiological
properties of rat-flea-borne bubonic plague;
(2) this seasonal pattern is incompatible with diseases spread by cross-
infection; and
(3) none of the alternative theories can explain this pattern.
35
Benedictow 2002: 40. My translation from the source into English.
36
Slack 1985: 239.
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410 chapter eleven
The plague epidemics at Penrith in 1597–8 and Eyam in 1665–6, which

both display a transseasonal pattern, are incompatible with any viral
theory based on interhuman transmission, but are easily compatible
with bubonic plague. Scott and Duncan’s discussion of these epidemics
is peculiarly strained and untenable.37 Eyam has been studied by
L. Bradley and M.P. Coleman on the basis of demographic parish
reconstitution techniques and the disease has been shown by both
scholars to be compatible with bubonic plague, including with respect
to the seasonal pattern,38 a fact which is conspicuously difficult to dis-
cern in Scott and Duncan’s discussion of it.
This seasonal pattern is incompatible with all epidemic diseases
spreading by cross-infection because it does not comply with the cen-
tral principle of epidemiology which is formulated so well by Burnet
(and White)39: “no matter by what method a parasite passes from host
to host, an increased density of the susceptible population will facilitate
its spread from infected to uninfected individuals.” All infectious dis-
eases spread by cross-infection flourish in chilly and cold weather: they
gain strength from people’s intuitive and practical reactions which are
to stay or huddle closer together, remain indoors more and restrict liv-
ing space for better and more efficient heating. The net effect is to bring
people closer together, in other words to increase population density at
the micro-level of human behaviour, which means that all interperson-
ally communicable diseases will gain increasing powers of spread. By
implication, all alternative theories based on assumptions that histori-
cal plague was spread by cross-infection must be untenable, namely the
theories of Morris and Karlsson, Scott and Duncan and Cohn. This
seasonal pattern is a defining feature of bubonic plague.
How do the advocates of alternative theories address the compelling
evidence on plague seasonality and defend their theories against its
potentially devastating effects? They employ three strategies:
(1) they attempt to reject the evidence of seasonality;
(2) they argue that seasonality did not apply to their alternative infec-
tion for some special reason;
(3) they argue that the Black Death did not exhibit seasonality, though
subsequent plague epidemics did, but that the Black Death and
37
Scott and Duncan 2001: 114–48 (Penrith), 261–83 (Eyam); Scott and Duncan
2004: 5–8, 153–62 (Penrith), 191–206, 212–3 (Eyam).
38
Bradley 1977a; Coleman 1986.
39
Revised edn. of 1972.
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subsequent epidemics were, nonetheless, the same disease, and

that the pattern of the Black Death proves that historical plague
epidemics were not bubonic plague.
Although anthrax is not generally, or is only sporadically, transmitted
by cross-infection between human beings, Twigg realizes the inherent
danger to his theory posed by the question of compatibility with plague
seasonality and presents some peculiar arguments which later are
picked up by Scott and Duncan, while Cohn relies mainly on his own
line of arguments and again more or less confines his attention to
northern Italy and Italian chroniclers. Twigg’s first climatic argument
against the possibility that the Black Death was bubonic plague is that
the epidemic, he asserts, moved (freely) across the Alps into southern
Germany in the winter of 1348–9, and Davis and Scott and Duncan
pick up the argument in closely related wordings.40 As shown above,
this is wrong. Twigg also launched the argument that the Black Death
ravaged Greenland, which would, of course, have been a good argu-
ment if it were not fictitious.41 Since Greenland is not mentioned in
Twigg’s index, the whole monograph must be read carefully in order to
discover the argument and reveal its true character.
Cohn starts his discussion of the seasonality of plague by citing
Burnet’s prestigious monograph Natural History of Infectious Disease
(3rd. ed.) to the effect that diseases of the past must be studied not only
according to clinical indications but also according to their epidemiol-
ogy. Of course, the seasonality of epidemic diseases is part of their
epidemiology. However, Cohn passes again in silence by Burnet’s pres-
entation of the central principle of epidemiology, the link between
increasing density of (susceptible) population and the powers of spread
of infectious diseases disseminated by cross-infection, whatever the
means or mechanisms of transmission. The reason for Cohn’s neglect
of this principle seems obvious: it would immediately reveal the unten-
ability of his alternative theory based on a viral disease spread by cross-
infection which would inevitably present itself as a disease thriving in
cold weather when people stay closer together and the density of peo-
ple is higher. All alternative theories on the microbiological and epide-
miological nature of historical plague must satisfy the criterion of a
40
Twigg 1984: 57; Davis 1986: 460; Scott and Duncan 2001: 87.
41
Above: 98–9.
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412 chapter eleven
disease strongly associated with the warmer seasons and exhibit weak
properties for spreading in chilly and cold weather.
Cohn’s approach also to this matter of seasonality is characterized by
his neglect of the work of historical demographers with their demand
for quantifiable source material in order to secure a high level of empir-
ical tenability. Instead, Cohn considers that the sources suited for the
study of the seasonality of historical plague are chronicles, which how-
ever are characterized by their inaccuracy and subjectivity, especially
in the relatively narrow perspective of Italian chronicles. However,
plague’s typical association with the warmer seasons is a very conspicu-
ous feature even of Cohn’s material and cannot simply be explained
away: a summary of his citations of various chroniclers will show a very
heavy preponderance of references to the warmer seasons.42 It is not
correct that “a reading of the chronicles might suggest that the medie-
val bubonic plague had no season and could strike at any time.”43 The
distribution of seasonal identifications of plague epidemics by chroni-
clers relates overwhelmingly to the warmer seasons. As underlined
above, in Southern Europe weather conditions may occasionally allow
plague in epidemic form in the winter, albeit at quite a low level of
intensity. Sporadic outbreaks in chilly weather or winter months, which
can reflect mild weather for the season, cannot override the fact that in
the overwhelming number of cases historical plague epidemics are
associated with the warmer seasons. It is erroneous not to take into
account the fact that bubonic plague can arrive in the late autumn or
winter with contaminated goods or luggage, progress slowly among the
rats and produce sporadic human cases for some time, and with the
advent of warmer spring temperatures develop into a serious epidemic
form that would impress chroniclers.
Also in the case of Italy, the results of studies on the seasonality of
plague by historical demographers are very clear, but since Cohn has
succeeded in avoiding all of them, some central findings shall be pre-
sented here. Herlihy and Klapisch-Zuber provide very strong material
on the seasonality of plague in Tuscany. For the period 1251–1500 they
succeeded in individualizing according to month the deaths of 939
persons who died in plague years and 1614 persons who died in plague-
free years. They found that 85.6 per cent of all deaths in plague years
42
Cohn 2002: 140–87, 209–10.
43
Cohn 2002: 140.
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occurred in the six months April to September, whilst 54 per cent of all
deaths took place in these six months in plague-free years, near the
normal distribution. They were also able to distinguish the cause of
death for 4711 persons in the period 1424–30. Among these 4711 per-
sons 3296 or 70 per cent died from plague, and among those who died
from plague 3091 or 93.8 per cent died in the six months May to
October.44 This reveals that 5.85 per cent of plague mortality in this
southern European city occurred in the months January to March and
almost the same percentage in the months November and December.
In Southern Europe, plague cases can occur in any month, but the
overwhelming majority take place in the warmer months or seasons. In
fact, with the arrival of the Black Death and subsequent plague epi-
demics in the period 1348–75 nearly a quarter of all Florentine deaths
took place in July, which contrasts sharply with the preceding period
1276–1347 when 9.4 per cent of all deaths took place in this month.45
Herlihy and Klapisch-Zuber conclude: “The concentration of the deaths
in the summer months corresponds well to the description which con-
temporaries make on the great plague epidemics,” and go on to cite
Giovanni Morelli, the chronicler, who writes that plague “begins to
make itself felt in February and goes on to grow until it peaks in July
[…].”46 This seasonal pattern corresponds quite closely to that of the
Black Death in Tuscany where the outbreaks were noted in Pisa in
January, in Lucca in February, and in March in Florence where accord-
ing to Matteo Villani the disease developed rapidly from April reaching
its peak in the summer and lasting until the end of September.47 This
pattern is strongly reflected in the dates at which many wills were writ-
ten, if we take into account the usual delay between the outbreak and
the time the will-producing social classes feel threatened.48
Del Panta provides other instances of transseasonal plague epidem-
ics in Italy, in Mantua 1575–6, in many localities in Tuscany 1630–1,
and in Genoa 1656–7. In all three cases, the original outbreaks were
quite late in the autumn, in October, and seemingly disappeared with
the arrival of winter weather, but recrudesced in the spring.49 In Rome,
44
Herlihy and Klapisch-Zuber 1978: 192, 465.
45
Herlihy and Klapich-Zuber 1978: 193–4.
46
Herlihy and Klpaisch-Zuber 1978: 192. My translation from French.
47
Matteo Villani Cronica 1995–1: 13; Falsini 1972: 432–3; Benedictow 2004: 93–5.
48
See Cohn 2002: 158. Cf. 150–71, 178–84. See above: 401; below: 431.
49
Del Panta 1980: 50–1, 53–4.
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414 chapter eleven
where the epidemic of 1656–7 broke out in July, the epidemic com-
pleted its course in the plague season, albeit with the peak skewed
towards the autumn months, indicating that if the contamination of
the city and the subsequent outbreak had been a little later, the epi-
demic process would not have been completed in the warmer seasons
and could have taken on the transseasonal form. Del Panta also points
out the association of bubonic plague with warmer seasons and under-
lines its connection with the role of rat fleas,50 the only viable explana-
tion. This helps to explain why Cohn, who relies so heavily on Italian
material, especially chroniclers and wills, passes in silence by this
standard work by a leading Italian historical demographer. Whatever
chroniclers wrote, the hard demographic statistical data speak loudly
to the effect that a new disease had arrived in Italy that dramatically
changed the usual seasonal pattern of mortality and produced a heavy
preponderance of mortality in the summer months and adjacent rela-
tively warm spring and autumn months. Only bubonic plague is char-
acterized by this seasonal pattern of mortality and only in the case of
bubonic plague can this pattern be epidemiologically explained.
Importantly, Herlihy and Klapisch-Zuber and Del Panta have made
both their data and their conclusions testable by other scholars. Italian
chroniclers can be shown to provide valuable information on the mat-
ter: they overwhelmingly relate plague epidemics to the warm(er)
seasons.
Cohn’s citations of various types of statistics regarding wills and
mortality in the form of figures associated with various hospitals and a
couple of burial grounds of ecclesiastical institutions in the period
1348–1400, mostly in Italy but also in other regions, overwhelmingly
show plague’s association with warm(er) months and seasons.51 Much
of Cohn’s presentation of this material deserves serious criticism, but
since he cannot get away from the pivotal point, historical plague epi-
demics’ close association with the warmer seasons or months, this can
be dispensed with. There is much more severe criticism to come.
However, seasonality is a material feature of epidemiology. Cohn starts
his chapter on seasonality by citing Burnet to the effect that historical
epidemic diseases must be studied according to their epidemiology,
but in the presentation and discussion of his material he ignores this
50
Del Panta 1980: 48–9.
51
Cohn 2002: 156–9, 161–73, 181–5.
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crucial point. Instead, he attempts to explain away the strong seasonal-

ity of plague epidemics with some rather peculiar arguments on fleas
and climate that he maintains prove that this seasonality, nonetheless,
was not an epidemiological reflection of the central role of rats and
their fleas.52
Cohn makes extraordinary comments on some of the developments
of plague seasonality in England, and claims that there should be peaks
in the late autumn and criticizes Slack and Schofield for maintaining
the established view of plague seasonality.53 As underlined repeatedly
above, the peaks of plague epidemics are affected by the time of arrival
in the plague season, and especially under favourable climatic circum-
stances late arrivals would make for late peaks. A couple of late autum-
nal peaks in Bristol in the sixteenth century do not constitute a change
of pattern, and Slack and Schofield, who know that plague epidem-
ics in England continued to be overwhelmingly associated with the
warmer seasons according to a long established systematic pattern,
have no reason to change their views on the matter. There will be occa-
sion to present much of this material below. Cohn tries to undermine
the rat-flea theory when he asserts in the concluding pages of his mon-
ograph that plague epidemics in the Mediterranean regions strike con-
sistently “during the hottest and driest months of the year” but “north
of the Alps” broke out “in the cooler and wetter autumn.”54 This is not
correct: all over Europe plague epidemics were associated with the
warmer months or seasons. The point is simply that since warmer
weather develops later north of the Alps, plague epidemics there will
tend to rise later and not complete their spread in the rat colonies
before later in the autumn, a pattern that is, of course, easily explicable
on the basis of the rat-flea theory of plague. Cohn naturally does not
make the point that this epidemiological pattern of seasonality which
is so easily compatible with the rat-flea theory of bubonic plague is
incompatible with his theory of a viral disease spread by interhuman
cross-infection.
Scott and Duncan enlarge on Twigg’s false arguments that the Black
Death crossed the Alps into Southern Germany in the winter of
1348–9 and his statements about plague in Greenland. They assert that
this “pandemic [the Black Death: my insertion] even reached the polar
52
Cohn 2002: 175–8.
53
Cohn 2002: 185.
54
Cohn 2002: 251.
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416 chapter eleven
regions,” reiterating six times that also Greenland and Iceland were
invaded by the Black Death and claim that this constitutes proof that
the epidemic could not have been bubonic plague: “It is inconceivable
that bubonic plague could have spread rapidly in winter, over alpine
passes and through sub-Arctic regions including Iceland, Norway and
Greenland.”55 The fact that I have written a monograph on plague in the
Nordic countries in the Late Middle Ages is ignored. The juxtaposition
and implied identity of the concepts “polar regions” and “sub-Arctic
regions” are quite extraordinary: according to dictionaries the term
polar means “of or near the North or South Pole,” hence “the polar
regions.”56 No scholars other than Scott and Duncan have asserted that
there ever was a bubonic plague epidemic on or near any of the poles,
for obvious demographic reasons. As shown above, the Black Death
never came to Greenland or Iceland, there is no factual basis for this
assertion, it has been taken out of thin air. And as shown below, the two
purported plague epidemics in Iceland in the fifteenth century cannot
for several independent sufficient reasons have been plague. In short
there never was an epidemic of plague in Iceland, neither bubonic
plague nor primary pneumonic plague.
Scott and Duncan also accept uncritically Twigg’s assertion that the
climate in Northern Europe was too cold to allow fleas to breed and
that for this reason there could not have been plague epidemics in
England, Scotland or Norway. This contrasts sharply with the brief
opening statement of the IPRC in a chapter on the “Distribution of
Fleas, Geographically and on Animals”: “Fleas are found in all climates
from the arctic regions to the tropical zones.”57 Scott and Duncan also
add unreservedly as an objective fact: “It is important to remember that
during the Little Ice Age, when the plague was rampaging most fiercely,
the conditions would have ensured that flea breeding was absolutely
impossible.”58 Obviously if flea-breeding was impossible in Northern
Europe there could not have been any fleas there or bubonic plague.
One may wonder how it could be that medieval and early modern
Scandinavians, obviously inhabitants of Northern Europe were plagued
by fleas in the period covered by the misnomer “the Little Ice Age” (see
below). Colloquially, with an element of black humour, old-time
55
Scott and Duncan 2001: 57, 81, 98, 108, 109, 357, 376.
56
Oxford Advanced Learners Dictionary 1990: 957.
57
IPRC 1908b: 245.
58
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Norwegians called their beds “fleaboxes,” so as the English “hit the hay,”
old-time Norwegians hit the “fleabox.” And how can it be that in the
Nordic countries many types of wild animals and birds are plagued by
fleas, although they do not live indoors in heated rooms but have to
endure the cold winter climate in nests and lairs in the “woods so wild”?
A shown above, this was also the case with rats, and the black rat was
the only rat in the Nordic countries in the Middle Ages. The modern
grey or brown rat, which was first described in the Nordic countries in
Norway around 1750 (which is the reason it is called Rattus norvegi-
cus), have substantial numbers of fleas in their nests in the Nordic
countries.
Scott and Duncan’s concept of the Little Ice Age is an exaggerated
version of a misnomer. In the period ca. 1540–1830, there was indeed
a slight fall in average temperatures in Europe, however, the tiny sig-
nificance of this development is demonstrated by the fact that the first
hundred years of this period saw the taking up of all lands all over
Europe that had become deserted in the late medieval period and the
recuperation of European populations after the precipitous decline of
that period.59 In the period c. 1520–1666, the number of agricultural
holdings in operation in such a northerly country as Norway increased
from c. 23,500 to 58,000; in addition many thousands of new underset-
tlers/ sub-tenancies were established within their territories, and the
number of both holdings and undersettlers continued to expand all
through the so-called Little Ice Age: even the deserted mountain settle-
ments were resettled and expanded. And this development took place
even in northern Norway. In a broader European perspective, this sub-
ject should certainly be discussed in relation to E. Le Roy Ladurie’s
sober works on the interaction of historical climate and historical
change with emphasis on the period in question.60
The implication that Norway is situated in the “polar regions,” what-
ever the meaning of this term, even in the implied highly unconven-
tional meaning of sub-Arctic, must be taken as an expression of great
geographical and conceptual confusion. Norway is not situated in a
sub-Arctic region, this is only the case for the northernmost parts of
Norway containing only a tiny part of the Norwegian population; in
59
The exception is England, but this was not due to climate but to profound demo-
graphic changes. Hatcher 2003.
60
Le Roy Ladurie 1965: 899–922; Le Roy Ladurie 1967. Le Roy Ladurie 1974:
3–30.
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418 chapter eleven
the Middle Ages this proportion was even smaller than it is today. It is
an expression of great geographical and conceptual confusion also
because the term is climatically and biologically determined and not
mechanically associated with latitude.61 One should note that the Gulf
Stream produces a climate in Norway with average temperatures about
10 °C. higher than would otherwise be the case.62 Central Norway
(Trøndelag), situated roughly at latitudes 63–65°, corresponding to the
southern half of Iceland and the region around Godthåb about 500 km
north of the southern tip of Greenland, is a rich agricultural area pro-
ducing, among other things, large amounts of Norway’s grain, vegeta-
bles and strawberries.
In the Middle Ages Norway was generally self-sufficient in grain,
and the central region of Trøndelag produced a surplus which was sold
in the adjacent eastern county of Jemtland, in the western coastal areas
of Namdalen and Fosen, and to some extent in southern parts of north-
ern Norway.63 The situation was entirely different in Greenland or
Iceland, in fact, early attempts at growing grain in those regions were
rapidly given up. Only the tiny fishing population in villages along the
coasts of northern Norway was largely dependent on importation of
grain from abroad, exchanging stockfish for grain with Hanseatic mer-
chants in Bergen. These fishing villages were mainly established on this
economic basis, and at the time of the Black Death this development
was in an early phase. Unfortunately, the fishers and fisher-peasants
61
It is also highly surprising that Norway should be thought to be part of sub-Arctic
regions in the ordinary scholarly meaning of a border zone between the Arctic regions
and the temperate climatic regions. Assuming that the point relates to the part of
Norway situated north of the Arctic Circle and the population living there at the time
of the Black Death, the following remarks will be relevant: this population consisted
mainly of an ethnic Norwegian population living up to or quite near to the border of
the most northerly county of Finnmark, on about 2400 individual agricultural settle-
ments (subsisting mainly on a combination of animal husbandry and fishing) compris-
ing a population of about 11,000 persons, and in addition those living in the few fishing
villages in operation at the time. At the time, Finnmark was mainly inhabited by Saami
people, nomadic hunter-gatherers numbering perhaps a couple of thousand persons
(at the most). In all, the part of Norway situated north of the Arctic Circle contained
some 14,000–16,000 persons or about 4–4.5 per cent of the national population. Thus
this line of argument is untenable. See Sandnes, 1968: 289; Benedictow 1996b: 179–81;
Benedictow 1996c: 155–6, 179–81; Benedictow 2003: 245, 248–9; Benedictow 2004:
147–8, fns. 5–6; Benedictow 2006: 125–7, 131–57, contains a new thorough discussion
of the size and composition of the Norwegian population at the time of the Black
Death, confirming, supporting and supplementing previous conclusions.
62
Eldevik 2006: 48.
63
Sandnes 1971: 69–70; Benedictow 2002: 161.
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who sailed to Bergen in the spring with their stockfish returned with
grain that could be contaminated with dangerous rat fleas, or Norwegian
traders could bring contaminated Norwegian grain with them from
Bergen or Trondheim.
A few later outbreaks of plague in northern Norway are mentioned
in the sources. The parson in Rødøy, a parish situated just north of the
Arctic Circle, provides in his chronicle-like notes information on out-
breaks of plague in Bergen and the devastating spread to Trondheim
and northern Norway in 1599–1600 and 1618. In 1618, he specified the
areas ravaged by plague in northern Norway as the contemporary baili-
wicks of “Helgeland, Salten, Lofoten, etc.,” comprising most of the
present-day county of Nordland; only the northernmost bailiwick of
Andenes is not mentioned.64 The northern part of the bailiwick of
Helgeland, where the parson’s parish of Rødøy is situated, and also
Salten and Lofoten are situated north of the Arctic Circle. Since skeletal
remains of black rats have been found in Trondheim (see above),
and the climate in the inland city of Trondheim is considerably colder
in the late autumn, winter and early spring than the coastal areas
around the Arctic circle, there is no reason why the black rat should not
have spread much earlier in sacks or barrels of grain or flour to north-
ern Norway in fishing boats or in ships belonging to Norwegian traders
from Bergen and Trondheim, and why black rats should not have
thrived there and provided a basis for epidemics of bubonic plague.
Some of the observations of the IPRC may here be usefully recalled:
We would, however, like to draw attention to the ease with which rats
with their fleas can be transported in certain kinds of merchandise. We
have seen rats dive, as it were, into bags containing bran and disappear, so
that the bags could be moved without any evidence of the presence of the
rats within. M. rattus [= Rattus rattus, the black rat] from its habits is
particularly liable to be transported in this way […].
From what has been said above it will be apparent that merchandise
and grain, which have been visited by rats, may have fleas deposited on
them and these fleas may be transferred with these articles to distant
places.65
These are important points that should be kept in mind. Twigg’s and
Scott and Duncan’s assertions on climate are arguably not the result of
serious scholarly work.
64
Benedictow 2002: 234, 240–3, 258–60.
65
IPRC 1908b: 254–5. Above: 105, 160.
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420 chapter eleven
The Seasonality of Plague and Mortality in England 1340–1666
Both Twigg and Scott and Duncan maintain that the Black Death
spread in the south-western counties or dioceses of England in the
winter months and that this constitutes proof that the Black Death
could not have been bubonic plague. The Black Death was introduced
into Norway from England and to the other Scandinavian countries
probably mostly from Norway. It has been shown that the Black Death
in these countries was temperature dependent, spreading only in
warmer seasons and disappearing with cold winter weather. In Norway,
it has been shown that there was never a winter epidemic of plague in
the country’s whole plague history of over 300 years. It has been shown
above that this was also the case with the Black Death all over Europe.66
In view of these facts, one should expect that the Black Death’s seasonal
pattern in England was similar.
Since Shrewsbury and especially Twigg and Scott and Duncan play
such a central part in this discussion, English evidence tends to play a
central and even disproportionate role. However, in defence of their
theories Twigg and Scott and Duncan focus only on small and selected
parts of the seasonal history of the Black Death’s spread in England and
base their arguments on sources which are highly problematic for
inference to the reality of these matters, as will be seen below. It is
therefore important to construct a rather complete overview of the sta-
tus of English research on the seasonal pattern of historical plague epi-
demics in England throughout the whole plague period of over 300
years and apply source-criticism in quantum satis (sufficient quantity).
An overview which is complete for all practical purposes will provide
the strongest possible basis for identification of the seasonal pattern of
plague and for inference to the causal nexus underlying the particular
form of correlation of plague epidemics and climate, i.e. their seasonal-
ity. Only a qualitatively secured and, for all practical purposes, com-
plete overview can provide a holistic perspective and framework within
which their arguments can be satisfactorily considered.
A methodological and source-critical point that may appear self-
evidently true must be stated for reasons that soon will be clear: only
empirical evidence consisting of generally accurate identifications of
66
There may have been a case of a mixed epidemic of bubonic and primary pneu-
monic plague which spread also in the winter in the pneumonic mode, or just possible
two cases. Benedictow 2004: 236–41.
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day of death or burial of a sufficiently large sample of persons dead

from plague can provide reliable information on the seasonality of
plague, providing that the registration is seasonally independent. The
reliability of information will decrease (1) with increasing temporal
distance or uncertainty as to the time of death of plague victims and the
registration of their demise, it will also decrease (2) as the number of
persons included in the sample diminishes, and it will (3) lose its evi-
dential power if the number falls under a critical minimum level.
The arrival of the Black Death and subsequent plague epidemics
caused a dramatic transformation of the seasonal distribution of mor-
tality in England throughout the Late Middle Ages and well into the
Early Modern Period, that is, for the duration of the plague period.
Russell produced data on the seasonality of the time of death of ten-
ants-in-chief, the noble class that held feudal land directly from the
king, in the period 1340–1450 and 1476–1500.67 The high social class
of the subject of Russell’s work will exclude direct influence from hun-
ger, malnutrition or undernutrition associated with bad harvests which
among the poorer classes would tend to cause increased mortality in
the summer and early autumn of the following year as reserves of food-
stuffs were being depleted and unavailable at affordable prices in the
market. Since tenants-in-chief had large households and an active
social pattern of behaviour, they would tend to be exposed to conta-
gious diseases as much as or perhaps more than the average population
without having normal consumption patterns of foodstuffs that would
significantly increase resistance to disease. This material will therefore
reflect more clearly the seasonal distribution of mortality caused by
epidemic disease and be reasonably representative in this respect also
for the general population. Tenants-in-chief lived at their manors or
estates around the country, and thus the material is probably geograph-
ically well distributed. Assuming that historical plague was bubonic
plague, this representativeness is negatively affected by the fact that
tenants-in-chief tended to live in stone buildings which were less ame-
nable to rats than ordinary housing at the time, and this fact would
presumably tend to reduce this disease’s impact on this social class
relative to peasants and burghers who lived in far more unfavourable
dwellings in this respect. In principle, the representativeness would
tend to deteriorate to the extent that the incidence and demographic
67
Russell 1948: 195–9.
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422 chapter eleven
impact of plague epidemics became relatively more urban, a develop-

ment that did not, however, become pronounced until about the mid-
1550s, and therefore does not affect Russell’s data here. As can be seen
from Table 8, the temporal coverage is sufficiently large to provide good
data.68 It should be noted that as outstanding medieval demographer as
Hatcher, who often is very critical of Russell’s material and his handling
of it, and rightly and fairly so, has no difficulty in accepting the useful-
ness of Russell’s data and the validity of the inferences drawn from it on
this point of the seasonality of mortality.69
Russell found that before the Black Death, in the eight pre-plague
years 1340–7, the “heaviest mortality was in the late autumn and win-
ter months, in January and February, in October and November,” and
he adds correctly: “The heavy mortality of the winter months requires
no other explanation than winter severity.” Traditionally, the months of
November and December were regarded as the first winter months, the
“forewinter.” With the advent of the Black Death, the seasonal distribu-
tion of mortality changed dramatically. In the period 1348–1375 cover-
ing the Black Death and the subsequent three plague epidemics (1360–1,
1369, 1374), Russell’s data show an abrupt surge of mortality in July,
the heaviest impact on mortality in September or more broadly the
months August to October, with an abrupt tendency of decline starting
in October. Conspicuously, the seven years of plague in this period
accounted for twenty per cent more deaths than the remaining twenty-
one non-plague years taken together.70
Twigg’s efforts to render these findings harmless to his theory are
curious: he divides his discussion of seasonality and Russell’s findings
into two parts more than hundred pages apart, which means that
important argumentative connections are severed, the critical reader is
put at a disadvantage, and the problematic character and lack of real
significance of his discussion in the second part tends to be veiled.71
Curious also is Twigg’s dismissal of Russell’s findings on the grounds
that in the first plague period 1348–75, “the death rate is only four in
68
One should note that even in countries the size of the U.K. or U.S.A. national
political Gallup polls are often based on a sample of about a thousand persons, which
provide national polls with an uncertainty margin of about 3 per cent. It is all a ques-
tion of reasonable or adequate representativeness.
69
Hatcher 1977/1987: 25–6.
70
Russell 1948: 195–8.
71
Twigg 1984: 59–69, 175–85.
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January,”72 which reflects his usual carelessness: in fact it is the number

of deaths that is four. If this figure is taken at face value, the death rate
as proportion of deaths in this month in the period is 0.9.73 Some sort
of numerical error is involved, since among the remaining seventy-one
mortality datapoints distributed according to month and temporal
subdivisions in the period February 1348 to December 1500 on which
the data presented in Table 7 are based, the lowest figure is 18. However,
on statistical grounds one should take heart from the fact that material
for correction is available: for the other months of January in the respec-
tive subperiods the figures are 42, 47, 56, and 53. The fact that these
numbers are quite closely bunched inspires confidence. The average is
49.5 deaths, and since there is a noticeable tendency of increase
throughout the period as a whole from 42 to the mid-fifties, it appears
reasonable, in our attempt to find the true figure for January in the first
plague period of 1348–75, to weight this average in the direction of
forty. Thus, it seems that the figure four is a slip of the pen for forty, a
zero has slipped away, and forty can readily be substituted for four in
the tables. This means that 52 per cent of total yearly mortality in the
period 1348–75 was distributed on the four months July–October. This
confirms that Hatcher’s use of Russell’s seasonality data is justified.
One could also remark that it does not seem that anomalous figures
concern Twigg much when they seemingly strengthen his case. Since
he must try to reduce mortality in the Black Death as much as he can,
Table 8. Percentage of mortality July–October 1340–1500 among

English tenants-in-chiefs
Period Nos. %
1340–7 159 33
1348–75 426/466 56/52
1376–1400 632 43
1401–25 759 42
1426–50 640 35
1476–1500 791 40
1348–1500 3248 43
72
Twigg 1984: 181.
73
Russell 1948: 197.
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424 chapter eleven
far more than anyone else has found possible, in order to make the
facts fit his alternative anthrax theory,74 he accepts without objections
Russell’s crude mortality data on the Black Death based on inquisi-
tions post mortem as a realistic factual basis, and not only for mortality
among the tenants-in-chief but also for the general population. In the
age group 0–1, this material contains no infants, implying, conse-
quently, a mortality rate of zero for this age, or alternatively, that there
were no infants, neither of which is a realistic possibility. In ages 1–5,
Russell’s material includes three young children, of whom one died.
Thus, in ages 0–5, Russell’s total child population consists of three per-
sons of whom one died, which he assumes permits the conclusion that
the mortality rate in ages 0–5 was a ludicrous 33 per cent.75 The result
is a very low mortality rate among the population of tenants-in-chief in
the Black Death as a whole that suits his case, especially when Russell
considers the mortality rate among tenants-in-chief representative for
the general population. However, Life Tables Model West for popula-
tions with life expectancy at birth of twenty-five years show a normal
infant mortality of 30.5 per cent for female infants and of 35 per cent
for male infants, and of 21 per cent for young children of ages 1–4.76
It should have been impossible not to note that the mortality rates
according to age imply that adult cohorts in this material were very
much larger than child cohorts since far more adults die according to
age cohorts in this social class than is warranted by the implied birth
rates. This should make it clear that Russell’s data are out of touch with
reality and do not allow any sort of statistical use but probably reflect
interesting aspects of culture and mentality. There can only be one
explanation for Russell’s registrations of children of these ages, namely
that the mortality rates of infants and young children were so high that
their deaths were taken for granted and parents quite generally did
not bother to register the deaths of their youngest children, only of
their somewhat older children who had greatly improved survival
rates and were of greater interest for questions of inheritance and line-
age. Thus, these data do not reflect realities of mortality in these age
cohorts but cultural and practical attitudes of parents. The use of statis-
tics and demographic sociology apart, Russell’s estimate of mortality
among infants and young children is at gross variance with medieval
74
Below: 595–608.
75
Russell 1948: 216.
76
Coale and Demeny 1983: 43.
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demography on these ages.77 This explains why Russell’s estimate of

mortality in the Black Death has been generally rejected.78 Twigg’s
peculiar efforts to reduce Russell’s mortality figure to c. 16.5 per cent
for tenants-in-chief in the Black Death and to argue that they are rep-
resentative for the general population will be commented on below.
Russell made the same type of estimate of the seasonality of mortal-
ity for the subsequent subperiods 1375–1400, 1401–25, 1426–50, and
1476–1500. The central data are presented in a highly concentrated
form in Table 8 which is so constructed that average mortality for a
four-month period is, other things being equal, 33 per cent; higher
percentages must reflect higher than average mortality, and vice versa.
The average of 33 per cent was the case in the months July–October of
the eight pre-plague years, importantly, in these years almost 45 per
cent of all mortality occurred in the four months January–February
plus October–November. This underlines the great change in seasonal
mortality heralded by the advent of the Black Death better than the
bare numbers in Table 8. In the period 1348–1450 and 1476–1500 as a
whole and in all its constituent subperiods there was a consistent super-
mortality in the four-month period July–October. A reservation is
called for in the penultimate subperiod 1426–50 as there was hardly a
statistically significant supermortality in these months. The main rea-
son is that a smaller or secondary peak had emerged in the months
April–May which drained off some of the relative distribution of mor-
tality.79 However, it is difficult to explain this as a real or factual change,
because in the next subperiod for which Russell provides data, namely
the last of 1476–1500, the seasonal pattern reverts by and large to the
previous level of supermortality in these months. It is therefore more
likely that there is some flaw in Russell’s material for 1426–50, which
also saw some very serious plague epidemics (see below). This may also
serve to explain the gap in the series caused by Russell’s inability to
present data for the implied following sub-period 1451–1475: there
seem to be serious problems associated with this specific material for
the decades around 1450, at least as collected by Russell. The data may
not be erroneous or skewed, but need further study, perhaps a heavier
input of source-criticism, and increased substantiation. Only Russell’s
data for the period 1340–1426 can be considered reliable and usable
77
78
See for instance Titow 1969: 68; Razi 1980: 100; Hatcher 1977/1987: 13. See also
below: 596–602, 605–07.
79
Ibid.
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426 chapter eleven
here. Fortunately, there are alternative sources of information on the

distribution of mortality according to season for the fifteenth century
which allow the development of an overview of the seasonality of mor-
tality in this period on independent material, and also correction or
adjustment of Russell’s data for the periods after 1426 (see below).
The seasonal pattern of mortality uncovered by Russell does not
mean that the incidence of mortality in the late autumn/early winter
months and central winter months had decreased significantly,
although, of course, persons with poor health now died from plague
who would otherwise have died in the subsequent winter months.
Mainly, it means that winter mortality now was overshadowed by new
forces of death with their greatest impact in the late summer and early
autumn as would be the case with bubonic-plague epidemics.
The sudden transformation of the seasonal distribution of mortality
from the pre-plague to the plague-era uncovered by Russell is a very
important finding. Certainly, it is entirely compatible with bubonic
plague with its basis in rats and fleas which would develop its highest
epidemic intensity in the months of (late) summer and early autumn
and subside and (almost) disappear with the advent of chilly and cold
weather in the late autumn and winter, as has also been pointed out by
several prominent historians.80 The easy explanation of this transfor-
mation of the seasonal distribution of mortality on the basis of central
aspects of bubonic-plague epidemiology strengthens the positive
assessment of Russell’s material and the good level of tenability of
observations inferred from it. Its incompatibility with diseases spread
by cross-infection should be clear: they would tend to increase winter
mortality.
The attainment of reliable general knowledge of the seasonality of

plague in the fifteenth century requires that information be collected
from several studies and pieced together. Hatcher has, as mentioned,
published an important study of the mortality among the monks of
Christ Church Priory, Canterbury. Obituary lists and other evidence
permit a complete registration of the day of death of the great majority
of monks who died there in the period 1395–1507, and to make good
assumptions as to the time of death for the remainder.81 In this period,
80
Hatcher 1977/1987: 25–6; Slack 1979: 43.
81
Hatcher 1986: 23–5; Hatcher 1977/1987: 17–8.
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plague visited the priory in 1413, 1419–20, 1431, 1447, 1457, 1465,
1467, 1470–1, 1487, 1501, 1504, 1507.82 There were also a couple of
epidemics there in the preceding eighteen years that could quite likely
have been plague as indicated by high mortality at the very end of the
fourteenth century and c. 1407, years corresponding to known or pre-
sumed national plague epidemics in the years 1400 and 1405–7.83
Since monks are a special social category and live in quite a different
way from the various segments of the ordinary population, the repre-
sentativeness and, thus, the usability of this material for the question
must be clarified and corroborated before inference to society at large
can be made. The monks were “exceedingly well fed, clothed and
sheltered,” and “they benefited from levels of sanitation, hygiene and
medical care which were wholly exceptional for the times.” On the
other hand, the monks did not live reclusive or isolated lives. There
were twice as many servants as monks, the priory housed an “unquan-
tifiable” number of permanent and temporary lay residents and corro-
dians.84 There was also a “constant stream of visitors,” so monks made
“frequent contact with the wider world,” and it was centrally located in
a bustling market town containing a population of about 4,000–5,000
persons with which there was lively social exchange, townspeople
visiting the monastery, and monks frequenting the town. In market
towns there was a strong confluence of people and with them of vari-
ous epidemic diseases which caused high urban mortality rates. Also
Canterbury’s population was declining throughout the fifteenth
century. Clearly, the monks were exposed to diseases transmitted by
cross-infection both by visitors who would quite likely suffer from an
unrepresentative incidence and array of diseases and by their own vis-
its in the town. The problem of cross-infectious diseases must have
been exacerbated by their communal living: the rank and file monks,
the younger monks or ordinary cloister-monks, “invariably slept in
common dormitories and ate the common meals,”85 which must have
“further facilitated the transmission of a range of diseases.”86
82
Hatcher 1977/87: 17.
83
Hatcher 1986: 26; Hatcher 1977/1987: 57; Shrewsbury 1971: 138, 141–3. Cf.
Harvey 1993: 125.
84
See for instance Harvey 1993: 179–209. “A corrody was a special form of pension
or annuity. Some corrodians enjoyed their privileges as a gift from the monks, but
many, as will appear, paid for them.”
85
Hatcher, Piper and Stone 2006: 682; Harvey 1993: 77.
86
Hatcher 1986: 34–6; Bailey 1996: 2; Hatcher 2003: 97.
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428 chapter eleven
The great similarity of the highly negative developments of life

expectancy of monks and their risk of disease in such distant localities
as Canterbury, Westminster and Durham (see below) to more general
demographic developments in English society at the time are striking.
Hatcher uses the terms “symmetry” and “synchronized” about this
concurrence of similar demographic patterns of people and monks in
the fifteenth century.87 Considering this concomitant demographic evi-
dence Hatcher first concluded that the monks’ health was “likely to
have been driven in major part by the same forces which were deter-
mining the health of the population at large.”88 In his latest paper, he
argues that there may have been a certain supermortality associated
with monastic life in the past, a view which tends to underline the
importance of infectious diseases spread by cross-infection in this spe-
cific environment.89 This may have been the case, but Hatcher also
argues convincingly that the size of the general population was falling
in the fifteenth century, markedly after 1450 until some time in the
early sixteenth century.90 It is therefore not clear that the possible
difference between the levels of mortality of people and monks was
pronounced, although the mortality profiles may quite likely have
diverged.
One point of importance could be that the monks lived in buildings
of stone or bricks that would, presumably, be an environment less ame-
nable to rats than ordinary housing at the time. This suggests that
monastic buildings would tend to reduce the numerical incidence of
rats and rat fleas in relation to monastic men compared to the situation
in environments of the general population in town and country. The
general analysis would therefore tend to suggest that these monastic
communities may have been relatively more at risk of contracting
infectious diseases spread by cross-infection and less at risk of con-
tracting bubonic plague than the general population. And this seems
to have indeed been the case. There is a clear increase of mortality in
the winter months among the monks. However, in general terms the
87
Hatcher 2003: 97; Hatcher, Piper and Stone 2006: 667: “[…] no doubt, the sym-
metry that has been established between mortality in three monasteries located in dif-
ferent parts of the country has important implications for our understanding of the
demographic history of late medieval England.”
88
Hatcher 2003: 97–8.
89
Hatcher, Piper and Stone 2006: 682–3.
90
Hatcher 1977/87: 43–57, 64–5; Hatcher and Bailey 2001: 31; Hatcher 2003: 95–9;
Hatcher, Piper and Stone 2006: 683–5.
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seasonal pattern of mortality among the monks at Christ Church Priory

in the period 1395–1504 still shows heaviest mortality in the months
July–October, a mortality profile that is clear all through the period,
but markedly stronger after 1450 than in the preceding period,91 which
may have been the case also for the “population at large” for the same
(main) causal reason, namely an increased incidence of bubonic plague
epidemics. Arguably, the supermortality among the monks in the
months July–October as a reflection of bubonic plague would tend to
understate the impact of bubonic plague on the ordinary population
in the same months and as such the importance of bubonic plague as
a demographic factor in the lives of the English population in the
period.
In a fine monograph, B. Harvey has studied the lives of monks at
Westminster Abbey, London, in about the same period. Unfortunately,
the material at her disposal for the demographic study of mortality is
considerably weaker, because, among other things, the obituaries are
lost, so that the day of death of the monks cannot be identified with the
same accuracy as in the case of Christ Church Priory in Canterbury.
However, other sources make it possible to address usefully the ques-
tion of the seasonal pattern of mortality in the period 1390–515. It hap-
pens that 28 per cent of deaths occurred in winter or early spring, 69
percent in the late spring, summer, and autumn, and 3 per cent of
deaths cannot be temporally accounted for. Furthermore, mortality in
the warmer seasons “claimed more victims in the crisis years” than in
years of “high mortality of the second order.” Importantly, in some of
the crisis years the summer and autumn were actually the “dangerous
seasons—and dangerous by any standards.”92 In a less specific and com-
pelling way, this material shows much the same pattern as was identi-
fied in the case of Christ Church Priory, that the mortality among
the community of monks, despite the particularly high level of expo-
sure to cross-infection, was much the highest in the warmer seasons,
especially in the summer and the autumn, and that this pattern is
closely associated with known plague epidemics in this period, namely
those in 1400, 1420, 1434, 1458, 1464, 1471, 1479, 1491, and 1500.
Evidently these studies of monastic mortality accord completely
with Russell’s findings, link up to his data around 1400, overlap his data
91
Hatcher 1986: 26.
92
Harvey 1993: 135–8.
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430 chapter eleven
for the periods 1401–26, and extend the seasonal overview up to about
1500, and as such also overlap and confirm the value of his data for the
period 1476–1500. The similarity of these findings based on unrelated
source materials is strongly corrobatory. They also strengthen the prob-
ability that Russell’s data for the subperiod 1426–50 are anomalous due
to some unresolved source-critical problem and should, as maintained
above, be left out of consideration.93
In his monograph on demographic developments in England in the
period 1430–80, R.S. Gottfried discusses to the seasonality of mortality
and its association with plague, especially in a chapter with the dra-
matic title “Season of Death.”94 In the period 1430–80 there appear to
have been seven epidemics of plague in England of a national or extra-
regional scale, in 1433–4, 1438–9, 1452–3, 1457–9, 1463–4, 1467,
1471–3, and 1478–80; locally there were many more.95 However, his
study is restricted to south-eastern England, more specifically to the
counties Suffolk, Norfolk, and adjacent parts of Cambridgeshire and
Hertfordshire, and it is mainly based on wills for its source material.96
The source-critical problems associated with the use of wills for demo-
graphic historical studies are many and must be taken very seriously.
Wills are a highly unrepresentative category of historical sources: those
who made wills belonged to the economic and social upper classes of
the population; a substantial majority of the population had little or
nothing to bequeath.97 Because of their “selective social coverage,” wills
constitute a poor indicator of the levels of mortality in general popula-
tions in epidemics of plague, since levels of mortality are socially une-
qual, higher among the poor than among the well-to-do.98
In times of a perceived serious threat of mass death from plague
many people would rush to make their wills. However, wills reflect
more fear of death than death itself, and at the end of the epidemic usu-
ally the (great) majority of those who made their wills would still be
93
It is unfortunate that the study of the superior demographic material relating to
the monastic community of Durham Priory in about the same period does not address
the question of the seasonality of mortality. Hatcher, Piper, and Stone 2006.
94
Gottfried 1978: 107–7.
95
Hatcher 1977/1978: 17, 57; Hatcher 2003: 97; Harvey 1993: 125; Gottfried 1978:
35–51, 238.
96
Gottfried 1978: Chapter 6.
97
Hatcher 1986: 22; Hatcher 1977/87: 28–9; Hatcher 2003: 95–6; Slack 1979:
12–4.
98
Slack 1979: 14.
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alive. The association between the making of a will and the day of death
is tenuous at best; “the frequency of probate was overwhelming.”99 Use
of wills as demographic sources for the study of levels of mortality is
therefore fraught with difficulties that cannot be satisfactorily or use-
fully resolved. In the words of Hatcher: “It will never be possible to
derive death rates from wills.”100
Nonetheless, wills are a usable source for the study of some aspects
of mortality, for instance, for the identification of years of mortality
crisis and the seasonality of mortality. However, this use also posesses
significant problems that must be taken into account. In urban centres
there was a social geography, a social differentiation of residential pat-
terns according to economic and social conditions. The poor classes
inhabited mainly the suburbs, while the central areas became more
strongly middle-class quarters, and this social geography was changing
in the direction of an increasing social polarization. Upper classes were
used to epidemic outbreaks among the poor classes. Increasing social
distance in residential patterns made for increasing time lag between
the outbreak of epidemic disease among the poor and observation of
and reaction to these events among the upper classes.101 Wills were
made when the upper classes recognized to their horror that epidemic
mortality among the poor was spreading and that also their own lives
would probably soon be at risk. Thus, a sudden strong rise in the
number of wills indicates quite a developed epidemic situation. This
means that there is generally a time lag of several weeks between
the outbreak among the poor and the surge of consternation among
the will-producing classes that causes a sudden and strong increase in
the making of wills. This is especially the case with plague because of
the characteristic slow and protracted incipient development of its
early endemic and epidemic phases.102
These source-critical comments must be kept in mind when Gottfried
states that the “fewest testators in the sample died in the summer quar-
ter, except during purported plague years, when mortality rose in late
August.”103 Taking into account the time lag between the outbreak of
plague and the time it began to impress itself on people in a way that
99
Gottfried 1978: 22–34.
100
Hatcher 1986: 22. Cf. Slack 1979: 14.
101
Slack 1979: 51; Slack 1985: 55–6.
102
See Benedictow 2004: 81, 136–7, 197–8, 272, 336.
103
Gottfried 1978: 107.
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432 chapter eleven
persuaded many of them to make their wills, it can be seen that the
plague season in general terms appears to have started in July, which
conforms to the pattern Russell uncovered for the preceding hundred
years. The severe plague epidemic of 1479–80 is clearly reflected in a
great rise in the numbers of probated wills, starting in the summer in
the town of St Albans; the epidemic then moved to Suffolk and Norfolk,
as reflected in a delay in the rise of the numbers of wills, which began
in August and September, reaching a sharp peak in the autumn, and
then a rapid fall set in.104 A chronicler states that plague this year broke
out in London in September and disappeared early in November.105
Quite likely, the epidemics of 1438–9 and 1479–80 took on a bimodal
form and broke out again in the spring.
The studies of Russell, Hatcher, Harvey and Gottfried cover among
them the seasonal pattern of mortality throughout the fifteen century.
Taken together they show a consistent and strong pattern with the
heaviest mortality in the months July–October; this was the new pattern
that emerged abruptly with the arrival of the Black Death and contin-
ued with the subsequent recurrence of plague epidemics in the follow-
ing 150 years.
This was also the characteristic seasonal pattern of mortality through-

out the remaining 166 years of the plague era. In his study of plague in
Tudor and Stuart England, Slack emphasizes that this was not only the
case in England, but a general European experience, demonstrating
that the same disease was at the heart of the matter all over Europe and
that there could only be one and the same reason for this general epi-
demiological manifestation:
outbreaks of bubonic plague have a characteristic seasonal incidence,
dictated by the climatic conditions favouring the development of the
fleas which carry the disease. All over Western Europe these epidem-
ics were marked by a rapid rise in the number of deaths in the summer;
burials normally reached their peak in the months between July and
September, and then fell more gently with the onset of colder weather
[…].106
104
Gottfried 1978: 35–51, 107–25. I do not, however, understand on what grounds
Gottfried 1978: 62, states that “the occurrence of bubonic plague in England is almost
always in late summer and early fall,” referring in the accompanying footnote on page
79 to Hirst 1954: 238, for support, where nothing to this effect is stated.
105
Gottfried 1978: 45.
106
Slack 1985: 65. Cf. Slack 1979: 24.
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The large epidemics in Devonshire in the years 1546–7, for instance,

exhibited the characteristic seasonality of bubonic plague: the “number
of burials began to increase in late spring and early summer of 1546 in
several parishes,” “the disease continued to cause havoc in the county”
even after the good harvest, and thus was not hunger-related. Only
seven of thirty-five parish registers showed no evidence of the disease,
while elsewhere there are all the characteristic signs of bubonic plague:
“summer peaks in the number of burials where the disease was worst,”
“the apparent slow movement of disease from place to place, burials
rising in one village a fortnight or a month after they had done so in
another a few miles away.”107 The last point is interesting in so far as it
constitutes evidence of short-range metastatic leaps and the latent
period conforming to and reflecting the rhythm of development of
bubonic plague in the plague season. Finally, Slack also points out that
people in London “noted the regular seasonal periodicity of plague and
acted accordingly.”108
All through his monograph Shrewsbury is clear on this unique pat-
tern of seasonality of plague and the reason for it, noting the winter
intermissions and the typical onslaught of plague epidemics in the (late)
summer which are characteristic of rat-flea-based transmission.109
However, he has little information on epidemic diseases for the period
c. 1375–1500, and hardly any seasonal information at all, for the simple
reason that little information was available at the time he wrote his
monograph. As was seen above, all studies containing significant or
important information on the seasonal pattern of mortality in the fif-
teenth century were published later except Russell’s. After 1500, Shrews-
bury’s account expands greatly and contains much detailed material.
Unfortunately, the term “seasonality” is not in his index, which makes
the task of systematizing his quite detailed empirical information on
this point very work-intensive. Fortunately, however, he is fond of sys-
tematizing his data in histograms (bar charts) and figures, which makes
much information showing the progression of plague epidemics
according to the monthly distribution of mortality easily identifiable
and usable. Although concentration on this material omits the occa-
sional piece of evidence noted by chroniclers on when the outbreak
began and ended, and also not rarely when they raged most intensively,
107
Slack 1985: 84.
108
Slack 1985: 239.
109
See for instance Shrewsbury 1971: 117. Cf. Creighton 1891: 217–33.
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434 chapter eleven
it provides quite a valuable and useful platform for insight. In all, his
book contains fifty relevant histograms or figures (mostly the latter) on
this topic, showing the seasonality of plague mortality according to month
in various locations in England, from London to tiny rural parishes. In
addition, a few tables show the time of the beginning and end of epi-
demics as reflected in plague deaths.110 Since display of the distribution
of seasonal mortality according to month requires individualized data
which for ordinary populations is mainly provided by parish registers
or bills of mortality, all of this material relates to the period 1548–1666.
This requirement for statistical identification of seasonality also ensures
good data quality and important detailed information on the progres-
sion of epidemics and reliability of inference to the reality of such
developments.111 This material shows a clear majority of urban epidem-
ics, which should be expected for the last hundred years of plague when
these epidemics increasingly became an urban phenomenon.
The material consists of fourteen histograms and figures showing
the distribution of plague mortality according to month (or season) for
the period 1548–99112 and thirty-six figures or histograms showing
mortality according to month (or season) for the remainder of the
plague period, the years 1600–66.113 All fifty figures and histograms
exhibit the same pattern without exception. All plague epidemics broke
out in the warmer seasons and began to decline with the advent of the
colder seasons in October, subsiding and disappearing in the following
months, causing only episodically some deaths in January.
Summing up, in the preceding pages substantial material has been pre-
sented on the seasonality of plague epidemics covering the whole
European plague era from 1347 to 1666/1722, with a particular focus
on the English evidence. The English material is based on diverse
sources, inquisitions post mortem, monastic studies, wills, parish
registers and bills of mortality, etc. The studies based on these sources
produce a comprehensive, continuous and consistent account of the
110
111
I will make source-critical comments below on the use of institutions of parish
priests during the Black Death.
112
Shrewsbury 1971: 176, 182, 183, 191, 197, 199, 214, 216, 238, 244, 249, 253, 396,
492.
113
Shrewsbury 1971: 267, 280, 296, 302, 310, 316–7, 320, 326, 328, 329, 350, 361,
364, (372), 374, 376, 378, 383, 386, 391, 396, 406, 411, 412, 417, 436, 438, 462, 463, 476,
500, 504, 511, 523.
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seasonality of plague which unambiguously associates plague epidem-

ics with the warmer seasons (spring, summer and autumn), with an
emphasis on the late summer and early autumn months. They consti-
tute together a powerful basis for inference that historical plague was
an epidemic disease that is systematically and by innate, systemic prop-
erties dependent on warmer seasons for developing epidemic
manifestations and functions. The occurrence of bimodal epidemics,
epidemics that break out (late) in the warmer season of one year, sub-
side and disappear with the advent of late autumnal and wintry weather,
and then break out again in the same locality in the spring to produce
another peak of mortality, is such a conspicuous and unique feature
that it strengthens this conclusion even more, if possible.114 The plague
epidemic at Colchester in 1665–6, exhibits a pattern as similar to that
of the epidemic in the Cathedral’s parish in Bergen a century earlier as
well-nigh possible in the real world. The epidemic started in September
with a fulminant development which was abruptly reversed by the
advent of cold weather which caused a rapid diminution and virtual
disappearance of the disease, which reappeared in Spring and produced
the last cases in December the following year, although, in the case of
Colchester, without producing a complete winter intermission as it
seems (if all deaths registered in Colchester were plague deaths), which
could quite likely be associated with the fact that Colchester is situated
over 900 km further to the south than Bergen with a correspondingly
milder winter climate in ordinary years.
This seasonal pattern was well known to contemporaries and is the
basis of the title of John Taylor’s book published in 1625 and reprinted
1636: The Fearefull Summer: Or Londons Calamitie, The Countries
Discourtesie, And both their Miserie. Printed by Authorities in Oxford, in
the last great Infection of the Plague, 1625.115 In 1641, a Londoner
claimed that a proposed day for religious humiliation to ward off plague
was unnecessary, because “winter was coming on, and then the plague
would be stayed.”116
This consistent seasonal pattern throughout the whole plague period,
which is based on various types of relevant source material and inde-
pendent studies, demonstrates that Twigg’s great efforts to discredit
Russell’s findings about the seasonal incidence of plague for the period
114
See for instance Shrewsbury 1971: 500, 504, 523.
115
Cox 1910: 149.
116
Slack 1985: 239.
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436 chapter eleven
1340–1500117 are untenable, and that the pattern Russell identified for
this period was similar throughout the remaining 166 years of the
plague era, 1501–1666. Twigg’s efforts reflect a great need springing
from the fact that this pattern of seasonality is easily compatible with
bubonic plague and incompatible will all the alternative theories of the
microbiological nature of historical plague including his own. Finally
when Twigg recognizes that his arguments are not convincing, he con-
cludes rather lamely, but as enthusiastically as he possibly can under
the circumstances: “I suggest, therefore, that the mortality patterns in
the post-1348 period, whether of epidemic or endemic years, are not
sufficiently different from the pre-1348 years as to allow us to believe
that bubonic plague was present.”118 This is clearly not correct.
Duration of Vacancies in Parish Benefices during the Black Death
Since Twigg and Scott and Duncan assume such a central part in this
discussion, English evidence tends to play an important and even dis-
proportionate role. However, to my knowledge it is not possible to con-
struct such a well-documented complete historical overview over the
correlation of seasons and plague epidemics for any other country.
Twigg and Scott and Duncan only address selected small parts of the
relevant material, focusing on a part of the seasonal history of the Black
Death’s spread in England, mostly based on a poorly suitable or, as we
shall see, more likely unsuitable category of sources, namely institu-
tions of parish priests. The time has come for an examination of this
source material and its usability.
Twigg was the first of the advocates of alternative theories to empha-
size the importance of the material on institutions of new parish priests
during the Black Death for the study of the seasonality of plague
because, in his opinion, they show in the southern dioceses a winter
incidence incompatible with bubonic plague.119 “The seasonal mortal-
ity pattern during the Black Death must be one of the most telling
arguments against it being bubonic plague.”120 Twigg’s line of argument
was enthusiastically picked up by Scott and Duncan who concluded
117
Twigg 1984: 181–4.
118
Twigg 1984: 183.
119
Twigg 1984: 60–2, 65–9, 176–85.
120
Twigg 1984: 185.
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triumphantly: “We can now abandon the idea, so firmly promulgated

in the literature, that the Black Death was an outbreak of bubonic
plague.”121
Remarkably, Twigg also states that “plague did not appear until late
1348.”122 Scott and Duncan accordingly state unreservedly: “In the dio-
cese of Salisbury, the epidemic was rampant through December to
February and reached its peak in March.”123 It is generally acknowl-
edged that the Black Death broke out in Melcombe Regis (Weymouth)
in the diocese of Salisbury shortly before 24 June,124 and spread in
England throughout the whole second half of 1348. Since these are
basic facts which are important for the discussion of the seasonality of
the Black Death in England, there will be ample opportunity to pro-
duce the evidence below. Hypothetically, Twigg could correctly have
meant that the effects of the Black Death did not appear in the form of
institutions of parish priests until late in 1348, in which case a danger
signal should start blinking with respect to the temporal connection
between the spatio-temporal progression of the Black Death and its
mortality effects and the reflections of this process in the form of insti-
tutions of parish priests into vacancies.
This material on institutions of parish clergy in a few months of the
Black Death in a small part of England, mainly the winter months of
1349, is supposed to undermine the consistent and strong link between
plague epidemics and the warmer seasons demonstrated for the
remainder of the Black Death and the remaining plague era of 320
years, i.e., 99.85 per cent of the history of plague in England in this
period, a fact which they refrain from attempting to explain or in the
case of Scott and Duncan even from mentioning.
Twigg falsely attributes to Shrewsbury the view that the Black Death
(and later plague epidemics) occasioned a different seasonal distribu-
tion of mortality from the pre-plague mortality pattern to the effect
that the heaviest mortality now occurred in the three autumn months
from August to October (see above). This distortion of research history
prepares the ground for Twigg’s defence of his view that the Black
Death and later plague epidemics could not have been bubonic
plague:
121
122
Twigg 1984: 181.
123
124
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438 chapter eleven
Despite what Shrewsbury says about the creation of a single peak in

August, September and October this fact does not emerge from the
Institutions to vacant benefices in the several dioceses, all vacancies being
generally but probably erroneously attributed to plague deaths.125
As shown above, it is not Shrewsbury but Russell who has documented
this peak in August–October. To characterize this finding as a “crea-
tion” is misleading; it is also disquieting because it appears to serve a
purpose. Next, Twigg goes on to use Shrewsbury’s extensive presenta-
tion of institutions of parish priests during the Black Death to argue
against the view he has erroneously attributed to him, disparagingly
implying that Shrewsbury has not noticed the gross contradiction
between his data and a conclusion which in fact he never drew.
One should also note the arbitrary assertion that “all vacancies being
generally but probably erroneously attributed to plague deaths”:126 this
is, to the best of my knowledge, not correct and is not substantiated by
Twigg with any reference to the scholarly literature. A few pages earlier,
he states that “some writers have assumed that all vacations during
1348–9 were due to death from plague,” which is very different from
asserting that this has “generally” been the case, and again there is no
substantiating reference that could clarify who “some writers” were.127
Are they serious scholars? However, identifications can be made: the
“accusation” can only be relevant for F. Seebohm 1865128 and perhaps
for some scholars up to the time Gasquet’s monograph was published
in 1893. In that work Gasquet makes it entirely clear that vacancies
were due not only to death, but also to “exchange, or resignation,”129
and he actually provides a rule of the thumb: “it is safe to say that two-
thirds were institutions to vacancies due to the plague.”130 It is another
matter that Gasquet does not consistently take this into account131 (but
then he was not a historian by training; nonetheless he made an impres-
sive pioneering achievement in an important field of historical study).
Twigg’s assertion on this point is untrue for all scholars who address
125
Twigg 1984: 65.
126
Twigg 1984: 65.
127
Twigg 1984: 59.
128
Seebohm 1865: 150–60.
129
Gasquet 1908: 86, 88–9. (I have used the 2nd edition of 1908 which is identical to
the 1893 edition for all practical purposes.) It should be remarked that Gasquet does
not seem to have consistently taken this into consideration, see, for instance, Pickard
1947: 25.
130
Gasquet 1908: 188.
131
Ziegler 1970: 184.
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the subject after Gasquet’s monograph was published and the appear-
ance of A.H. Thompson’s two pioneering papers on institutions during
the Black Death in the dioceses of Lincoln and York in 1911 and
1914—in other words, the assertion has not been true for at least a
hundred years. Also, Twigg does not indicate the proportion of vacan-
cies that have been “erroneously attributed to plague deaths” and pro-
vides, thus, no clue as to the possible (in)significance of the argument.
In reality, Twigg pursues an anti-source-criticism line which serves to
confuse the discussion and allows arguments to slip into the discussion
that in the interest of its quality would better have been left out.
In view of the great importance they attribute to institutions as evi-
dence on the seasonality of the Black Death, one can legitimately be
surprised by the scant source-critical interest Twigg and Scott and
Duncan take in this type of source and especially in the crucial ques-
tion of the temporal link between the deaths of incumbents and the
institution of successors. Twigg is surprised by Shrewsbury’s remark
that, according to J. Lunn’s thesis on institutions (see below), there was
a time lag of about a month between deaths of incumbents and the
institution of successors, but appears willing to accept it.132 Shrewsbury
does not indicate that Lunn’s assumption had any empirical basis, and
since Lunn’s thesis has been lost, the crucial scientific tenet of testabil-
ity has vanished as well.133 However, since his assumption is identical
with A.H. Thompson’s statement on this point in his paper on the insti-
tutions in the diocese of Lincoln in the plague period, Lunn’s statement
may quite likely have come from this paper. Thompson’s view will be
discussed below and found to be based on a misunderstanding or mis-
conception. Scott and Duncan have not taken interest in this problem,
presenting their case on the assumption of contemporaneity between
the two events. Their figures or histograms show numbers of institu-
tions according to month (taken from Twigg’s monograph) and are
presented as if they provide direct information on the mortality among
parish priests in time and space. This is erroneous and misleading. In
his admirable and still useful account of the Black Death in England,
Ziegler maintains that there was a “usual gap of a month to six weeks
between mortality and replacement,” however, as there is no support-
ing footnote the statement is also arbitrary, though it may be based on
132
Shrewsbury 1971: 59; Twigg 1984: 65.
133
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440 chapter eleven
Thompson’s statement on the matter.134 Therefore, this important point

appears to have been largely neglected, but in the present context this
question is at the heart of the matter and must be seriously and satisfac-
torily addressed.
Only Thompson refers to a material basis for his statement on the
matter and can as such be taken seriously. All others who express an
opinion on the matter seem to base their view on his statement, with-
out having tested the material basis. For this reason, it is of crucial
importance to examine the basis for Thompson’s view and assess its
tenability. If tenable, this will be an important fact, but its geographical
limitation and specificity will limit its representativeness with regard to
seventeen bishoprics and will also have a corresponding limiting effect
on its significance. If it is untenable or problematic, a new study of the
matter is called for.
Thompson has produced two of the classic studies of institutions at
the time of the Black Death, for the diocese of Lincoln (1911) and the
diocese of York (1914). In his study of the diocese of York’s bishop’s
register, he states that “It may be fairly assumed that the institutions in
any given month represent deaths which took place during the previ-
ous three or four weeks,”135 however, he provides no evidence or even
explanatory considerations for why this should be a reasonable or “fair”
assumption. It is in his study of the bishop’s registers of the diocese of
Lincoln that Thompson provides the material basis for his assumption
on the time lag between the death of incumbents and the institution of
successors and the method of estimation: by comparing the dates of
institutions to benefices “which were at this time in the hands of the
king […] and the death of tenants-in-chief, with the dates of the letters
of presentation which fill the patent rolls for this year, one is lead to the
conclusion” that the average period which elapsed between the death of
an incumbent and the institution of his successor was “at least a
month.”136
Unfortunately, four big problems immediately present themselves:
(1) Thompson appears to have misstated his case on this point: this
material does not reflect the time elapsing from “the death of an incum-
bent to the institution of his successor,” but covers the time elapsing
134
Ziegler 1970: 148.
135
Thompson 1914: 105.
136
Thompson 1911: 317.
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from the day a candidate for the crown was presented to the bishop’s
administration to the day of institution as entered in the bishop’s regis-
ter. The question that can be answered on the basis of this material is
therefore the average time which elapsed from the day the crown pre-
sented a candidate for a parish benefice until the institution of the pre-
sentee. It does not relate to the crucial question of the average period of
time elapsing from the death of incumbents until the crown’s presenta-
tion of candidates for vacated parish benefices took place, which
together with the average time elapsing from the presentation until the
time the institution was entered in the bishop’s register, constitute the
time elapsing from the death of incumbents to the institution of their
successors.
Thompson, an exemplary scholar, provides the source material on
which his estimation is based in an appendix, which makes testing
readily possible. The time of all presentations by the crown and the
time of the corresponding institutions in the period 25 March 1349 to
25 March 1350 as supplied in Thompson’s Appendix II have been stud-
ied.137 There are in all sixty-nine presentations by the crown, and the
time that elapsed from the day of presentation to the day of institution
was, on average, 33.5 days or 4.8 weeks, which may be taken to support
the assertion that this was the period of time which Thompson had in
mind with his reference to “at least four weeks” and Ziegler’s statement
of “a month to six weeks.” This means that the trust I placed in
Thompson’s statement in my monograph on the Black Death was mis-
placed and that the standard assumption I developed based on his
statement and on Ziegler’s statement on this matter138 falls apart.
Thompson provides no evidence on the time elapsing from the deaths
of parish priests to the institution of their successors.
(2) Nothing is said about benefices in the king’s gift for which no
candidate was found at the time of the epidemic, for which institutions
were performed in the following couple of years. As will be shown
below, this appears to have been the case with 15–30 per cent of the
parish benefices for which the bishop had the right of institution, and
one could reasonably surmise that much the same would be the case
with the vacancies for which the king was in the position of the patron.
137
Thompson 1911: 339–56. No usable material of this kind is given in the bishop’s
register of York diocese, Thompson 1914: 135–40, 148.
138
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442 chapter eleven
This perspective implies substantial additions to the average lapse of

time as estimated for the plague period.
(3) The type of source used by Thompson in this case is subject to
very serious source-critical objections or reservations. In a small pas-
sage in Appendix III in the paper on the institutions of the diocese of
York some formidable weaknesses with respect to this material are pre-
sented: “a crown presentation is no guarantee that the person presented
actually received institution, as such presentations were frequently
made without proper references to facts, and in such cases often proved
inoperative or were actually revoked.”139 In his later monograph on the
English clergy in the Later Middle Ages, Thompson actually empha-
sized the Crown’s role as a mess of such proportions that it certainly
implies much confusion and reservations as to its practical usability for
clarification of the present topic.140
(4) Since the crown’s candidates are presented by a parallel organiza-
tion that was not specialized in religious functions, as is clear from the
amateurishness that appears to characterize its functions in these mat-
ters according to Thompson, it might not function according to the
same time schedule as the episcopal organization, which also intro-
duces a serious source-critical problem of (un)representativeness.
Ignoring for the moment the problematic source-critical nature of
this material, the crucial question that remains to be answered, and
which cannot be answered on the basis of Thompson’s data, is the aver-
age period which elapsed from the time of death of incumbents in
cures to which the king had the right of presentation until a candidate
for succession was presented to the bishop’s administration. The aver-
age period from the death of incumbents to the institution of their suc-
cessors must have been much longer than 33.5 days.
Twigg only touches the crucial problem of the average lapse of time
between the monthly numbers of institutions in the histograms and
these numbers’ spatio-temporal relationship with the deaths of the
incumbents, and the basis for this “touch” has been shown to be unten-
able. Scott and Duncan do not address the issue at all. Since they adduce
no testable material or study in support of their argument, their
assumptions on this point appear arbitrary and their climatic or sea-
sonal arguments can be dismissed. Evidently, here is a problem that
needs elucidation.
139
Thompson 1914: 148.
140
Thomspon 1947: 104.
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A useful start could be to address some basic factors that affected the
lapse of time between the two events, keeping in mind that this is only
a start, and that other factors will be presented below:
(1) When a parish priest died (retired, or resigned to exchange for
another parish benefice), this set in motion a complex process
leading to the institution of a successor. In this process, first the
system of patronage on which the medieval church depended at
every level was activated.. In the case of parish churches, the
patrons were the possessors of church advowsons which gave the
right of presentation to a benefice or living. The patrons of local
benefices could be the bishop, the dean and chapter, heads of
wealthy families, religious houses, the local ordinary, often the
Crown, tenants-in-chief, or groups of local parishioners. The
Crown’s important role should be emphasized and explained, in
the words of Thompson:
An immense number of presentations to rectories by the Crown are
recorded on the patent rolls. These for the most part were benefices
in the patronage of tenants-in-chief which escheated to the Crown
during the minority of an heir or the vacancy of a religious hose, or
in consequence of a forfeiture of estates. Such presentations did
not always take effect: they were frequently made upon false infor-
mation, and instances of two or more concurrent presentations to
the same benefice through mere inadvertency are not uncommon.
But they gave the Crown a good opportunity of providing for its
clerks.141
Possession of an advowson and the consequent rights of presenta-
tion could be divided into shares or portions (medieties), in which
case the grant of presentation could alternate in turn from one
owner to another or the portioners could act as a collective patron
in presenting a cleric to the cure. The bishop’s registers show that
the king in many cases enjoyed temporary ownership of advow-
sons pending the inheritance of property or the filling of a
vacancy.142
Then there are the problems of pluralism and absenteeism, and
so on. Hopeful non-beneficed clergymen in the parish or district
would take the initiative to start the process and take up contact
with the possessor(s) of the advowson, but often the possessor(s)
141
Thompson 1947: 104.
142
Dohar 1994: 26–9, 110–2.
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444 chapter eleven
would take the initiative. The beginning of the process of replace-

ment would therefore often be complicated and quite time-con-
suming, and might involve a considerable journey for the hope-
ful, or some prominent person in the parish, to the patron just to
provide information about the vacancy, and in those days the
whereabouts or identity of a patron might not be obvious and need
clarification that could take some time. If the patron were local(s),
the process would probably be simpler, but not necessarily in the
case of multiple possessors of the advowson.
(2) The patron would then be obliged to find a suitable replacement;
this could take time, and the vacancy could be sought by various
interests and candidates with consequently lengthy discussion and
dispute.
(3) When the patron had reached his decision, he would contact
the archdeacon who might not be readily available and ask
him to perform an enquiry into the legal circumstances of the
vacancy and the suitability of the candidate, which could be a
complex and time-consuming process, especially when, as in the
time of the Black Death, there were many such requests, and
numerous vacancies and candidates which needed to be screened
or scrutinized.
(4) If the candidate was suitable and the legal circumstances of the
vacancy unproblematic, this would be made known to the bishop
and his staff who would consider the candidate, especially if he was
presented by the king or a tenant-in-chief. The candidate would
then be notified that his candidacy was accepted and he could
come to the bishop’s residence in order to be instituted in the
vacancy.
(5) The candidate would then prepare for the journey, find the bishop,
whose whereabouts might not be readily known if he was circulat-
ing in his diocese or had sought refuge at some peripheral manor,
and wait for the ceremonies of admission to the vacancy and of
institution into the benefice to take place.143
(6) The size of dioceses varied greatly and affected the time required for
the various processes of contact between the hopeful candidates,
patrons and the bishop’s staff at a time when travelling also on
horseback was quite slow and could also be dangerous.
143
See, for instance, Wood, Ferrell, and DeWitte-Aviña 2003: 430.
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Taken together, the various elements of this process could evidently

take months before being completed even at the best of times, and in a
time of great distress and catastrophic mortality it could obviously take
much longer time and the average lapse of time which is in focus here
could be considerable (see below).
As this introduction to the underlying problems of the topic should

indicate, the use of registers of institutions for determination of the
time and seasonality of deaths of incumbent parish priests during the
Black Death is far more problematic than implied by Twigg and Scott
and Duncan. In fact, to attempt to do so is to open a can of methodo-
logical and source-critical worms that would make Medusa’s head pale
in comparison.144 The connection between the two crucial events, the
death of an incumbent and the institution of his successor, is in source-
critical terms very indirect and circumstantial: the institution may not
be caused by the incumbent’s death, and when caused by his death may
have quite a distant and variable relationship to the time of his death,
especially at a time of almost incomprehensible mortality among the
beneficed parish priests and high mortality in the bishops’ administra-
tive staffs that should handle an enormously increased number of insti-
tutions and other types of ecclesiastical business. The crucial point or
defect is, as there will be ample opportunity to consider, the lack of
information on the time of death of incumbent parish priests. Only the
bishop’s register of the diocese of Coventry and Lichfield registers time
of death of the previous holder of the benefice, but in the present con-
text the representativeness and significance of this are quite limited
(see below). The lapse of time between the death of incumbent priests
and the institutions of their successors and its effects on the usability of
institutions for the study of the seasonality of the Black Death and
plague epidemics more generally will be in focus in this subchapter, in
accordance with the importance ascribed to this material by Twigg and
Scott and Duncan.
Importantly, the institution of a new parish priest could also be due
to resignation or exchange of living. Resignations and exchanges must
be deleted from the material for estimation of mortality rates or deter-
mination of time of the epidemic, since they are not caused by death
144
The following discussion of methodological and source-critical problems associ-
ated with the use of institutions is based on the quite detailed discussion in Benedictow
2004: 343–59.
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446 chapter eleven
and will often relate not to the presence of the epidemic but to frighten-
ing hearsay of the epidemic’s ravages and clerical mortality in other
districts or counties or dioceses. In fact, the number of resignations
increased sharply in many dioceses under the Black Death partly or
mostly but not only (see below) because of a wish to avoid dangerous
priestly service. This also affects the time horizon of the epidemic as
reflected in institutions. It is important to take into account the fact
that resignations from fear of plague and the desire to move away before
the arrival of the epidemic would have to be initiated significantly ear-
lier, which means that there would tend to be a considerable or at least
significant difference in time between the two causes of voidance, by
resignation and by death, which would tend to affect the distribution of
institutions over time and the time perspective of the process.
The importance of a sharp increase in resignations in the face of the
approaching epidemic is also due to another effect: it added many
vacancies to those caused by the mortality among the parish priests. It
increased the pool of vacancies in good cures for which not only non-
beneficed auxiliary parish clergy but also many incumbents would vie,
since resignations could be prompted by a wish for an exchange of liv-
ing into a better cure. According to Thompson, “in the course of the
fourteenth century the custom of exchanging ecclesiastical benefices
had reached serious proportions.”145 Great mortality among the parish
clergy together with great fear of the plague triggered great clerical
social mobility not only vertically in the form of the rise of clerics in
auxiliary service into the ranks of beneficed parish priests but also
diagonally, so to speak, in the form of exchange or preferment from
poor to good livings.146 Unfortunately, the information on these mat-
ters provided by the bishop’s registers is of uneven quality (see below).
There are still other problems with this material. The right to per-
form institutions was not the bishops’ prerogative, which is the impres-
sion conveyed by Twigg and Scott and Duncan. The right to institute
parish priests was to a considerable but variable degree granted to other
ecclesiastical dignitaries, and especially archdeacons quite often pos-
sessed this right in their archdeaconries. In the diocese of York, the
145
Thompson 1947: 107.
146
Much the same social pattern of mobility took place in the manorial social sys-
tem where not only landless men but also smallholders entered vacant customary ten-
ancies and therefore improved their social standing by moving upwards vertically or
diagonally.
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number of parishes was somewhat below 1,000 but the bishop had the
right of institution to only 536 benefices. Thus, a substantial proportion
of the deaths of parish priests would not be reflected in the bishops’
registers. Inevitably, this weakens at least significantly and quite likely
considerably the usefulness of the registrations of the bishops’ institu-
tions as a source for identifying when exactly the Black Death entered
and ravaged considerable parts of England.
Further, as mentioned above, pluralism and absenteeism represent
serious problems. It was quite usual that clerics in the service of the
king or a noble patron held benefice in more than one parish and, by
implication, a significant number of parish priests were absent from
their livings for this reason. They would be represented in the parishes
from which they were absent by non-beneficed clergymen who acted
as their vicars. Also ordinary rectors who held only one benefice were
quite often, for various reasons, allowed to be non-resident on condi-
tion that they arranged for non-beneficed clergymen to be their vicars
and to perform their functions for pay or a share in the living’s income.
Since the death of vicars and other clergymen acting on behalf of absent
rectors would not be reflected in institutions, the effect of pluralism
and absenteeism was to weaken the correlation between the spread of
the Black Death in(to) parishes and institutions as reflections of cleri-
cal mortality and its seasonal distribution in the parishes.
In addition, the bishops’ administrations did not escape unscathed
from the onslaught of the Black Death. In considering this aspect of the
problem one must take into account the fact that a bishop’s administra-
tive staff had two forms, a complete household staff at his principal
residence, the bishop’s palace, and a small one consisting of selected
members of his household staff when he was circulating in his diocese.
Bishops were assumed to be travelling round their bishoprics for a con-
siderable part of the year in order to inspect or superintend religious
matters, but also, to a considerable extent, in order to consume the
bishopric estate’s local manorial incomes in the form of liveries in kind
that were not carted or carried by pack horses to his palace in the cathe-
dral city (prandial perambulations). This meant that it was usual that
bishops, for a considerable part of the year, were travelling with a small
staff and many institutions were performed in this context, while oth-
ers were postponed until the return of the bishop to his cathedral city
and residence. Thus even in normal times institutions occurred in cir-
cumstances that would often cause considerable delay for various prac-
tical reasons.
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448 chapter eleven
In times of dramatic general mortality, the connection in time

between an incumbent’s death and the performance and registration of
the institution of his successor would tend to be seriously affected both
when the bishop was resident at his palace and even more so when he
was perambulating. Important reasons for delay were:
(1) the bishop’s whereabouts were unknown and had to be ascer-
tained and the bishop contacted before a patron could present his
candidate for a vacant benefice and apply for his recognition as
successor;
(2) extraordinary mortality among the ordinary staff of the bishop’s
administration would reduce its normal organizational capabili-
ties, at least during some periods;
(3) the bishop’s small travelling staff would tend to be overwhelmed by
an exceptionally large increase in number of institutions which it
was never designed to handle;
(4) the functioning abilities of the small staff which travelled with the
bishops were vulnerable to the loss of members, and also because
replacement(s), if available at the bishop’s palace, would have to be
called for, a process that would tend to take quite some time;
(5) lack of suitable candidates for replacements of dead members of
the staff.
These points can be illustrated concretely. A prominent contemporary
chronicler, William Dene, a monk of Rochester, relates that the Bishop
of Rochester “out of his small household lost four priests, five gentle-
men, ten serving men, seven young clerks, and six pages, so that not a
soul remained who might serve him in any office.”147 Even though a
rhetorical exaggeration can be noted, and it is difficult to believe that
the bishop’s staff succumbed completely, the severity of the onslaught
on the staff and the great administrative problems it must have caused
can hardly be doubted.
During the epidemic onslaught, these factors relating to bishops’
administrations would tend to affect seriously the temporal connection
between the resignations or death of parish priests and the institu-
tion of successors. The concrete effects on the functioning abilities
of the episcopal administrations as observable in the quality of their
147
Gasquet 1908: 120.
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production of sources, as historians will call it, can be concretely dem-

onstrated (see below).
Furthermore, when the successor had eventually been instituted, the
archdeacon would be given mandate to induct him into the living,
which meant that the would-be successor would have to contact him
with the mandate and ask for induction to be effected.
One must also take into consideration the spatio-temporal aspects of
the Black Death’s impact on the bishops’ administrations: the first dio-
ceses which were attacked were taken completely by surprise and over-
whelmed by the exceptional mortality of the epidemic, having no expe-
rience on which to base their reactions in order to cope with the
onslaught and little or no time to prepare for the catastrophe. Further
to the north, however, the bishops and their administrations could pre-
pare themselves mentally and practically for the approaching disaster
based on what had happened in the southern dioceses. One should
therefore expect that the bishops’ administrations in central and north-
ern dioceses would have coped considerably better with the disastrous
events.
In 1937, J. Lunn earned a PhD degree in Cambridge for a thesis on
the study of eleven of the thirteen surviving registers (from a total of
seventeen dioceses in England at the time) titled The Black Death in the
Bishop’s Registers (the registers of the dioceses of York and Lincoln had
already been studied by A.H. Thompson). Unfortunately, Lunn’s thesis
has been lost because a copy was not deposited in the University
Library, but some of the data are cited by G.G. Coulton and Shrewsbury
who had the opportunity to read it before it was lost. Thus the work’s
methodological and source-critical premises cannot be examined and
the quality or problems cannot be clarified.148 Also importantly, the
accuracy of citation cannot be tested at the source itself (see below).
According to Shrewsbury, Lunn stated that the best kept and “most
valuable registers are, in order of importance: Lichfield, Lincoln,
and York, with Worcester and Hereford of considerably less value.”149
According to Shrewsbury, Lunn also asserts that five of the bishop’s
registers, namely those of Bath and Wells, Exeter, Winchester, Ely, and
Norwich, do not give the causes of the voidance of their benefices and
that Lunn should have concluded that “included in the great number of
148
Coulton 1947; Shrewsbury 1971. See also Twigg 1984: 224, fn. 4.
149
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450 chapter eleven
plague institutions must be many which were not caused by death.”

However, Pickard asserts that resignations and exchanges are specified
in the diocese of Exeter’s bishop’s register, and Ziegler that in the bish-
op’s register of “Somerset [Bath and Wells] about a quarter of the new
institutions were the result of the resignation of the previous incum-
bent rather than his death.”150 Both K.L. Wood-Legh and J. Aberth who
independently studied the bishop’s registers of the diocese of Ely also
found resignations, Wood-Legh only one and Aberth three, of which
the larger number must be accepted. The difference may appear sur-
prising but gives little cause for concern, since the order of magnitude
appears quite trustworthy, this was a small diocese, and the average
yearly number of institutions before the plague was 3.5.151 I have previ-
ously had occasion to point out a tendency towards carelessness in
Lunn’s work,152 but now I recognize that I may have been unfair: pos-
sibly Shrewsbury has cited Lunn’s thesis inaccurately and in a way that
would support his own “campaign” to reduce the mortality rates among
the parish clergy as estimated by Lunn. We will enlarge on this point
below.
The state of the Exeter episcopal registers in this period is described
in very negative terms by (Rev. Prebendary) Hingeston-Randolph, as
cited by Gasquet, and reflects strongly the impact of the Black Death on
the diocesan administration:
The Registrum Commune, which is wonderfully full before and after the
fatal year, records scarcely anything during the year itself. The ordinary
work of the diocese seems to have been all suspended, with a single
exception. The register of institutions—a separate volume—is a record of
incessant and most distressing work. Its very outward aspect for this
period tells a tale of woe. The entries are made hurriedly and roughly, in
striking contrast with the neatness and regularity of the rest of the
Register. They are not longer grouped, as before, in years, but in months,
and the changes in each month exceed the changes of a whole ordinary
year, when there was no pestilence. The scribe leaves off the customary
‘vacant per mortem’, as if he dreaded to write the fatal word.153
This does not confirm that the diocese of Exeter’s register of institu-
tions in this period did not indicate whether parish benefices were
150
Benedictow 2004: 344; Pickard 1947: 25; Ziegler 1970: 130, I have not been able
to identify Ziegler’s basis for this assertion.
151
152
Benedictow 2004: 353–4, 356–7.
153
Cited by Gasquet 1908: 100.
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vacated by resignation, as stated by Lunn according to Shrewsbury,

only that vacation by death was not specified. The register has also two
sizeable lacunae that may reflect the deaths of the scribes who kept
them. Lunn is cited to the effect that the lacunae could be reasonably
filled in with an estimated two institutions per day.154
However, the general geographical outline of Lunn’s assessment of
the bishop’s registers, the poor quality of those of the southern dioceses
at or around the place of arrival of the Black Death and the better qual-
ity of those produced in northern dioceses, fits very well into the out-
lined spatio-temporal perspective on how the bishops’ administrations
should be expected to cope with the disastrous events.
In his study of the institutions entered in the diocese of Lincoln’s
bishop’s register Thompson points out that
The presentee could often have a long journey to make to reach the
bishop; and again and again, in classifying the institutions, one is struck
by the appearance on the same day of several candidates who had been
presented to churches in adjacent parishes […]. This looks as though the
clergy, who were largely drawn from the neighbourhood in which their
parishes lay, waited until they could get one or more companions to make
the journey with them.155
The practice of non-beneficed priests who wished preferment to a local
benefice vacated by the Black Death of waiting to set out on the journey
to the bishop until they could get one or more companions would cer-
tainly entail at least some delay. However, one may wonder if they
would take the chance of postponing departure if they really had good
prospects of being instituted, and this question raises that of the central
role of patrons and advowsons. Thompson seems to have overlooked
the fact that the real reason for the postponement was that these hope-
ful men needed to receive the support of the patron or group of medie-
ties holding the advowson to the parish church in question, who would
then contact the archdeacon and ask him to enquire into the legal cir-
cumstances of the vacancy and the suitability of the candidate. If the
response was positive, the patron would present his candidate’s service
to the authority who possessed the right of institution, the bishop
or the archdeacon, and receive confirmation of the candidacy for the
benefice. Next, this piece of news would be conveyed to the candidate,
154
155
Thompson 1911: 316–7.
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452 chapter eleven
who only then would optimistically set out on a journey to be insti-

tuted in the benefice. This account of the process accords better with
Thompson’s own wording, understanding the term “presentee” to apply
to those who set out on the road to the bishop to be instituted, which
implies that they had already been presented by a patron and officially
approved, and had then received a notification, at which point they
could prepare for the journey to the bishop to be presented and insti-
tuted. This means that several non-beneficed priests in a district where
the Black Death was raging would be in this situation, awaiting eagerly
confirmation of preferment, which also can explain that they could set
out on the journey together. This process would obviously be quite
time-consuming.
Thompson also provides some material that indicates quite a long
time lag between the occurrence of vacancies and the institution of
new incumbents in the diocese of Lincoln, namely, that “some of the
six institutions in September were to churches which had fallen vacant
before the end of July.” In Nottinghamshire, “where we might expect to
find the earliest ravages of the plague, there is only one such institution
before July [1349]” and it is known “that on 15th May archbishop
Zouche licensed the dedication of a cemetery at Newark, owing to the
alarming growth of the pestilence.”156 Newark is situated deep in
Nottinghamshire, and the Black Death must be assumed to have been
spreading for a longish time before attacking this town. If we add to
this time the usual time of the disease’s development among the rat
colonies and unobtrusive endemic phase of about six to seven weeks
before demonstrating its presence by a significant number of deaths,
and the additional time before the disease had caused a great mortality
necessitating the establishment of a new cemetery,157 we see that the
Black Death had ravaged Nottinghamshire for at least several months
before there was any reflection in the incidence of institutions.
Cures vacated by the death of incumbents would quite often not be
reflected in institutions for quite a long time of variable duration simply
because the number of deaths among the beneficed parish clergy ex-
ceeded the number of substitutes competent to fill them, a point that
there will be occasion to enlarge upon. Another closely related point
that will also tend to distort the connection between the time and
location of the death of parish clergy and institution of successors is that
156
Thompson 1914: 105–6.
157
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the best cures would be taken up first whilst the poor cures would go
begging, a fact strongly criticized and deplored by contemporaries.158
Studies of institutions which cover not only the period of the Black
Death but also the pre-plague and the post-plague years exhibit some
conspicuous features that have been generally overlooked. However, in
this context they must be closely examined because they imply a much
longer average lapse of time between vacancies and institutions than
has been envisaged up to now. In particular the high numbers of insti-
tutions in the post-plague years deserve comment. In the diocese of
Exeter, which comprises the two counties of Devonshire and Cornwall,
Devonshire was invaded in the summer of 1348, and it is known that in
August the Black Death was causing terrible mortality in religious
houses on the River Otter about twenty-five km from the border of
Dorset; Cornwall was invaded in the late autumn, implying that by this
time the Black Death had spread across Devonshire.159
Exeter was a largish diocese with 642 parishes.160 Pickard found an
average of twenty-five institutions for the period 1338–47 and the
yearly variation was 8–31. Thus when the number of institutions in
1348 was twenty-eight, the difference from the average is not signifi-
cant and cannot be taken as evidence of supermortality caused by the
Black Death. In 1349, the number of first institutions was 331, in 1350
seventy-five, and twenty-nine in 1351. The fact that the Black Death
raged in Devonshire in August, but that there is no noticeable increase
in the number of institutions before January 1349, shows that there
must have been a usual lapse of time between the death of incum-
bents and (the registration) of the institution of their successors of
something of the order of five to six months. This must reflect the fact
that the diocesan administration broke more or less down under the
impact of the Black Death, as was suggested above would be the case
for the dioceses that were attacked first and had scant time to prepare
administratively and mentally for the ferocious onslaught. This shows
that a large proportion of the vacancies caused by the Black Death was
filled in after the epidemic had disappeared, especially in Devonshire.
When this is not taken into account, the level of normal mortality
among the beneficed parish clergy will be substantially underestimated
158
Benedictow 2004: 347; Campbell 1931: 138.
159
Benedictow 2004: 128–9, 131–2; Shrewsbury 1971: 60.
160
Pickard 1947: 22.
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454 chapter eleven
and the spatio-temporal aspects of the epidemic process become

strongly skewed. In the following period of 1352–60 the average yearly
number of institutions diminished to 16.4, reflecting the fact that the
normal mortality rate among the new and younger parish priests was
much lower than the normal mortality rate among the elderly pre-
plague incumbents; in fact it was almost halved. This implies that
thirty-three of the 104 institutions in 1350–1 were due to normal mor-
tality, resignations or exchanges and that about seventy-one were due
to plague,161 many of them quite likely pertaining to Cornwall where
the Black Death petered out in the autumn of 1349. Also some of the
deaths in the plague period were, of course, due to other causes than
plague, but many of those that would otherwise have died from such
ordinary causes now died from plague instead, and this aspect of cleri-
cal mortality therefore loses much of its significance. This shows also
that the real mortality rate among the parish priests in the Black Death
was considerably higher than 51.5 per cent as estimated by Pickard.
However, not all post-plague institutions were first institutions, some
were successive institutions in the same living, second, third or even
fourth. These successive institutions must be deleted in order to ascer-
tain the pool or population of original incumbents which can serve as
a base for estimation of mortality rate, the proportion of them who
died, and for constructing an outline of the temporal progression of the
epidemic throughout the parishes.162 The numerical relationship
between first institutions and successive institutions in the same bene-
fice is reasonably well known only in the case of the diocese of Coventry
and Lichfield. Lunn and R.A. Davis agree that the period of the Black
Death in this diocese was April to October of 1349. In this period 208
parish priests were instituted. Twenty-three of them were successive
institutions to the same benefice; when this number is deducted, the
number of first institutions was 185, and successive institutions con-
stituted 11 per cent of the total.163 Assuming that this percentage is
161
Pickard 1947: 22–7. Gasquet 1908: 199–200, gives considerably higher figures,
but they are dismissed by Pickard who asserts that they do not refer to first institutions
in parish benefices but to all sorts of institutions, also successive institutions in the
same living.
162
The size of the population of auxiliary priests from which new incumbents were
recruited into the vacancies is not known and must therefore be deleted from the mate-
rial. See also Davis 1989: 86.
163
Davis 1989: 86. According to Lunn, as cited by Shrewsbury 1971: 77, the number
of first institutions was 188. Here Davis’s figures are preferred, since Lunn’s thesis has
been lost and his premises cannot be tested.
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reasonably representative of the proportion of successive institutions

among the total number of institutions in the following couple of years
in the diocese of Exeter, this indicates that of the seventy-one institu-
tions in the years 1350–1 caused by plague, sixty-three were first insti-
tutions. This means that the total number of first institutions caused by
plague was 331+63 = 394 first institutions performed in 642 parishes.
Consequently, post-plague first institutions constitute 19 per cent of
the number of institutions in the plague period and 16 per cent of the
total number of vacancies caused by plague. It also means that 61.4
percent of all parish priests serving in the diocese of Exeter at the time
it was invaded by the Black Death died in the epidemic. This indicates
that the average lapse of time between incumbents’ death by plague
and the institution of successors must be much longer than the average
of the institutions that were being performed during the plague epi-
demic in the diocese. It must be underlined that the accuracy of these
estimates is dependent on that the assumption that the proportion of
successive institutions in the same cure in Coventry and Lichfield is
reasonably representative also of this diocese.
Taken together, the information relevant to the question of the time
lag between deaths of incumbents and institution of their successors in
the diocese of Exeter has uncovered a high proportion of long delays
that considered together indicate an average time lag of at least several
months between the death of incumbents and the first institution of
successors, quite likely on the order of five or six months or longer.
The considerable proportion of plague mortality related institutions
in 1350–1 must reflect great difficulties in filling in many vacancies
during the epidemic and a high incidence of long delays in the plague
period that would not show in the bishop’s register. This is confirmed
by another feature of the register. Gasquet remarks that
It is curious to note in these years that numerous benefices lapsed to the
Bishop. These must have been vacant six months, at least, before the dates
when they were filled by Bishop Grandisson [of Exeter].164
The time perspective of the relationship between the death of incum-
bents and institution of successors should also be seen in the light of
the frequency of lapses of benefices.
The magnitude and importance of these problems can be seen in
other dioceses as well. In the diocese of Ely (Cambridgeshire), the
164
Gasquet 1908: 200.
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456 chapter eleven
number of institutions in 1349 was about eighty-five. In the pre-plague

years, the average number of institutions was 3.5, but conspicuously,
after the Black Death had disappeared, in 1350 and 1351, there were
thirteen and eleven institutions respectively. Since the new parish
priests tended to be considerably younger than the incumbents they
succeeded, their natural mortality rate was, as could be expected, con-
siderably lower than before the plague, a factor that would be concealed
by the total figures of institutions during the immediate post-plague
years. In the years 1352–5, the average number of institutions in the
diocese of Ely was 1.75, down from 3.5 before the plague, in fact,
halved.165 Thus, the twenty-four institutions of 1350–1 represent an
“excess” of vacancies related to the plague period of twenty or twenty-
one parish priests (not seventeen), making the total number of plague
mortality related vacancies 105–6. This constitutes strong evidence that
a considerable proportion of institutions of successors to cures were
performed in the two years after the plague had disappeared, in fact a
proportion of 24 per cent of the institutions of 1349 or 19.5 per cent of
the total number of plague-mortality related vacancies. Obviously, this
implies that a significant or rather substantial proportion of voidances
remained unfilled for many months in the plague period, but that this
is concealed by the way institutions are recorded in the bishop’s registers,
since they (with one exception) do not note the time of the incumbent’s
death (or resignation). Taking into account the fact that the post-plague
institutions do not reflect mortality in the dying days of the epidemic
but rather a variable number of months earlier, the time lag between
these institutions and the incumbents’ deaths was even longer, quite
likely around 1.25–2.5 years later. Again, this shows that the average
lapse of time between the death of incumbents and the first institution
of successors must have been quite a number of months.
In the diocese of Hereford the average number of institutions during
the three pre-plague years was, according to Gasquet, thirteen, while in
the plague year of 1349 175 institutions were recorded in the bishop’s
register.166 According to W.J. Dohar’s count in his recent study of the
Black Death in this diocese, the average number of institutions in the
years 1345–7 was six,167 and in 1349 160, almost twenty-seven times
165
Benedictow 2004: 354–5; Aberth 1995: 278–9.
166
Gasquet 1908: 165.
167
In 1348 the number was 11, affected by the intrusion of the Black Death into the
southern districts of the diocese at the end of the year, and can therefore not be included
in estimation of the pre-plague average. Dohar 1994: 41–2.
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higher. The discrepancy is rather disquieting. Dohar’s figures include

all sorts of reasons for vacancies, including death, retirement, resigna-
tion and exchange, and apparently also all subsequent institutions in
the same parish in 1349, which means that no mortality estimate can
be made. However, according to Lunn, as cited by Shrewsbury in a his-
togram, only about 127 institutions were performed in the months
March to December,168 representing a yearly total of 132 when five
institutions in January and February are added.169 Perhaps meticulous
registration of the institutions would have allowed Lunn to delete
successive institutions in the same benefice from the material, which
might fit quite well with the difference and should perhaps have been
accepted instead. All other explanations tend to be disquieting, and
would tend to give the following simple calculations the character of
guesstimates or indicative exemplifications. According to Gasquet and
Dohar, there were forty-five more institutions in 1350,170 7.5 times the
pre-plague average, while in 1351 and 1352 the numbers of institutions
were twenty-five and twenty-six respectively, and in fact, the yearly
number of institutions did not revert to the pre-plague figure until 1358
(7), then jumped to eighteen in 1359, to return to seven in 1360.171
Thus, in the decade 1350–9 there were 207 more institutions, an aver-
age of about 21.
If, for the sake of comparability, it is assumed according to the previ-
ous data that the post-plague normal yearly attrition rate of the new
and young(er) parish priests was roughly half of the level among the
pre-plague incumbents, this suggests that thirty of the post-plague
institutions resulted from normal deaths and that the remaining 177
institutions presumably reflected the ravages of the Black Death with
the caveat in this special case that successive institutions to the same
cure must be deducted. Data discussed above suggest that successive
institutions in the same parish benefices could have constituted around
11 per cent of the total. On these premises, forty-two of the forty-five
institutions in 1350 could be assumed to be due to plague, of which
11 per cent or five institutions may have been successive institutions,
and thus the number of first institutions would be thirty-seven. In the
168
169
Dohar 1994: 46.
170
Gasquet 1908: 165; Dohar 1994: 42. This confirms that Gasquet tends to register
all institutions whatever the cause of vacancy.
171
Dohar 1994: 42.
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458 chapter eleven
case of the fifty-one institutions of 1351–2, the same considerations

would provide a number of first institutions of forty. When normal
mortality and successive institutions are deducted, this means that
there were seventy-seven institutions in the years 1350–2, which con-
stitute 58 per cent of the first institutions in 1349 and 37 per cent of the
total number of first institutions of 209 in the years 1349–2. Again it
must be clear that a substantial proportion of parish benefices vacated
by the Black Death was not filled in until several years after the epidemic;
in Hereford diocese, as it seems, not until the end of the following dec-
ade. If seventy-six institutions performed in the five years 1353–7 are
also taken into account, fifty-four of these would on the same premises
be first institutions vacated by the Black Death. This implies that the
number of first institutions in the period 1349–57 was 263, and that in
this diocese only half of the vacated parish cures were filled in during
the epidemic. No matter which of these estimates are applied, a very
long average lapse of time is implied between the death of incumbents
and the institution of successors. The usability of institutions for fol-
lowing the process of epidemic spread of the Black Death is further
undermined, or rather their unsuitability for this task is confirmed.
Gasquet realizes that there is something important associated with
his registration of forty-five vacancies that were filled up in the first
post-plague year: this “points to the fact that many livings had probably
remained for some months without incumbents.”172 Importantly, he
goes on to add:
This suspicion is further strengthened by the frequent appearance of the
words “by lapse” in the record of institutions at this period, which shows
that for six months the living had not been filled […].
Gasquet’s comments show an incomplete understanding of the real sig-
nificance of his findings, but the pioneering character of his work must
be underlined. One might also consider the effects of the bishop’s anti-
epidemic strategies: he did not stay much at his palace in Hereford, he
moved away from the progress of the epidemic to episcopal manors in
his diocese, and next to manors belonging to his diocese in the neigh-
bouring diocese of Worcester.173 For all parties concerned this would
inevitably cause considerable additional delay and extra difficulties in
the process of filling in the vacancies.
172
Gasquet 1908: 165.
173
Dohar 1994: 56–7.
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At the episcopal level of analysis, the Bishop of Bath and Wells con-
veys relevant comments and views in a circular letter to his clerical
personnel in the diocese of 17 January 1349:
the pestilence which is spreading itself far and wide has left many parish
churches and other cures, and consequently the people of our diocese,
destitute of curates174 and priests. And inasmuch as priests cannot be
found who are willing out of zeal, devotion, or for a stipend to undertake
the care of the foresaid places, and to visit the sick and administer to
them the Sacraments of the Church (perchance for dread of the infection
and contagion), many, as we understand, are dying without the Sacrament
of Penance.175
Thus the bishop conveys information and impressions which in his
religious perspective imply that in mid-January 1349 dramatic and
unacceptable duration of voidances of priestly benefices was usual in
the parishes of the diocese which covered most of the county of
Somerset, which in the Middle Ages stretched all the way to the River
Avon and Bristol. Since this was a circular letter to his clergy, its con-
tents would not be mere rhetorical imaginings, and it seems likely that
the recipients would accept its main thrust on this point, that there was
a great dearth of clergy and priestly services and that many people were
dying in the diocese without priestly spiritual services in their dying
hours. At a time of great religious devotion and the belief that the last
rites were a necessary condition for salvation, this was an extremely
grave situation indeed. The time perspective of this letter makes it clear
that, in the autumn of 1348, the Black Death had raged so severely in
Somerset that the situation was critical at the latest at the end of the
year. This corresponds perfectly well with the fact that most of the ten-
ants at manors in the south-eastern part of the county and at Frome
Braunch in the north-eastern part of the county were dead by the
beginning of August and that the Black Death broke out in Bristol
15 August.176 If institutions followed “some little time” after the deaths
of incumbents, how could it be that the spread of the Black Death all
over the diocese or county in the autumn of 1348, which caused a
widespread and grave lack of parish priests by the end of the year, an
increase in the number of institutions was noticeable in November at
174
The term “curates” refers to the positions of parish priests who had “the actual
cure of the souls.”
175
Gasquet 1908: 92–3.
176
Rees 1923: 29; Benedictow 2004: 128. See also below.
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460 chapter eleven
the earliest?177 However, this small increase in November is quite likely

not significant: it is independently explicable by Russell’s finding of a
normal pre-plague peak of mortality at this time of the year and at the
beginning of winter weather when vulnerable persons with poor health
were more likely to die than in the warmer seasons (see above). And in
view of the early outbreak in Bristol and shortly thereafter in Gloucester,
how can it be that there is not an indisputable clear plague-related
increase in the institutions of the diocese of Worcester until May of
1349?178 The small increase in December 1348 and January 1349 is also
explicable by Russell’s finding which means that such an increase in
this month was normal.
Independently, other contemporary observers made the same point
as the bishop, and as early as 1348 a chronicler asserted that “there is
such a scarcity of priests and others serving churches that many of the
latter remained without incumbents.”179 Again it must be asked, why is
this situation not reflected in the registers of institutions? Can it be any
other explanation than that there is a usual time lag of around six
months, quite likely significantly longer, between the death of incum-
bents and the institution of successors, at least in the southern dioceses
that were attacked first, unprepared and terror-stricken?
A recent paper offers a fresh discussion of the bishop’s register of the
diocese of Coventry and Lichfield. This is, as mentioned above, the
only such register that provides information both on the dying day of
the incumbent and the day of the institution of his successor. It is
important to note that this diocese’s bishop’s register is generally
characterized as the best, most detailed and most neatly kept bishop’s
register (see above). Impressively, this was also the case throughout the
epidemic period, thus, the staff managed to maintain these standards
under circumstances of immense distress and workload. In a source-
critical perspective, this reflects the workings of a diocese with a strong
tradition for high administrative standards and indicates that the
bishop and his staff put, accordingly, a special emphasis on being well
prepared for the coming onslaught and being able to uphold their
standards, which was not the case with the bishops’ registers of the
south-western dioceses. This paper shows an average time lapse
between the death of incumbents and the institution of their successors
177
Gasquet 1908: 96; Shrewsbury 1971: 64; Benedictow 2004: 128.
178
Shrewbury 1971: 66, 68.
179
Campbell 1931: 137.
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of 39.4 days for the first eight months of the epidemic.180 As should be
clear by now, such a time perspective for the study of this subject is
insufficient and will not cover a substantial proportion of institutions
caused by plague deaths among incumbents. One may wonder why
there were no lapses of cures into the hand of the bishop in this diocese
and why or how, in contrast to other dioceses, substitutes could be so
readily found for all incumbents who died in the epidemic.181 One
should note that only those vacancies which were filled and for which
institutions were performed were entered in the bishop’s register, and
that those which remained vacant for the duration of the epidemic or
which lapsed to the bishop are not mentioned. This means that the
estimate of the average lapse of time between the death of incumbents
and the institution of successors provided by these scholars are not rel-
evant for the present discussion. According to the course of events in
other dioceses, a longer perspective of several years would presumably
have uncovered further important information. Assuming that the
proportion of institutions which was performed in the following four
months and the proportion in the following two or three years resem-
ble those of other dioceses for which data are available, the complete
average lapse of time was no doubt considerably longer. This paper also
reflects some of the misconceptions with respect to the spread rates of
plague and the reasons for the differences between historical plague
and modern plague that have been thoroughly discussed above. These
misconceptions reflect the fact that the authors have not acquainted
themselves with the primary studies or standard works on bubonic
plague.182 Fortunately, R.H. Davis and also Lunn, as cited by Shrewsbury,
provide valuable information on the Black Death related developments
in this diocese on the basis of this bishop’s register (see above).
Also from a source-critical perspective there is truth in Shakespeare’s

words: “When sorrows come, they come not single spies,/but in bat-
talions!” Twigg is surprised by Shrewsbury’s remark that, according to
Lunn, the peak in institutions in March in the diocese of Salisbury
indicated that the epidemic reached its peak in February, implying that
this, in his opinion, was an unexpectedly long average lapse of time
180
Wood, Ferrell, DeWitt-Aviña 2003: 441, 439.
181
Wood, Ferrel, DeWitt-Aviña 2003: 445.
182
See also Wood and DeWitt-Aviña 2003: 327–8, and Wood and DeWitt-Aviña
2004: 485.
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462 chapter eleven
between the deaths of parish priests and the institutions of their suc-
cessors.183 As should now be clear, this assumed duration of the average
lapse of time between the death of a parish priest and the institution of
his successor must be considered unrealistically brief; and as shown
above, the reason is that it is based on a misconception or misunder-
standing by Thompson. Certainly, in the case of the southern dioceses
there is much evidence for assuming average delays of quite a number
of months and much longer delays for a substantial proportion of the
parish benefices vacated by the Black Death.
The central insights that can be learned from this discussion are that
there was apparently great variation in the standards of the diocesan
staffs or administrations, that there was great dissimilarity in the oppor-
tunities to prepare for the onslaught, and that the interaction between
these main structural factors caused great variation in the lapse of time
between the death of incumbents and the institution of their successors.
Another factor is the size of the dioceses, which varied greatly and
affected the processes in co-variation with the bishops’ various strate-
gies in the face of the threat of the spread of the Black Death, particu-
larly their strategies of taking refuge on peripheral manors or being on
the move away from the approaching plague, settling provisionally on
various episcopal manors, and if necessary even moving into a neigh-
bouring diocese. Each diocese must be considered individually, there is
no such thing as a usable standard average lapse of time for all dioceses
in this respect. It has been well documented above that a flexible time
horizon of around half a year is relevant for several dioceses, especially
the southern dioceses closest to the Black Death’s landing ground in
Melcombe Regis/ Weymouth, which are central to the present discus-
sion. This implies that Twigg’s and Scott and Duncan’s use of institu-
tions to determine the time of mortality in the parishes on the basis of
an assumption of contemporaneity or proximity in time between mor-
tality and institution is untenable (also within wide margins of
uncertainty).
The substantial incidence of long lapses of over six months and of
one to two years indicates that the usual estimates of the mortality
among parish priests on the basis of institutions in assumed close
association with the epidemic will tend to be substantial underestima-
tions and that the real mortality rate of parish priests quite likely was
183
Shrewsbury 1971: 59; Twigg 1984: 65.
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considerably higher than usually assumed, on the order of 50–60

percent. This supports the direction of my discussion of the various
source-critical problems associated with the use of bishop’s registers for
estimating mortality rates among parish priests in my monograph on
the Black Death.184
Temporal Relationship between the Territorial Spread of the Black

Death and Increase in Institutions
At the present state of research, this conclusion based on the study of

bishops’ registers can only be further tested by examining independent
data on the spread of the Black Death in time and space and by com-
paring these data with the reflections of the mortality among the parish
priests in the form of institutions of successors. Twigg’s brief account of
the arrival and spread of the Black Death in England and, consequently,
also of Scott and Duncan who follow Twigg’s account closely and
dependently, are quite misinformed and misleading (see below).185
Instead, the discussion will be based on the most recent synthetic and
fully documented presentation of this important historical event which
is given in my monograph on the Black Death and supplemented with
additional information.186 Given this background, the discussion of
this topic will focus directly on the dioceses where they assert on the
basis of institutions that the beneficed parish clergy exhibited high
mortality in the winter months, and that these months coincided at
least mainly with the time the ordinary population there were visited
by the Black Death. If this view can be shown to be reasonably tenable,
the epidemic would have to be something else, since bubonic plague
does not spread efficiently in the winter.
The dioceses that have been central in the previous discussion exactly
for the same reason are the south-western dioceses of Salisbury, Exeter,
Bath and Wells, and the south-western part of Winchester (county of
Hampshire). Twigg and Scott and Duncan are completely dependent
on Shrewsbury for their material on institutions, so their data is a sec-
ondary selection of data from Lunn’s lost and untestable thesis, which
also means that Shrewsbury’s rendering of it is untestable. As repeat-
edly shown above, there are serious grounds for concern with respect
184
185
Twigg 1984: 58–69; Scott and Duncan 2001: 88–91.
186
Benedictow 2004: 123–43, 342–60.
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464 chapter eleven
to this important point (which, unfortunately, has dawned upon me

quite belatedly). Twigg purportedly cites Shrewsbury’s data by month.
Scott and Duncan do it differently and more inaccurately in the chapter
where they discuss the seasonality of the Black Death in England: they
indicate only the month when the epidemic started and the months of
the peak of the epidemic, in both cases according to an assumption of
identity in time between institutions and the progression or main
phases of epidemic developments.187
These approaches to the material and their dependence on
Shrewsbury’s monograph will shape much of the discussion here,
because also Shrewsbury has a negative agenda. His objective is to
reject the conclusion that plague could cause high mortality in medie-
val England because the densities of people and rats and rat fleas in his
opinion were too small to allow efficient powers of spread, and for the
same reason mortality rates would have to be very much smaller than
ordinarily assumed by demographers and agricultural historians at the
time he wrote his monograph. This agenda suits Twigg’s and Scott and
Duncan’s objectives, namely to deny that the epidemic could have been
bubonic plague, which clears the way for an alternative theory that also
involved very much smaller mortality rates. In their opinion, the epi-
demic was, as mentioned, anthrax or the filoviridal Ebola or Marburg
diseases, diseases that are so extremely different that apparently very
little of an empirical nature restricts their choice of microbiological
alternative: in this situation choice of alternative can be made quite
arbitrarily, which undermines their validity.
It has been shown above that Twigg’s, Scott and Duncan’s and Cohn’s
assertions to the effect that bubonic plague spreads only contiguously
between rat colonies are not based on the research literature and are at
variance with the studies in India and elsewhere; they are, in short,
erroneous. On the basis of my quite complete analysis of the Black
Death’s spread in England, average spread rates of 1–1.5 km a day by
land,188 corresponding to spread rates elsewhere in Europe, including
in Norway,189 will be assumed as normal under not unfavourable con-
ditions. This range of spread rates should be considered within a wider
registered range of spread rates of c. 0.5–2.5 km a day, with the caveat
187
Twigg 1984: 65–7, 175–80; Scott and Duncan 2001: 88–90, 105–7.
188
189
Benedictow 1993/1996: 78–80; Benedictow 2004: 227–31; Benedictow 2002:
33–8; Benedictow 2006: 90–4, 107–8.
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that in chilly or cold weather epidemic spread would be greatly reduced

or halted altogether.190 One should also take into account bubonic
plague’s ability to spread easily by metastatic leaps. In the history of the
Black Death in England it is possible to identify a number of metastatic
leaps over considerable distances by ship transportation both along the
coasts and along estuaries and rivers which established new centres of
spread. Among the most important are the early leaps by ship from
Melcombe Regis to the Pale in eastern Ireland, to Bristol, to London, to
East Anglia and up the River Stour to Sudbury, perhaps from an origi-
nal infection at Harwich, which can explain why Cambridgeshire was
invaded several months earlier than Oxfordshire and Buckinghamshire,
and by ship from south-eastern England to Grimsby (or possibly Hull)
in the autumn of 1348,191 and so on.192
The diocese of Salisbury is where discussion of the Black Death’s sea-
sonality in England starts. The point of departure must be the original
outbreak of the Black Death in England shortly before 24 June 1348 in
Melcombe Regis (Weymouth), a town situated on the coast of the
county of Dorset in the diocese of Salisbury which also included the
inland counties of Wiltshire and Berkshire. This makes it very difficult
to understand the reality or substance of Twigg’s assertion that “plague
did not appear [in England] until late 1348”193 or Scott and Duncan’s
corresponding and dependent assertion to the effect that “In the dio-
cese of Salisbury, the epidemic was rampant through December to
February and reached its peak in March.”194
Dorset comprises an area of 2559 sq. km; the maximum distance
along the west-east axis is slightly above ninety km, and slightly above
fifty km along the south-north axis. Melcome Regis where the Black
Death was introduced into the county (and England) is situated at the
most about fifty-five km from the borders of the county in any direc-
tion. This implies that the epidemic should or could have spread to all
corners of the county around mid-August, if the time of the outbreak is
taken as the point of departure and not the time of introduction which
190
191
Benedictow 2004: 128, 127–34, 139–40, 144.
192
At the end of September, the prior of Christ Church Priory in Canterbury wrote
an alarmed letter to the Bishop of London informing him about various invasions of
the Black Death in the diocese. Benedictow 2004: 134.
193
Twigg 1984: 181.
194
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466 chapter eleven
is followed by the latent period when contaminated rat fleas could

unobtrusively have been transported in goods by land and sea.
Importantly, there was great mortality in religious houses on the
River Otter in the south-eastern corner of Devonshire about sixty-five
km west of Melcombe Regis in August.195 Gillingham is situated at the
very northern end of central Dorset, in a longish territorial protrusion
between the southern parts of Somerset and Wiltshire. At the sitting
of a manorial court held at the royal manor of Gillingham on the
Wednesday after the feast of St Lucy (13 December) 1348 it was
recorded that heriots (“death duties”) were paid on the deaths of about
twenty-eight tenants, furthermore, the bailiff noted that he had in hand
the lands and tenancies of about thirty tenants, which means that they
had died without heirs who could succeed into their holdings. In many
cases, it was declared that no heriot had been paid, although receipts of
this kind at the court were unusually numerous.196 This means that the
Black Death had raged there for quite some time, since such a large
number of heriots was being paid on tenants who had died since the
previous sitting of the court, and since at this time about thirty hold-
ings had reverted into the hand of the lord, and since there was already
a large backlog of unpaid heriots, which must be assumed to reflect the
cumulative process over some significant length of time.197 Consequently,
at the latest in the first half of November, and quite likely considerably
earlier, the Black Death had broken out in this district almost as far
away from Melcombe Regis as one could possibly get in any direction
within the county and about as deep inland as one could possibly get.
There is no reason to assume that this was the first manor in the area or
in the northern parts of the county to be attacked. On the contrary, the
survival of medieval manorial records is quite fortuitous; as is, to some
extent, the concrete information in this case, since it is a result of
Gasquet’s personal request for permission from the Squire of Gillingham
to have a look at them. One hopes that more manorial material waits to
be studied that can shed more light on these events. This analysis is
confirmed by the large number of institutions performed in Wiltshire
in 1348, over seventy (see below), which shows that the Black Death
had crossed Dorset’s border in the north and spread devastatingly there
for a considerable period of time in the autumn.
195
196
Gasquet 1908: 194.
197
Ibid.
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This evidence indicates that the whole of Dorset was engulfed by

the Black Death by November at the very latest, probably considerably
earlier, although there were no doubt districts or territorial pockets
that remained to be invaded or were passed over by the epidemic. Th is
view is supported by the fact that the experienced ecclesiastical histo-
rian J.C. Cox found 140 institutions in the diocese in the years 1345–7,
a yearly average of c. 47, but registered 190 institutions in 1348 and 140
in 1349. When the average number of institutions in the preceding
three years are deducted from the 190 institutions performed in 1348,
this produces a net number of 143 institutions that must reflect quite
closely the effect of the Black Death in the second half of 1348, repre-
senting twelve times the normal average for half a year.198 In fact, the
number and proportion of plague-related deaths must be higher,
around 155, since incumbents that would have died from ordinary
causes in the previous years, now died from plague instead. This makes
it rather disquieting that Lunn, according to Shrewsbury’s histogram,
found only c. sixty institutions in the last six months of 1348 for the
whole diocese, and not a noticeable rise until November.199 Cox’s regis-
tration means that the peak period of vacancies and institutions in the
diocese of Salisbury was the last six months of 1348, which is corrobo-
rated by the large number of institutions in Wiltshire. In fact, Gasquet
and Fletcher found seventy-three and seventy-two institutions respec-
tively in Wiltshire in 1348, higher numbers of institutions for this
county alone than Lunn registered for the whole diocese according to
Shrewsbury, which is even more disquieting.200 One should note that in
the diocese of Salisbury there were thirty institutions in 1345 and fifty-
six in 1346, so the normal yearly variation is at least hundred per cent,201
since there is no reason to believe that the figures for these two years
represent maximum variation in numbers of institutions in the preced-
ing decades. This means that seventy-two or seventy-three institutions
in Wiltshire in 1348 represent a level of mortality among incumbents
corresponding to the normal attrition of incumbents for two years for
the whole diocese.
The high number of institutions in Wiltshire in 1348 must reflect the
fact that this county to the north of Dorset was invaded in the early
198
Cox 1907: 13.
199
200
Gasquet 1908: 189; Fletcher 1922: 11; Shrewsbury 1971: 59.
201
Cox 1907: 13.
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468 chapter eleven
autumn at the latest and that the disease had spread widely, which con-
forms to the prediction of the of normal spread rates of bubonic plague
as presented above. This makes it quite inexplicable that Dorset should
not have been engulfed by the Black Death in these months, and dem-
onstrates that the tiny number of institutions registered by Lunn
(according to Shrewsbury) before November cannot reflect the real
number of victimized incumbents in this period but can be explained
as normal attrition by death although within the higher reaches of the
range of normal variation. Thus, from the outset of this examination
of the relevant data, Twigg’s and Scott and Duncan’s assertions and
assumptions crumble.
How does this spatio-temporal picture of the spread of the Black
Death in Dorset correlate with known institutions? In his paper on the
Black Death in the county of Dorset which is mainly based on the study
of institutions, Fletcher states that he had found four institutions in
Dorset in October, but he seems to have included one of 30 September
in West Chickerell “which appears to have been the first parish to be
deprived of its incumbent.”202 Does this not appear very surprising?
Should not the first institutions have occurred in Melcombe Regis
where the Black Death first broke out shortly before 24 June? If the
Bishop’s register is reliable and institutions followed incumbents’ death
after a month’s time, how can it be that the local incumbents seemingly
escaped unscathed at least until the end of the year (and possibly later,
as no institution in Melcombe has apparently been identified)? One
institution elsewhere at the very end of September and three in October
constitute an incidence within the confines of normal variation. The
registered institutions occurred 30 September, 9 October, two on the
19th, and then nothing occurred until the beginning of November and
again, as it seems, on 9 November (Bridport).203 Institutions are part of
the normal clerical events and business of the diocesan organization.
There is no reason to consider these four institutions as being due to
the Black Death, since they do not represent a statistical incidence out-
side of normal variation. Neither is there a territorial relationship
between these institutions, which display great territorial dispersion,
a haphazard distribution unconnected by the movement of an epi-
demic disease. These institutions do not suggest an epidemic pattern or
202
Fletcher 1922: 7.
203
Fletcher 1922: 7–11.
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rhythm but an ordinary episodic character of clerical deaths. There is

no clustering of institutions in Dorset until after mid-November when
there were eight from the 17th to the 20th, which makes it likely that
the remaining seven institutions for November (out of 17 in all)
occurred in the following ten days. In December, there were twenty-
eight more institutions, which indicate a strong acceleration in the rate
of registrations of institutions from about mid-November.
Thus, the effects of Black Death appear not to be reflected in the
institutions until almost five months after the outbreak at Melcombe
Regis, until it had spread all through the county and crossed the bor-
ders into the neighbouring counties and had raged there throughout
the autumn. Remarkably and rather suspiciously, the number of insti-
tutions in Dorset in the second half of 1348 was only a fraction of the
institutions in the county situated north of it, namely Wiltshire, which
raises serious doubts as to the administrative process by which institu-
tions were entered in the bishop’s register at the time. Taken at face
value, this should mean that the Black Death reached this county to the
north of Dorset at a time which allowed it to spread according to a pat-
tern of pace and intensity which caused a much higher level of mortal-
ity among incumbents than in Dorset. Certainly, this feature needs
explanation since it may seem rather farfetched or unrealistic, and as
such must rather be taken as evidence to the effect that the bishop’s
register does not reflect the reality of mortality among the parish priests
in Dorset. And why are there, as it seems, no data for Berkshire? Perhaps
it would be useful to take a much closer look at the bishop’s itinerary
and, if possible, what happened to the bishop’s staff, and identify pos-
sible difficulties of effectuating and completing the process leading to
institutions (did he flee away early to Wiltshire?).
The main thrust of the evidence is that it took almost five months
from the outbreak of the Black Death in Melcombe Regis before effects
of the Black Death were reflected in institutions in Dorset; any possi-
ble deviation from this conclusion must have been insignificant. This
demonstrates that institutions as reflections of and evidence of the
process of spread and the mortality among parish priests in the Black
Death are only distantly related or correlated to the actual epidemic
process or at least that this was the case in this southern diocese. This
indicates that parish priests died in great numbers through the sum-
mer and autumn, but that this tragic and disastrous development was
not reflected in the bishop’s register until much later, and probably
imperfectly and in an order that did not reflect in any clear-cut way the
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470 chapter eleven
territorial progression of the epidemic. The institutions recorded in

the bishop’s register of this diocese are clearly unusable for the purpose
of identifying the Black Death’s spatio-temporal pattern of spread in
Dorset. Twigg’s and Scott and Duncan’s use of institutions for this dio-
cese is untenable and reflects the absence of source-criticism.
Also, the fact that Gasquet and Fletcher registered far more institu-
tions in Wiltshire than in Dorset in 1348 reflects badly on institutions
as sources on the spread and mortality effects of the Black Death in this
diocese. According to Shrewsbury, Lunn registered about sixty institu-
tions for the whole of the diocese in the months June to December. This
means that Lunn found a much smaller total number of institutions for
all three counties than Gasquet and Fletcher found independently of
each other for Wiltshire alone, and Fletcher is very clear on the point
that he has excluded all vacancies “caused by resignation or exchange”
from his material.204 Either Lunn’s registration is very deficient or, as
there has repeatedly been occasion to point out, Shrewsbury’s render-
ing of his data is highly inaccurate. This is unfortunate for Twigg and
Scott and Duncan who base their cases on Shrewsbury’s rendering of
Lunn’s results—“purported results” would now seem a more appropri-
ate choice of words. The registration of such a large number of institu-
tions for Wiltshire in 1348 indicates that the Black Death must have
spread widely and ravaged a large part of the county in the autumn of
1348. Fletcher registered 103 institutions in Wiltshire in 1349, which
also proportionally indicates that quite a large part of the county was
ravaged in the autumn of 1348. However, since it must be assumed that
a substantial portion of the parish benefices vacated by the Black Death
in 1348 was not filled in before the next year, an even larger part of the
county must be assumed to have been ravaged in these months, half or
more. This is not at all reflected in the numbers and seasonal distribu-
tion of institutions presented by Twigg and Scott and Duncan, which
means that their case again breaks down. It also appears rather incom-
prehensible how the pattern or rhythm of spread should in any way be
compatible with anthrax or any viral disease spread by physical contact
and the direct transmission of infected living cells as required by filo-
viridal diseases.
The diocese of Exeter lies immediately to the west of Dorset. It is
England’s south-westernmost diocese comprising the two counties
204
Fletcher 1922: 7.
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Devonshire and Cornwall. According to Twigg’s and Scott and Duncan’s

account of the events there, the number of institutions in the diocese of
Exeter did not begin to rise until January of 1349 and the Black Death
continued unabated through the winter months and into the spring
and summer of 1349. Twigg’s figures for monthly institutions in the
diocese deviate quite markedly from those given by Shrewsbury,
they are considerably higher, although he asserts that they are “after
Shrewsbury 1971.”205
The poor state of the diocese of Exeter’s bishop’s register cannot
explain the gross disparities between the number of institutions in the
months November 1348–September 1349 produced by Hingeston-
Randolph, as cited by Gasquet, and Lunn’s number of institutions, as
cited by Shrewsbury in a histogram (bar chart), namely 361 and c. 257
respectively.206 Later in his monograph, Gasquet states that the number
of vacancies in 1349 was 382.207 Pickard, who has made a new and inde-
pendent study of the institutions of this diocese, dismisses Gasquet’s
figure, asserting that it must include all sorts of institutions, for exam-
ple those to non-parochial benefices as well as exchanges and resigna-
tions. He found 331 first institutions in 1349,208 which means that he
very disquietingly found seventy-four more first institutions than
Lunn, almost 30 per cent more. Again these considerations raise seri-
ous doubts as to the quality and usability of Lunn’s work or perhaps
rather Shrewsbury’s rendering of it, and consequently serious doubts
over Twigg’s and Scott and Duncan’s use of it.
Devonshire is conterminous with Dorset 35–40 km west of Melcombe
Regis where the original outbreak occurred shortly before 24 June
1348.209 At the heart of Twigg’s and Scott and Duncan’s argument is a
willingness to accept as fact that when the incidence of institutions
does not begin to rise until January 1349 this proves that the Black
Death began its ravages at or around this time, half a year later, instead
of taking it as evidence of the problems in using institutions as sources
for this purpose. Assuming a normal spread rate by land of 1.25–1.5 km,
205
Twigg 1984: 179–80.
206
I again have an uneasy feeling about Shrewsbury’s figure which seems out of
line.
207
Gasquet 1908: 199.
208
Pickard 1947: 24–5.
209
Grandsen 1957: 274: “Isto anno apud Melcoumbe in comitatu Dorsate parum
ante festum nat’ sancti Iohannis Baptiste […].”
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472 chapter eleven
the Black Death would have crossed the border into Devonshire
14–20 July. Two religious institutions in the south-eastern corner of
Devonshire suffered heavy losses in August, namely the canons of the
collegiate church of Ottery St Mary and the Cistercian house of
Newenham in Honiton about 10 km north-east of Ottery. The time
perspective leading to full-blown outbreaks in the second half of August
suggests metastatic leaps, either by land, perhaps by pilgrims seeking
comfort in the religious institutions, or perhaps the contagion had been
transported by ship from Melcombe Regis to the estuary of the River
Otter, possibly to the small town of Budleigh Salterton and from there
by boat or barge some way upstream. One must also take into account
the possibility that the spread of the contagion started before the out-
break in Melcombe Regis by transportation in merchandise loaded
from a contaminated ship in the harbour and carried by ship, cart or
pack horse. The account of the Grey Friars’ Chronicle that contagion
was transmitted in the harbour from the contaminated ship which had
arrived from Gascony to a ship from Bristol210 is a sharp reminder of
this possibility. The process of spread could also have been accelerated
by people fleeing from the outbreak in Melcombe Regis, transporting
infected rat fleas in their clothing or luggage, which is an ordinary fea-
ture of bubonic plague’s epidemiology. Like many other counties,
Devonshire was apparently invaded from several directions, by epi-
demic spread over land, by carriage of goods or by the movement of
people and their luggage over land, and in this case also by people flee-
ing from Melcombe Regis, or by metastatic leaps by ship or boat.
Gasquet and Ziegler both comment that transportation by fishing boats
and ships along the coast and up the estuaries and navigable rivers
played a major role in the process of dissemination of the Black Death.211
Coulton, who also had the opportunity to read Lunn’s thesis, cites him
to the effect that “navigable rivers and estuaries did much to dissemi-
nate the plague.”212 More instances will be presented below.
Gasquet cites a source which states that the Black Death was raging
in the area of the modern district of North Devon on the Bay of
Barnstaple: it was raging 7 November at Northam on the estuary of
River Torridge, the same day also in the parish of Alverdiscott about
210
See for instance Benedictow 2004: 126–7.
211
212
Coulton 1947: 496.
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five km south-east of Northam, the next day it is mentioned in the vil-

lage of Fremington situated on the estuary of River Taw at the northern
end of the Bay about ten km from Northam, 23 December it was present
also in the small town of Barnstaple situated also on River Taw a little
over one km east of Fremington. All of these localities are situated
about fifty to sixty km north-west of Exeter (as the crow flies).213 This
pattern is entirely compatible with the marked tendency of bubonic
plague to linger in the same area for five to eight months, because it
needs to develop through phases taking around twenty-three days at
each place or house of arrival before the first death occurs, and almost
six weeks to develop into a local epidemic. Thus, the datings of the
epidemic presence in these neighbouring localities reflect a time-
consuming process of arrival and local spread, and imply that the dis-
ease had first broken out in the area at least several months earlier and
that the contagion had reached there almost six weeks before the first
outbreak, a pattern or process which would be repeated in all the sub-
sequent outbreaks in the area. Barnstaple and Northam could easily
have been contaminated by ship and have been included in a more
comprehensive spread along the coast that started in the summer and
caused the outbreak which was recognized at Bristol 15 August. The
Black Death was also raging in villages on the River Exe in November,214
a river that is navigable for a long part of its course, far north of Exeter,
all the way to Tiverton in north-eastern Devonshire, only about forty-
five km south-east of Barnstaple. Again transportation by ship or boat
may have played an important part, in this case from the south.
These data on the spread of the Black Death in Devonshire indicate
that the whole of Devonshire had been engulfed by the Black Death by
the late autumn and that the county had been invaded from several
quarters, by landings from ships or boats sailing along the coasts, espe-
cially in villages or small towns on the estuaries of major rivers, from
where the epidemic leapt inland by river transport and by spread over
land. This makes it rather incomprehensible that there is no sign of any
increase in institutions before January 1349, if institutions were useful
sources for determination of the spatio-temporal progression of the
Black Death. The validity of the assumption that institutions were use-
ful in this regard should be considered in light of the distance from
213
Gasquet 1908: 102.
214
Ibid.
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474 chapter eleven
Melcombe Regis deep into Wiltshire where the Black Death caused
over seventy institutions in the autumn of 1348. How could it be that
parish priests in Devonshire should collectively have remained
unscathed in the autumn of 1348, although outbreaks and great mor-
tality are documented in August and the epidemic raged in northern
Devon later in the autumn, while the parish priests of Wiltshire were
exposed to catastrophic mortality? And how could it be that much the
same must have occurred in the county of Somerset north of Devonshire
(see below)? Instead, this outline of the spatio-temporal progression of
spread of the Black Death according to institutions appears highly
unlikely or inexplicable, at variance with other independent types of
sources constituting further proof that institutions are at best poor
sources or rather unusable or misleading sources regarding the spread
of the Black Death, especially in the early phase of the epidemic. This
means that they do not constitute evidence of a winter epidemic of
plague in Devonshire. It is also important to note that no winter epi-
demic of plague was recorded in this county after the introduction of
parish registers which allows a closer examination of plague seasonal-
ity for the period 1546–645.215
By failing to consult Hatcher’s fine monograph on late medieval
Cornwall, Twigg and Scott and Duncan lost the opportunity to study
his specification of numbers of institutions by month for this county,
which is at variance with their assertion of a winter pattern: in Cornwall,
the incidence of institutions does not show significant increase until
March 1349, the highest figures for institutions occur in the months
April to July, and then numbers begin to fall, reaching quite ordinary
levels in the late Autumn.216 Thus, it is erroneous to include Cornwall
in their argument for the spread of the Black Death in the winter
according to institutions.
On the same assumption of normal spread rates, the Black Death
should have moved across Devonshire the c. 100 km from the border
with Dorset to the border with Cornwall in sixty-seven to eighty days,
that is, some time between about 20 September and early October, a
pace of westwards spread of plague across the county that is recorded
also later.217 The whole of Devonshire should have been ravaged by the
Black Death in the summer and autumn of 1348. This is by and large
215
Oswald 1977: 77–81, 87–91.
216
Hatcher 1970: 103.
217
Oswald 1977: 78.
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confirmed by an entry in the register of the Church of Friars Minor at

Bodmin where it is stated that the Black Death broke out there shortly
before Christmas,218 which means that epidemic manifestations
occurred about thirty km into Cornwall from Devonshire by the end of
the year and that most of this county presumably was ravaged in 1349.
Importantly, Pickard registered seventy-five institutions in 1350 and
twenty-nine in 1351, which compared with the average of twenty-four
institutions in the pre-plague decade show that the diocesan organiza-
tion did not succeed in filling in the vacancies caused by the Black
Death until 1351; in the following years the situation normalized. Since
the average number of institutions in the following nine years 1352–60
was eighteen due to the lower age of the new incumbents who had a
correspondingly lower normal attrition rate, it appears that sixty-eight
of the institutions in 1350–1 were replacements of incumbents killed
by the Black Death. This means that 331+68 = 389 institutions in the
years 1349–51 were caused by the Black Death and that the mortality
rate among the 642 parish priests at the start of the Black Death was
60.6 per cent. This estimate will only be marginally affected by some
minor factors that are not accurately accounted for. It is unlikely, for
instance, that all parishes had their formal incumbents in place and
were not represented by vicars who would not be replaced by institu-
tions after their death, which would tend to reduce the mortality rate
among the pool of functioning priests.
The diocese of Bath and Wells comprised the medieval county of
Somerset which stretched from the borders of Devonshire and Dorset
in the south all the way to the River Avon. Bristol is situated on the
other riverside where the county of Gloucestershire and the diocese of
Worcester began. According to the data furnished by Shrewsbury, there
was a small increase in institutions in November followed by quite a
strong increase in December. One should note Russell’s finding of a
general pre-plague mortality increase in November, which means that
the small increase in November has an alternative explanation and that
there is no clear plague-related evidence of an increase of institutions
before December. A higher level of institutions prevailed through the
winter months and the early spring months (January–April).
The crucial question is: How can this temporal pattern of institu-
tions reflect the spatio-temporal spread of the Black Death in the
218
Creighton 1891: 116: “parum ante nativitatem Domini intravit villam
Bodminiae.”
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476 chapter eleven
diocese? The distance from Melcombe Regis to the border of Somerset

is about thirty-five km. Taking as the point of departure the original
outbreak of the Black Death in Melcombe Regis shortly before 24 June
and applying normal spread rates of 1.25–1.5 km a day, the Black Death
would cross into Somerset about twenty-three to twenty-eight days
later, 14–19 July. However, the process of spread could have started ear-
lier, before the outbreak, through transportation of contaminated
goods by ship, cart or pack horse. The process of spread must also be
assumed, as mentioned above, to have been accelerated by people flee-
ing from the outbreak in Melcombe Regis and surrounding areas who
transported infected rat fleas in clothing or luggage, since this is an
ordinary feature of bubonic plague’s epidemiology.
It is as should be expected, therefore, that “by the beginning of
August, most of the tenants of Frome Braunch in Somerset were dead
and there were other deaths in North and South Cadbury.”219 The two
manors and villages of Cadbury are situated in the south-eastern cor-
ner of Somerset around forty-five km north of Melcombe Regis, and
Frome about thirty km further to the north, in the north-eastern part
of Somerset. In the area between these three localities, the Black Death
is reported to be raging 19 November in Evercreech, a village situated a
couple of km north of Castlecary, and a fortnight later in Castlecary
itself and the adjacent village of Ansford.220 This is the same pattern
noted above for North Devon. It is entirely compatible with the marked
tendency of bubonic plague to linger in the same area for five to eight
months for easily explicable epidemiological reasons, and with late
arrival in the plague season, the epidemiological processes could be
suppressed by cold winter weather to recrudesce in the spring and
complete their course among local populations of rats and human
beings. This means that it can be shown that the Black Death was rag-
ing in quite a large area in eastern Somerset from early August at the
very latest, which means that it must have broken out in the second half
of July in order to have attained a serious character in early August and
maintained it throughout the autumn. North and South Cadbury are
situated about fifteen km west of Gillingham, which broadens the doc-
umented area for the Black Death in this part of the country. Very seri-
ous developments in Somerset by early August at the latest can explain
219
Rees 1923: 29; Benedictow 2004: 128.
220
Gasquet 1908: 97; Holmes 1911: 25–6.
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that that the Bishop of Wells and Bath issued prayers for general use in
the diocese in August.221
One might like to surmise that Frome Braunch was contaminated so
early by goods from Bristol loaded on boats moving up the River Avon
to be unloaded at various places and transported to various destina-
tions. However, the recognized outbreak in Bristol is dated to
15 August,222 more than a week after the plague is known to have been
raging at Frome Braunch which may appear a problem for the chronol-
ogy of the epidemic’s development. One could realistically assume that
the epidemic had reached an early phase among poor people living in
the harbour area before its extreme mortality caught the attention of
chroniclers among the social elites. Assuming a normal time horizon
for the development of bubonic plague epidemics from the arrival of
contagion to the recognized epidemic outbreak in the city, i.e. seven
weeks, it must have arrived at the end of June. Since ships in those days
sailed at an average pace of about forty km a day,223 the voyage from
Melcombe Regis of around 700 km would normally take about seven-
teen days, thus, the ship transporting the contagion must have left
Melcombe Regis around 10 June, almost a fortnight before the recog-
nized outbreak in this town. Interestingly, in the chronicle providing
the best account of the first phase of events there, it is stated that two
ships came alongside in Melcombe Regis’s harbour, one from Bristol,
one from Gascony, presumably the ship that originally brought the
contagion from Bordeaux, although the account is dramatically con-
densed in time as was so typical of medieval chroniclers. Since the
Black Death broke out in the Pale in Ireland at the very beginning of
August, the same type of analysis of the time horizon of epidemic
developments suggests that the ship transporting the contagion from
Melcombe Regis to towns on the coast of the Pale must have put to sea
around 1 June.224 This means that it is quite possible that Frome Braunch
was contaminated with goods shipped upstream from Bristol before
the outbreak in the city itself. This accords with Gasquet’s assertion that
small towns along the coast of Somerset, namely Bridgewater, Clevedon,
Weston-super-Mare, Portishead and also Bristol, “were among the
221
Holmes 1911: 25.
222
Boucher 1938: 34.
223
Benedictow 2004: 102, fn. 20.
224
Benedictow 2004: 127–8, 143–4.
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478 chapter eleven
earliest places in the county to be attacked,” and that this demonstrated

that “the contagion was carried to these coast towns by a boat passing
up the Bristol Channel.”225 This outline accords with the pattern that
was observed in North Devon in localities in the vicinity of or on
Barnstaple Bay. Thus, the Black Death spread in cargo by ship to many
localities along the coast and up the estuaries and rivers, producing
multiple contaminations of towns and villages. One should also envis-
age how the epidemic was spread with more and more broadly by goods
and by people fleeing from these localities, the powers of spread devel-
oping almost according to a multiplicative pattern of progression.
On this basis of all available data on the spread and whereabouts of
the Black Death in Somerset and the possible origins of contagion
I cannot see how they can be made compatible with the temporal per-
spective provided by institutions. The Black Death had broken out in
the north and south of eastern Somerset by some time in July, presum-
ably in the second half of the month, and was raging from the early
August at the very latest. The Black Death can be shown to be present
in quite a number of other localities later in the autumn. The early out-
break in Bristol must have functioned as a powerful centre for the
spread of the epidemic into Somerset, not only by goods, but certainly
by people who fled the city when they saw the horrors and likely death
awaiting them if they stayed. On the premise that institutions should
be suitable for spatio-temporal determination of the spread of the Black
Death, the time perspective inherent in these data makes it rather
impossible to understand that there was no institution in September,
and that a clear plague-related increase in the number of institutions
first occurred in December.
Obviously, one would like to have more data. Interestingly, a number
of mortality studies has been performed on manors in the eastern half
of Somerset, for Walton, Mells, Pilton, Batcombe, Ditcheat and High
Ham (and for Marnhull in Northern Dorset).226 One may hope that the
manorial sources from which these mortality estimates are produced
can provide information on the arrival and spread of the Black Death
in the eastern parts of the county and diocese. Razi for instance has
shown that the Black Death invaded the parish of Halesowen in May
1349 on the basis of information given in the court rolls.227
225
Gasquet 1908: 97; Holmes 1911: 26.
226
Benedictow 2004: Map 361, 364, 375.
227
Razi 1980: 102.
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The diocese of Winchester is the last area to be examined in this way

in order to study the relationship between the temporal distribution of
institutions and the time of the Black Death’s spread. The diocese of
Winchester is constituted by the counties of Hampshire and Surrey.
Then as now, Hampshire was conterminous with Dorset’s eastern bor-
ders. According to Shrewsbury, for 1349 Lunn registered 228 institu-
tions in Hampshire and thirty-one institutions in the county of Surrey.228
Gasquet found both 204 and 228 institutions in Hampshire and, con-
fusingly, eighty and ninety-one institutions in Surrey, 2.5–3 times more
than Lunn found there, according to Shrewsbury. Although the lower
figures presumably reflect unspecified deductions for institutions not
caused by plague,229 something must plainly be erroneous. The tempo-
ral distribution of institutions does not show a tendency of extraordi-
nary increase until January 1349;230 the slight increase in the previous
month is so modest that it may reflect the ordinary late autumn–early
winter mortality increase identified by Russell. Unfortunately, in the
case of Hampshire there are few secular data with which to test the
incidence and temporal distribution of the institutions which is at
the heart of the matter in this subchapter.
Melcombe Regis is situated about sixty km from the border with
Hampshire, and at a normal spread rate by land of 1.25–1.5 km per day
it should have taken the Black Death forty to forty-eight days to the
border into Hampshire. Assuming that the spread started at the time of
the recognized outbreak, the crossing of the border should have
occurred sometime between 29 July and 6 August, though as men-
tioned above, the spread could have started earlier and the border have
been crossed earlier. Since Hampshire is a little over sixty km along the
west-east axis to the border with Sussex, this distance should have been
covered by about mid-September. However, it is hard to imagine that
the Black Death should not have been introduced quite early in locali-
ties along the coast of Hampshire as has been shown to have occurred
in Devonshire and Somerset. This was in fact the case, the Black Death
was spread efficiently by ship also eastwards along the coast: at the end
of September, the prior of Christ Church Priory, Canterbury, wrote in
alarm to the bishop of London about the outbreaks of the Black Death
228
Gasquet 1908: 130, 208–9; Shrewsbury 1971: 90–1.
229
Gasquet 1908: 209.
230
Cf. Watts 1998: 22.
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480 chapter eleven
in the latter’s diocese,231 at the same time the outbreak in London was
recognized. The bishopric of London included also the county of Essex
and the Black Death had spread further up the south-eastern coast at
least as far as the estuary of the River Stour on the border between
Essex and Suffolk and had been transported up the river at least as far
as Sudbury.232 This makes it rather unreasonable to assume that the
coasts of Hampshire were passed by. Against this background, it seems
reasonable to mention that Henry Knighton, a contemporary chroni-
cler, asserts that the Black Death first broke out in Southampton, which
could be taken as an indication of a very early outbreak there.233
Fortunately, in recent years some concrete evidence of this process
has been provided by preliminary studies of transactions at manorial-
court sessions at the manor of Titchfield on the coast of Hampshire.
Titchfield is a village and small port on the estuary of River Meon which
empties into the Solent around twenty km south-east of Southampton.
In 1347, five heriotable deaths among the villains were recorded at the
sittings of the manorial court, and in the first seven months of 1348
another five cases were recorded, which in itself is a suspect increase
bringing to mind the outbreaks in the second half of July at manors in
Somerset which had caused great mortality by the beginning of August.
Next, there was a long break from the July session of the court until
eight heriotable deaths were recorded at the court held 31 October.
Very unusually, only a week later there was a new sitting of the court in
which twenty-five more deaths were reported, which suggests a weakly
functioning court organization that did not manage to carry out much
work at the previous sitting. Since the normal rhythm of the court’s sit-
tings is not known, the analysis of the events becomes uncertain.
However, in the last seven months of 1349 there were four sessions of
the court, a court session being, on average, held each seven weeks.
Against this background, the eerie silence in the over three months
between the implied July session of the court and the last day of October
suggests that two sessions of the court would ordinarily have been held
in this period. This also suggests that the manorial scribe was an early
victim and that the onslaught of the Black Death temporarily broke
down the manorial organization and that this could have occurred
231
Ziegler 1970: 161.
232
Benedictow 2004: 134–5, 137–8.
233
Benedictow 2004: 132; Ziegler 1970: 123.
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before the expected court in the second half of August. Under the cata-
strophic circumstances, the court could only be workably reconstituted
after several months when two court sessions were hastily held, before
it broke down again and no session of the court was held again until
over four months later, on 11th March.234 This reflects the fact that great
amounts of court business were accumulated and hastily taken down
in the records at very uneven intervals in catastrophic circumstances
making the temporal links between the recording and the events tenu-
ous. The two sittings on 31 October and 7 November may quite likely
have recorded mortality effects of the Black Death in September, pos-
sibly also from August, and we cannot assume that these two courts
actually managed to bring the records up to date: it is possible that
many deaths which actually occurred in the autumn of 1348 remained
unrecorded until the next court in mid-March.
The events on the small neighbouring manor of Swanwick are even
more clouded, but it appears that the Black Death certainly was making
its presence felt in the late autumn when two deaths were reported in
the court held 25 November, but then another court was not held for
3.5 months, which could be taken to suggest that this manorial organi-
zation had also broken down.235
As can now be seen, court rolls and other manorial records also tend
to be quite problematic sources for determination of the time the Black
Death visited a given location. They are also problematic because a ten-
ancy could have changed hands several times owing to the death of
subsequent holders as they died in rapid succession without being for-
mally noted in the court’s records.236 The pace of change of hands of
tenancies could easily have been increased when new tenants moved
into the houses of the previous holders before the epizootic process had
come to an end and infective rat fleas had died. Obviously, this is a
process which would tend to distort the time-link between the epi-
demic impact and the recording of heriots, lending the process some
disquieting resemblance to the temporal and organizational process
occurring between an incumbent’s death and the institution of his suc-
cessor. However, no other types of sources seem to be available that
could help detail the spatio-temporal progression of the spread of the
234
Watts 1998: 23–4.
235
Watts 1998: 25.
236
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482 chapter eleven
Black Death in this county. Fortunately, there appears to be interesting

manorial material available, and mortality studies have been performed
for some Hampshire manors, for Bishop’s Waltham, Corhampton
and Damerham, and more in-depth studies of the extant sources of
Titchfield and other manors in the surrounding districts seem to offer
some promise.237 Recently P. Arthur has written an outstanding thesis
on the study of eleven of the Bishopric of Winchester’s manors in
Hampshire providing, among other things, valuable mortality data, but
without paying attention to the temporal aspect of the Black Death
with respect to arrival and spread.238 At least some of the records of
these manors which could be used for mortality estimates of custom-
ary tenants and social classes paying money heriots in the Black Death
must be assumed to contain valuable indications of the time of their
death.
Admittedly, this is not much evidence with which to test the usabil-
ity of institutions for determination of the time the Black Death’s spread
in Hampshire. However, the available evidence indicates that the Black
Death spread in the county in the early autumn of 1348 and that this
process is not reflected in the number or spatio-temporal distribution
of institutions.
Summary and Conclusion
This chapter’s objective has been to examine all material bearing upon
the connection between seasonality and the spread of the Black Death
and later plague epidemics in England. It has appeared that through
the whole plague era of 1348–1666 plague epidemics spread efficiently
only in the warmer seasons and subsided and more or less disappeared
with the advent of chilly and cold weather. This pattern is incompatible
with all diseases spread by cross-infection, by droplets or by personal
contact, which flourish in cold weather when people stay closer together
and droplets last longer and drift further. All ascertained facts and con-
clusions are consistent and compatible with the conclusion that the
epidemics were bubonic plague.
Twigg and Scott and Duncan argue that institutions of beneficed
parish priests in the period of the Black Death show a clear winter
237
Benedictow 2004: Map 361, 364–5; Watts 1998: 25–6.
238
Arthur 2005.
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incidence in the south-western counties which disprove that the Black

Death was bubonic plague. However, they have neglected to exercise
source-criticism and to examine critically the evidence for a temporal
link between the death of incumbents and the institution of successors
which in this case is the crucial piece of information. Instead, this task
has been performed in this chapter. It has appeared from the critical
examination of sources and studies on the matter that the use of insti-
tutions to determine the spread of the Black Death in time and space is
highly problematic for several serious reasons.
The study of the intermediate process between an incumbent’s death
and the institution of his successor has uncovered a time-consuming
and complex system often taking several months or longer. A signifi-
cant amount of secular evidence reflecting the time and whereabouts of
the Black Death in the south-western counties has revealed that the
epidemic was widespread and causing great mortality in the south-
western counties and dioceses without being reflected in institutions.
Despite the fact that the Black Death broke out in Melcombe Regis in
Dorset shortly before 24 June, there is no reflection of the widespread
severe mortality which it must have caused among the beneficed parish
priests until the turn of the year, the second half of November being the
earliest time such a mortality process can be discerned, but in most
cases not until January 1349. A similar situation appears also to have
been usual in other southern dioceses around the epidemic epicentre
in Melcombe Regis (Weymouth). This shows that institutions in these
counties and dioceses reflect incumbents’ death in the Black Death in a
clearly discernible way with a time lag of five to six months. However,
it has also been shown that that lapses of six months or longer were
frequent, and that a substantial proportion of vacancies was not filled
until one or two years after the incumbents’ death. Taken together these
data indicate a long average time-lag but also suggest that more focus
should be placed on the process of filling in vacancies after the Black
Death.
This study has uncovered a serious lack of congruence between
our source-based knowledge on the outbreak of the Black Death in
Melcombe Regis shortly before 24 June 1348 and the epidemic’s spread
in the south-western dioceses in the following six months and the spa-
tial and temporal reflections of mortality among parish priests in the
statistics of the institutions of parish priests according to Shrewsbury’s
rendering of Lunn’s data, which constitutes the material used by Twigg
and Scott and Duncan. This makes it an even larger scholarly tragedy
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484 chapter eleven
that Lunn’s thesis was lost at least a couple of years before Shrewsbury’s
monograph appeared,239 with the serious consequence that the correct-
ness of Shrewsbury’s use of it or Lunn’s application of source-criticism
cannot be examined or tested. Taken together, the many problems
which have been uncovered with respect to the data rendered by
Shrewsbury which are purportedly taken from Lunn’s thesis, the gross
incongruence between these data on institutions and the facts on the
ground with respect to the Black Death’s arrival and spread in time and
space in south-western England, as well as the loss of testability, mean
that Twigg’s and Scott and Duncan’s reliance on this lost study of insti-
tutions for their argument of seasonality appears materially untenable
and methodologically invalid. Their use of this material in order to
prove that the Black Death spread in these regions in the winter breaks
down as untenable. One can only hope that the institutions in the bish-
op’s registers for this period will be studied again and now with a keen
eye to possible information on the lapse of time between the time of
death of incumbents and the time of institution of their successor and
an awareness that this requires a study of the entries in at least a ten-
year perspective comprising the years preceding and following years of
the Black Death.
Using institutions as sources for the seasonality of the spread of the
Black Death in England is not for faint-hearted medievalists, and schol-
ars of other disciplines are respectfully advised to avoid them.
239
Ziegler 1970: 297, fn. 22.
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PART FIVE
THE ALTERNATIVE THEORIES
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INTRODUCTION: THE HISTORY AND ESSENCE
OF THE ALTERNATIVE THEORIES
In the history of alternative theories of the identity of historical plague

epidemics, the two first and the fourth, those put forward by Shrewsbury
(1971), Morris (1971), and Karlsson (1996), respectively, are closely
connected in two important respects. Firstly, Morris’s theory reflects or
represents a strong negative reaction to Shrewsbury’s theory and
Karlsson’s theory is very much inspired by Morris’s theory. Secondly,
they have in common that they all accept that the microbiological agent
was Yersinia pestis, albeit in the case of Karlsson’s theory an unspecified
mutated variant. This chain of development of alternative theories
reached a dead end with Karlsson’s theory. Nonetheless, Karlsson’s the-
ory represents a sort of link to the following theories in so far as he is
the first to make use of the arguments against the bubonic-plague the-
ory that Twigg presented in the third alternative theory (1984) on
which I will comment next among the alternative theories.
The three other alternative theories have in common that they are
based on other microbiological pathogens. An abrupt and sharp proc-
ess of radicalization took place that started with Twigg’s anthrax-based
theory, was followed by Scott’s and Duncan’s theory of a filoviridal
virus, the type of microbiological agent causing Ebola disease and
Marburg disease (2001) or, perhaps, even a disease that has since disap-
peared (2004) and therefore is caused by an unknown and microbio-
logically unverifiable and unidentifiable virus. Similarly Cohn argues
in his alternative theory for a viral disease spread by cross-infection
that has since disappeared and is therefore also caused by an unknown
and microbiologically unverifiable and unidentifiable virus (2002).
These theories are in the process of being overtaken by the rapid devel-
opment of paleomicrobiology (see above). Firstly, because paleomicro-
biologists have developed fully-fledged techniques for the testing of
skeletal remains in historical graves for bacterial causes of death and
on this basis several studies have been published which show that all
the great historical pandemics of plague have been caused by a geneti-
cally stable unmutated variant of the biovar Yersinia pestis Orientalis.
This leaves Scott and Duncan’s and Cohn’s theories only the faintest
hope for survival, that their purported pathogen(s) may have spread
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488 introduction
concomitantly with bubonic plague without having been revealed by

the presently available techniques. However, these diseases are so dif-
ferent from bubonic plague in their transmission and pattern of spread
that they can for all practical purposes be excluded as alternatives by
traditional historical and medical sciences.
All six advocates of alternative theories have in common that they
flatly reject all other alternatives in addition to the established bubonic-
plague-cum-Yersinia-pestis theory, and since they are incompatible at
least five of them must be untenable and massively erroneous, and why
not all six? However, there is a close and cordial connection between
Twigg and Scott and Duncan, the only instance of open mutual respect
and co-operation within this field of study. The relationship is princi-
pally shaped by Scott and Duncan’s ambition to develop their own
alternative theory, but they take over lock, stock and barrel Twigg’s
arguments for rejecting the bubonic plague theory, which spared them
the effort of developing their own platform but also exposed them to
very serious problems. Much the same goes for Cohn who also eagerly
grasps Twigg’s arguments against the bubonic plague theory, but other-
wise is much more independent in his approach. As now can also be
seen, Twigg is the central scholar in the later developments of alterna-
tive theories of historical plague; his anthrax theory is apparently gen-
erally rejected, but his arguments against the bubonic-plague theory
are eagerly employed by all later advocates of alternative theories.
Twigg’s central arguments against the bubonic-plague theory have
been discussed above in various chapters and have been shown to be
untenable, specifically his denial of the broad European presence of
black rats, the implications of the mortality rates in the Indian plague
epidemics, and with respect to the importance of metastatic spread in
the epidemiology of bubonic plague. Karlsson’s theory will be discussed
first, since it is closely associated with Morris’s paper.
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CHAPTER TWELVE
THE BEGINNING: THE ALTERNATIVE THEORIES OF

SHREWSBURY AND MORRIS
Shrewsbury: the Composite, Low-Intensity Theory
It is often overlooked that J.F.D. Shrewsbury is the pioneer of alterna-

tive theories of the microbiological nature of the Black Death and later
plague epidemics in his monograph A History of Bubonic Plague in the
British Isles of 1971. He did not reject the role of bubonic plague alto-
gether. He argues that rat-borne bubonic plague was introduced into
England with the Black Death, but that it caused a specific mortality
rate of only about 5 per cent at the most. Instead, he asserts that the
fact that there were numerous plagues other than bubonic plague in
fourteenth-century England is commonly ignored; but smallpox, mea-
sles, diphtheria, pertussis [= whooping cough], influenza, and dysentery
undoubtedly occurred in widespread and deadly epidemics, and the
“burning ague” in Langland’s list was almost certainly typhus fever […] it
is obvious that he was acquainted with a variety of communicable dis-
eases and other disorders, as anyone would expect who was not obsessed
with the notion that bubonic plague was omnipresent in fourteenth-
century England.1
Thus, Shrewsbury addresses the problems posed by the advent of
plague and the abrupt and long-lasting late medieval population decline
by underscoring the epidemiological and demographic importance of
other microbiological agents which caused other serious or severe epi-
demic diseases, but which had been around all along. The central line
of argument throughout his monograph is that the introduction of
bubonic plague meant only a small but significant increase in the pre-
vailing generally high level of epidemic mortality of those times.
Shrewsbury’s monograph is characterized by his huge and systematic
efforts to play down the significance of the Black Death and subsequent
epidemics of bubonic plague.
1
Shrewsbury 1971: 36, 42.
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490 chapter twelve
It is, therefore, misleading when Twigg and Scott and Duncan por-
tray Shrewsbury as an irrational, incompetent and rigid defender of
the bubonic plague theory of historical plague epidemics.2 They have
completed his line of argument by rejecting the possibility that there
could have been epidemics of bubonic plague in England excepting,
perhaps, the sporadic incidence in port cities, particularly London.
However, since their lines of argument are strongly restricted to
England, they needed to use his monograph but must argue that
he systematically misunderstood the obvious microbiological and
epidemiological facts on the ground and claim that the epidemics
he designated bubonic plague either were anthrax or “haemorrhagic
plague” respectively. At the same time, they miss no opportunity to
avail themselves of Shrewsbury’s efforts to minimize the significance of
bubonic plague.
In contrast to Karlsson, Cohn, and Scott and Duncan, Shrewsbury
does not invent or introduce new or unknown diseases or mutated
forms of other diseases unknown to modern medicine, but presents a
composite alternative theory in which plague plays only a minor con-
tributory role. I cannot see how it was possible at that time (the early
1970s) to assert that the Black Death caused relatively high mortality
only in urban centres and that the mortality rate for the whole country
was at most 5 per cent. At the time, quite a number of manorial studies
were available to him showing, on average, at least ten times higher
mortality in the countryside than his estimate of 5 per cent, but not a
single mortality estimate for any English urban centre was available
to him and is still not available.3 Another independent and suffi-
cient reason for rejecting his theory is that the main alternative dis-
eases of his composite theory, such as exanthematic typhus and also
probably smallpox, apparently did not arrive in Europe until around
1490.4 Although he cites H. Zinsser’s authoritative monograph on
typhus where it is concluded that this disease did not arrive in Europe
until the end of the fifteenth century,5 Shrewsbury emphasizes on the
2
Scott and Duncan 2001: 14, 16–15, 94, 98–100, 102, 110–1, 149, 151–4, 166–8,
202, 209, 212.
3
4
See, e.g., Zinsser 1985: 71–6, 241–53, 278–9; Copeman 1960: 127–8; Cartwright
1977: 76–8; Snyder 1965: 1059–60; Greenwood 1935: 172–4, 227; Ackerknecht
1963: 67.
5
Zinsser (1934)1985: 241–4.
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the alternative theories of shrewsbury and morris 491
same page the importance of this disease during the Black Death and
subsequent plague epidemics.6 And there are other serious objections
to his conclusions.
Morris: the Primary Pneumonic Theory
In a sharply critical review paper of Shrewsbury’s monograph,

C. Morris launched another alternative theory, namely that the Black
Death and later plague epidemics were primary pneumonic plague,
i.e., caused by the same pathogen Yersinia pestis but disseminated by
interhuman spread of infected droplets. He makes this contention
for British plague history but the implications for other countries are
clear.7 Morris’s review is the basis of Karlsson’s paper to the same
effect and will be discussed briefly as part of a thorough analysis of this
paper. However, it must be pointed out that Morris confuses second-
ary pneumonic plague with primary pneumonic plague. He castigates
Shrewsbury, for example, for citing the Irish friar of Kilkenny John
Clyn’s clinical description of plague cases in the Black Death without
including the element “some died spitting blood”. However, even these
few words must reflect that the majority of plague cases did not spit
blood and therefore, presumably, were bubonic cases, and that the clin-
ical characteristics of the Black Death in this area had the normal inci-
dence of cases which developed secondary pneumonia and were
“spitting blood” before they died. Morris avoids citing the part of John
Clyn’s clinical description that would make this absolutely clear and
justify Shrewsbury’s view on the medical and epidemiological nature
of the Black Death in the British Isles:
[…] many died of boils and abscesses, and pustules on their shins [= legs]
and under their armpits; others frantic with pain in their head, and oth-
ers spitting blood […].8
As can be seen, the references to buboes and pustules and carbuncles
dominate the clinical picture, and the extreme headache which often
6
Shrewsbury 1971: 125. See also register ibid: 660, typhus fever and smallpox.
7
Morris 1971: 205–15.
8
Hirst 1953: 13. There is an insignificant deviation from Hirst’s translation in
Morris’s citation, substituting “others” with “some.”
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492 chapter twelve
drives patients to irrational, desperate action is a typical clinical feature

of bubonic plague. John Clyn’s observation that some were spitting
blood indicates a normal proportion of cases of secondary pneumonic
plague in epidemics of bubonic plague. This account contains quite a
good description (for the time) of an ordinary epidemic of bubonic
plague and as such constitutes empirical evidence to this effect.
Morris is also sharply critical of Shrewsbury for denying the exist-
ence of pure epidemics of primary pneumonic plague,9 a modality of
plague that is not dependent on a basis in bubonic cases which develop
secondary pneumonia. Morris’s erroneous assertion on the existence
and importance of pure epidemics of primary pneumonic plague is
commented on below in the discussion of Karlsson’s alternative the-
ory, and urgently raises the question of the origin of the epidemic.10
However, in contrast to the more recent advocates of alternative theo-
ries of the nature of historical plague epidemics he recognizes that
“a rodent migration is not necessarily required for the spread of plague
since infected fleas, and occasionally infected rats, can travel long dis-
tances in grain, clothing or other merchandise.” In other words, he
acknowledges the importance of metastatic leaps in the epidemiology
of bubonic plague.11 I cannot see how the notion of plague-infected rat
fleas can be separated from the notion of bubonic plague cases and the
spread of epidemics of bubonic plague.
9
Morris 1971: 207–9.
10
11
Morris 1971: 206–7.
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CHAPTER THIRTEEN
GUNNAR KARLSSON’S ALTERNATIVE THEORY:

THAT HISTORICAL PLAGUE WAS PURE EPIDEMICS OF
PRIMARY PNEUMONIC PLAGUE
Introduction
G. Karlsson presented his alternative theory to the international com-

munity of scholars in a paper published in Journal of Medieval History
in 1996 where he argues that two late medieval epidemics in Iceland
and more generally that plague in medieval Europe were pure epidem-
ics of primary pneumonic plague.1 For his epidemiological interpreta-
tion, Karlsson bases his alternative theory directly on Morris’s assertion
of the occurrence of pure epidemics of primary pneumonic plague,
a modality of plague disease spread by interhuman cross-infection by
droplets. The concept of a pure epidemic of primary pneumonic plague
implies that the origin of the epidemic is not a case of bubonic plague
which develops secondary pneumonia but a case in which the first vic-
tim contracted pneumonic plague directly by inhalation of infected
droplets into the lungs.
Karlsson’s paper follows quite closely and draws heavily on a paper
he published together with S. Kjartansson in an Icelandic journal in
1994 on two supposed plague epidemics in Iceland in 1402–4 and
1494–5 respectively.2 He is clear about its objective: “The present article
[as the first in Icelandic] can be seen as a defence of the late Jón
Steffensen against Benedictow’s critique of his conclusions,” namely,
that these epidemics, and also the Black Death of 1348–9 in Norway
were primary pneumonic plague.3 Thus, the central feature of Karlsson’s
(and Karlsson’s and Kjartansson’s) paper on the two supposed plague
epidemics in fifteenth-century Iceland is a comprehensive and sharp
criticism of my doctoral thesis (1993, repr. 1996). The apparent objec-
tive was to clear the way for his own theory that the epidemics were
1
Karlsson 1996: 263–84.
2
Karlsson and Kjartansson 1994: 11–74.
3
Steffensen 1973. 40–55.
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494 chapter thirteen
pure epidemics of primary pneumonic plague: the epithet “pure” deter-

mines that they were without any basis or origin in flea-borne plague
from rats (or other rodents) or cases of human bubonic plague.4 Thus
he thinks that the contagion was the bacterium Yersinia pestis, as in the
case of bubonic plague, but the process of dissemination was interhu-
man cross-infection by droplets and not transmission by rat fleas at any
stage of the epidemic process. This immediately presents the insur-
mountable problem of how primary pneumonic plague could arise in
the complete absence of bubonic plague and in the complete absence of
rats, a problem he surprisingly does not identify or try to explain (and
the editors and consultants of the Journal of Medieval History did not
find significant). Alternatively, he might have launched a theory of
importation, which he conspicuously fails to do and, as we shall see, for
the very good reason that this would disclose another insurmountable
problem, which is that there is no place abroad whence plague in any
form could have been imported into Iceland in these years (another
problem which the editors and consultants of the Journal of Medieval
History did not find significant).
The Icelandic epidemics exhibit such peculiar features that Karlsson,
as the first of the advocates of alternative theories, has to invent some
suitable mutations in order to defend his theory. He does not consider
that his assertion as to the occurrence of these mutations can move
from the status as arbitrary or speculative to the status as tenable
(at any level of validity) only by meeting some elementary methodo-
logical requirements, namely to explain to the scholarly community:
(1) why and how and by which process of evolutionary selection
this mutant strain or biovar came into being;
(2) when and where, in Iceland or abroad, this mutant strain of
primary pneumonic plague originated and developed;
(3) whether this mutated variant miraculously came into being twice;
and
(4) where on earth (literally) it had been in the meantime (another
problem which the editors and consultants of the Journal of
Medieval History did not find significant).
Undaunted by these formidable problems, Karlsson expands the per-
spective of his theory from its tiny and isolated Icelandic territorial
base in the middle of the North Atlantic to argue that historical
4
Karlsson 1996: 265.
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gunnar karlsson’s alternative theory 495
plague in Europe generally was pure epidemics of primary pneumonic

plague.
On this basis, Karlsson concludes triumphantly that by having
removed the black rat from the medieval plague he has more generally
paved the way for asserting that the medieval plague epidemics in gen-
eral, all over Europe, were primary pneumonic plague, presumably
caused by that unknown mutated variant. These assertions will be
addressed in this chapter.
The principal interrelationship between the advocates of alternative
theories is the usual one in this case: that they accept his view that there
were not rats in Iceland and that the fifteenth-century epidemics con-
sequently could not have been rat-borne, which suits their alternative
theories, but they flatly reject his theory that these epidemics or the
medieval plague epidemics generally were (pure) primary pneumonic
plague.5 The gist of these counterarguments is, thus, that there never
was a plague epidemic in Iceland, neither bubonic nor pneumonic, and
Karlsson’s assertion that there were not rats in Iceland offers an excel-
lent explanation. The obvious implication is that the severe epidemics
in Iceland were another epidemic disease or other diseases. To my
knowledge, no other scholar has supported Karlsson’s view, at least not
outside the Icelandic scholarly community where opinions apparently
differ sharply.6 One should note that there is a remarkable qualitative
difference between the way Cohn and Scott and Duncan argue their
rejections of Karlsson’s theory, and in my opinion, only Cohn makes
his case on this point in a scholarly and scientifically tenable way.7
Karlsson and Benedictow
I consider Karlsson’s reading of my thesis so bizarre and skewed that

it is, in my opinion, grossly misleading and I hope I may be excused
for considering it an expression of the weakness of his case.8 In my
5
Cohn 2002: 23, 51; Scott and Duncan 2004: 182. See also Twigg 1984: 68, 161–8.
6
Karlsson’s (and Kjartansson’s) paper’s were discussed at a conference in Iceland
and met with much criticism; papers from this conference are published in Sagnir
1997.
7
Cohn 2002: 22–3.
8
This is even more the case for the original paper in Icelandic, Karlsson and
Kjartansson 1994, but since very few read Icelandic or Icelandic scholarly journals, this
is not important in this context, only to the Icelandic scholarly community. Also the
offensive comments on my work can, therefore, be ignored.
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thesis, I presented a detailed account of the scholarly literature on pri-

mary pneumonic plague, however, to no avail so far as Karlsson was
concerned.
This highlights another feature of Karlsson’s paper: although he
argues very strongly for a theory to the effect that the Icelandic epi-
demics of 1402–4 and of 1494–5 were pure primary pneumonic plague
and ends up with a triumphant conclusion with a much wider territo-
rial sweep, linking the nature of “medieval plague” to this disease, he
has not made any attempt to acquire scholarly knowledge of primary
pneumonic plague. Not a single medical study on primary pneumonic
plague can be found in his footnotes. According to traditional academic
principles, this ought to mean that he cannot discuss the disease that
constitutes the cornerstone of his theory with the competence that only
familiarity with the primary research studies and standard works on
this disease can provide. The reason for this extraordinary approach by
a scholar is presumably that the Icelandic epidemics exhibit many epi-
demiological characteristics or features that are not compatible with
the studies on primary pneumonic plague.
This is where wishful thinking about mutations is introduced into
his arsenal of arguments. For the same reason, he cannot avail himself
of the fact that I provided a comprehensive summary of all primary
studies on primary pneumonic plague and the presentation of this dis-
ease in the standard works in my thesis. My endeavours to track down
and present the gist of these studies does not earn me any praise, it
represents, on the contrary, a significant problem that has to be man-
aged. Since Karlsson cannot use the corpus of scholarly works on pri-
mary pneumonic plague in order to form a basis for his theory and
likewise cannot use my complete presentation of it, he must find a way
out of this problem. His solution is to base his arguments on a second-
ary paper which is profoundly flawed, namely Morris’s sharply critical
review article of Shrewsbury’s monograph where Morris was the first
scholar to launch a theory that the Black Death was an epidemic of
primary pneumonic plague.
Karlsson starts in this way: “Other diseases [than bubonic plague]
are hardly considered by him [Benedictow], and all other forms of con-
tagion are excluded, mainly because they are said to be insufficient to
explain epidemics of the dimension under discussion here.”9 Firstly,
9
Karlsson 1996: 264.
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one should note the logical and factual contradiction in the opening
part of the statement, that “other diseases are hardly considered by
him” and that “all other forms of contagion are excluded:” since all
other forms of contagion unavoidably relate to many other diseases,
I cannot have excluded other forms of contagion without having dis-
cussed other diseases.10 Secondly, he fails to mention that I made a
complete presentation of the corpus of primary research on primary
pneumonic plague, and this omission allows him to present a spurious
explanation as to why I reject his theory. Thirdly, one should also note
that in the second part of the statement he sharply criticises my
approach, saying that I exclude all other forms of contagion “mainly
because they are said to be insufficient to explain epidemics of the
dimension under discussion here.”11 Thus, the truth shows through,
albeit indirectly and involuntarily, that I have discussed other alterna-
tive diseases based on other forms of contagion, but have found that
they have, inter alia, insufficient mortality-generating properties.
Notably, Karlsson acknowledges in his paper that the Icelandic annals
do not contain any clinical or diagnostic information that would per-
mit the microbiological identification of these Icelandic epidemics.
However, he contends that these chronicles provide information that
can be used for producing estimates of the population loss in both epi-
demics, and that the extreme estimated mortality level could only have
been caused by primary pneumonic plague.12 In other words, in prac-
tice he avails himself of exactly the same approach that he criticizes me
sharply for using (although I do not use it as a fundamental argument
but only as an additional argument).
Later in Karlsson’s paper, there is another sudden but indirect indi-
cation that he has read my presentation of primary pneumonic plague.
This occurs with a parenthesis within a citation from Morris’s paper to
the effect that
the great pneumonic epidemic in Manchuria would have spread much
more, “but for the heroic counter-measures taken by the great Chinese
10
Benedictow 1993/1996: 121–5, 214–27.
11
Benedictow 1993/1966: 16, 125, 266–74. As this statement is inaccurate and could
produce misconceptions about my view, I would like to point out that I have discussed
not only the size of the epidemics, as Karlsson may be taken to state, but also properties
that combine tremendous powers of spread with tremendous lethal powers, and I ar-
gue explicitly why that is a rare combination (see also above).
12
Karlsson 1996: 265, 268–84.
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doctor Wu Lien Teh [one of Benedictow’s greatest authorities on plague]

who most fortunately was put in charge.”13
However, Morris continues, unquoted by Karlsson:
Wu Lien-Teh’s classic treatise on pneumonic plague is significantly absent
from Shrewsbury’s very extensive bibliography.14
This treatise is also “significantly absent from” Karlsson’s few footnotes.
One could also note the distortion inherent in Karlsson’s combined
reference to me and “Wu Lien-Teh [one of Benedictow’s greatest
authorities on plague],” since Wu Lien-Teh is the indisputable and
uncontroverted towering expert on primary pneumonic plague, not
on “plague.” Morris’s aim was to reject Shrewbury’s theory to the effect
that the Black Death and later plague epidemics in Britain could have
caused only a minor part of the national mortality rate, about 5 per
cent, and that exanthematic typhus, smallpox and other serious epi-
demic diseases caused most of the mortality (see above). Because
Morris has insufficient knowledge of bubonic plague to effectively
counter Shrewsbury’s arguments, he launched another and appar-
ently relevant alternative theory, namely that plague in Britain was pri-
mary pneumonic plague. However, he had poor knowledge also of
primary pneumonic plague, and many of his central assertions are
unfounded. This subject is discussed below after the substance of Wu
Lien-Teh’s and other researchers’ studies on this modality of plague
have been presented, in order to perform a systematic comparison
between these studies and Morris’s and Karlsson’s assertions.
Karlsson bases his paper and theory on Morris’s ten-page review of
Shrewsbury’s monograph instead of on the primary research studies on
primary pneumonic plague because they in important respects have
the same ambition, namely to prove that the medieval plague epidem-
ics, at least in Britain and in Iceland, were pure epidemics of primary
pneumonic plague. However, Shrewsbury’s rejection of primary pneu-
monic plague as a significant causal factor of mortality is in full accord-
ance with all primary research on this modality of plague, the same
research that persuaded me to reject in my thesis the theory that the
Black Death or subsequent plague epidemics could have been pri-
mary pneumonic plague. Apart from the fact that Morris referred to
13
Karlsson 1996: 283.
14
Morris 1971: 208–9.
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Wu Lien-Teh in his text and mentioned his monograph in a footnote, it

can hardly be demonstrated that he has read his work or knows more
about primary pneumonic plague than Karlsson. Karlsson based his
case on the quotation from Morris’s paper for two crucial reasons:
(1) because it provided an impression that primary pneumonic plague
has great powers of spread, but in this case was halted by the coun-
termeasures introduced by Wu Lien-Teh;
(2) because Morris introduced the concept of pure pneumonic plague,
which Karlsson makes the cornerstone of his theory. Both asser-
tions are, as we shall see, at complete variance with Wu Lien-Teh’s
presentation of primary pneumonic plague, where it is emphasized
that epidemics of this disease arise from cases of bubonic plague
which develop secondary septicaemia with subsequent lung con-
solidation and a bloody cough spreading infected droplets. Thus,
Wu Lien-Teh maintains that epidemics of primary pneumonic
plague never are pure, never arise de novo from a first or original
case of primary pneumonic plague droplet infection.
The heart of the present monograph is the identification of epidemic
diseases of the past. This objective requires that some elementary meth-
odological rules are followed in order to ensure the validity of identifi -
cation of diseases, otherwise any mention of a severe or disastrous
epidemic in the sources can be arbitrarily taken as evidence of plague
(or any other serious communicable disease). An illustration of the
consequences of an approach unguided by methodological considera-
tions is provided by Scott and Duncan who assert that “there are said to
have been 233 outbreaks [of bubonic plague] in China between AD 37
and 1718.”15 They have used Wu Lien-Teh’s general list of epidemics in
China, for some reason leaving out the first of 224 BC.16 However, Wu
Lien-Teh does not at all suggest that all these epidemics were or could
have been bubonic plague. He emphasizes that it is possible to identify
only a couple of these 233 epidemics as bubonic plague. He has not
succeeded in finding clinical or epidemiological evidence of bubonic
plague in chronicles or literary accounts, only in three medical works.
Two of these medical works were from the first half of the seventh
century; their clinical descriptions are unambiguous but cannot be
15
16
Wu Lien-Teh 1936a: 43–51; Benedictow 2004: 40–2.
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correlated or associated with any specific epidemic(s) in China. Only

in a medical work of 1642 is a clinical description of bubonic plague
given within an epidemic context, obviously referring to the epidemic
of 1641–2.17
Identification of an epidemic disease, in this case as plague (either
bubonic or pneumonic), requires specific evidence of at least one defin-
ing epidemiological or clinical feature or a combination of features that
are unique (see above). In weak or inconclusive cases, it must be pos-
sible to demonstrate at least a possible link of dissemination from a
known epidemic of plague to the epidemic under study which may
allow formation of a hypothesis to the effect that it may have been
plague. This does not, of course, constitute any proof that it actually
was the plague; the function of a hypothesis is to legitimate research
and direct the search for corroborative evidence. This requirement is of
particular importance in the case of epidemics in a highly isolated
island like Iceland. This clarifies the basic methodological, empirical
and source-critical requirements that Karlsson should meet in order to
justify his theory of the aetiology of the purported fifteenth-century
plague epidemics in Iceland.
The Icelandic sources that provide information on these epidemics
consist mainly of brief accounts in two chronicles for each epidemic;
translations of these accounts into English are supplied in my thesis
and by Steffenson. My translation into English is provided in Appendix
2 below.18 As is most often the case with this type of source, the quality
of the information they provide is quite deficient (in the eyes of mod-
ern scholars). They have nothing to say about whence the contagion
arrived in Iceland or about defining or weaker indicative clinical fea-
tures, excepting perhaps on the typical duration of the illness. They
contain some comments on spread and mortality that are incidental
and sensational in character as would be expected from this kind of
source. Since Karlsson asserts that this “information” can be used for
17
Wu Lien-Teh 1936a: 10–3; Benedictow 2004: 35–42. This means that also McNeill’s
use of the same list is unfortunate, and his choice of a Chinese epidemic of 1331 as the
origin on the Black Death that subsequently spread all the way to the Crimea is com-
pletely unsupported by clinical or epidemiological evidence; see McNeill 1979: 152–4.
Instead, McNeill let himself be victimized as a scholar by “the overwrought imaginings
and hopelessly inaccurate quantification of the chroniclers,” to cite yet again Hatcher’s
apt description (1977/87: 21). His theory is also contrary to a number of other empiri-
cal facts, for instance, the fact that the communication lines between China and the
Crimea were severed long before the Black Death broke out in the Crimea or
Constantinople. See Benedictow 2004: 44–51.
18
Benedictow 1993/1996: 211–2; Steffensen 1974: 457, 50–1.
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estimates of mortality which are indicative of plague, this point will be

discussed below.
An intriguing question presents itself immediately and with great
urgency: how can it be possible in such evidential circumstances to
identify with a (very) high level of certainty the aetiology of the
fifteenth-century Icelandic epidemics, in this case specifically as pure
primary pneumonic plague caused by some mutant variant of the con-
tagion Yersinia pestis? This problem is exacerbated by the fact that in
his paper Karlsson does not perform source-criticism in accordance
with scholarly standards, stating only with reference to his and
Kjartansson’s paper that: “It would be tedious here to repeat all the
arguments and reservations concerning our use of Icelandic sources,
let alone all the references to sources and literature that only people
who read Icelandic could use.” Inevitably, it means that his paper, on
this crucial point, represents incomplete methodology and scholarship.
There is also another serious matter of deficient methodology of source-
criticism that will be discussed below.
Karlsson’s theory is characterized by at least three independent fatal
flaws of both empirical and methodological nature, in the sense that
each represents a sufficient condition for rejecting it as untenable or
invalid. (1) In the circumstances, when the two requirements for iden-
tification of epidemic diseases outlined by Shrewsbury cannot be met
by the Icelandic sources, it is a serious deficiency that Karlsson has
completely neglected to investigate the possible provenance, the pos-
sible territorial origin of the contagion that was introduced into Iceland
and that unleashed the purported plague epidemics there in the years
1402–4 and in 1494–5. In reality, this question is composed of two
independently decisive parts that must each be satisfactorily resolved
in order to keep the theory afloat: he must for each epidemic be able to
identify at least (1) one contemporary plague-stricken port town in
Europe which (2) was sending ships to Iceland at the time these epi-
demics arrived there. These two crucial questions or problems for the
tenability of his theory are passed by in silence. In 2002, I published a
complete Norwegian plague history from 1348–1654 which covers
more than thirty waves of plague epidemics, without finding evidence
of any epidemic of primary pneumonic plague, let alone of a pure epi-
demic of primary pneumonic plague; in fact all epidemiological evi-
dence is compatible with bubonic plague.19
19
Benedictow 2002. See also Benedictow 2006.
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Could Plague Have Come to Iceland from Anywhere?
Only a few ships came to Iceland from abroad at the beginning of the
fifteenth century, only Norwegian ships or Icelandic ships returning
from Norway, normally from Bergen. The first English fishing ship is
reported to have arrived in Icelandic waters in 1412.20 It was prohibited
by law for the Icelanders to trade with foreigners. In order to illustrate
this point one could note that in 1409, there was an intensive discus-
sion at the Icelandic all-moot (‘Alþingi’) about what to do with all the
royal incomes that had piled up in the island.21 Iceland was part of
the Norwegian kingdom, normally administered by a royal governor
(‘hirðstjóri’), and taxes were mostly paid in homespun woollens and, to
some extent, in stockfish (wind-dried cod). Evidently, the cause of the
problem was that too few ships arrived from Bergen, and that not even
the commander of the King’s Mansion22 in Bergen who was responsible
for collecting the royal incomes in Iceland, regularly sent a ship there to
collect them. In the following years the New Annals (Nyi Annáll) occa-
sionally provide telling pieces of information, for instance, under the
year 1412 we are told that “No news came from Norway to Iceland,” i.e.,
no ship arrived from Norway; next year we are told that “A ship came
from Norway,”23 a fact that the annalist finds worth mentioning. In
1419, the Icelanders wrote a letter to the king complaining that for
several years no ships had arrived from Norway according to the old
agreement with the Crown, which had been gravely detrimental to
their poor country. They therefore considered it unreasonable that the
old prohibition against trading with foreigners was still in force.24
British sources tell the same story. Ships from Britain were sailing to
20
Carus-Wilson 1966: 161.
21
Steffensen 1974: 48.
22
The ‘King’s Mansion’ is a translation of ‘Kongsgården,’ the royal administrative
centre of western Norway in Bergen. At the time, this was not a castle built in stone, but
consisted of wooden buildings surrounded by a wooden palisade and had no real de-
fensive capabilities.
23
Annales islandici posteriorum sæculorum. Annálar 1400–1800: 18–9. Also the
Icelandic Vatnsfjarðarannáll hinn elzti relates to this epidemic but it is written so long
after the event and is so infested with source-critical problems that it is not mentioned
by Gunnar Karlsson (or Jón Steffensen) who in other works shows good knowledge of
these important types of sources to Icelandic medieval and early modern history.
Annales islandici postseriorum sæcolorum, 1933–8: 22.
24
Diplomatarium Norvegicum, vol. 2, no. 651; Diplomatarium Norvegicum, vol. 4,
no. 330.
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Iceland at the time: the first English fishing ship arrived in 1412 to be
followed by many others in the subsequent years. However, throughout
the fifteenth century only English fishing ships and merchant ships
sailed to Iceland; Scottish ships do not seem to have been engaged
in fishing in Icelandic waters or trading with Iceland during this
century.25
Crucially, there is not a single account of plague in these countries in
1402. Not a single plague epidemic has been registered in England
between 1400 and 1405–7, nor was there any outbreak of plague in
Ireland or Scotland during this period,26 nor for that matter in Northern
Germany between 1396 and 1405–6, nor in the coastal commercial cit-
ies of the Netherlands between 1400–1 and 1409.27 Since the epidemic
broke out in the autumn of 1402, after the return of an Icelandic ship,28
it is also clear that the disease would have to have been imported from
a city or region where it was spreading in this year.29 In Norway, the
sources provide no certain information of plague between 1391–2 and
1452, although there are some indications that there could have been
plague in 1438–9. Norwegian sources are particularly sparse in these
decades, and it is likely that one or more plague epidemics may have
gone unnoticed. However, it is improbable that plague contagion could
have been imported into Norway and re-exported to Iceland in years
when there was no plague epidemic in the countries whence plague
was imported to Norway, and this was throughout the Late Middle
Ages mostly England, and at least once the Netherlands.30 There is no
evidence that plague was imported from Northern Germany before
25
Carus-Wilson 1966: 155–82.
26
Shrewsbury 1971: 149–50, mentions that “some time in 1402 there was ‘some
disease in Scotland that ‘caused several deaths’ in Dundee.” Evidently, he does not con-
sider it to have been plague, referring to it only as “some disease,” and since the only
concrete information on mortality is restricted to the statement that it “caused several
deaths” no impression is conveyed of a dramatic epidemic situation. And one must
keep in mind that no ships from Britain were sailing to Iceland at the time and that also
later in the century only English fishing ships and merchant ships sailed to Iceland,
Scottish ships do not appear to have been engaged in fishing near or trading with
Iceland. Carus-Wilson 1966: 155–82.
27
According to Blockmans 1980: 854, there was an outbreak of plague in Guelders,
an inland city situated in the south-eastern part of the Netherlands near the border of
Germany.
28
“Nýi Annáll,” in Annales islandici postseriorum sæcolorum, 1922–7: 9–10;
“Lögmanns-annáll” in Islandske Annaler indtil 1578: 286.
29
30
Benedictow 2002: 102–11. Evidently the reason is that Denmark’s pattern of inter-
national trade was very different from Norway’s.
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1500 (or more accurately before 1628), and for the year 1402, with a
substantial margin of safety of years around it, plague is not recorded
in this area.31 According to the extant sources, plague was never
imported from Denmark in the whole plague history of Norway, and
no plague epidemic has been registered in Denmark from the end of
the fourteenth century until possibly in 1405.32
Steffensen, who recognizes that notions on provenance cannot be
dispensed with and that this question therefore cannot be ignored,
asserts that the supposed plague contagion came to Iceland with a ship
from England. His source is Sticker’s old pioneering standard work on
plague of 1908, where plague is mentioned as having occurred in
England in 1402, but without indication of his source.33 Probably
Sticker has misunderstood a reference to the epidemic in Iceland in the
Danish scholar F.V. Mansa’s proto-scientific monograph of 1875 on the
epidemic history of Denmark.34 It is a mistake or rather a slip of the pen
on the part of Sticker that Steffensen could easily have corrected by
using Shrewsbury’s recent monograph on the history of plague epi-
demics in Britain and, as we shall see, Steffensen knows the work
and has consulted it, which makes his silence on this point the more
remarkable. In fact, in another context Steffensen remarks that Sticker’s
mention of a plague epidemic in Denmark in 1402 with reference to
Mansa’s monograph is erroneous,35 apparently he knows that this pas-
sage in Sticker’s work is not correct. Furthermore, Steffensen does not
attempt to assert that ships sailed directly from Denmark to Iceland at
the time which also can be checked and corroborated in Icelandic
annals and other sources. The staple36 was in Bergen and the Iceland
trade a privilege for Norwegians. At the time of this epidemic, Icelanders
were living in isolation with only sporadic contacts abroad and, for all
practical purposes, abroad was Norway.
31
Shrewsbury 1971: 138, 141, 149–56; Ibs 1994: 206; Blockmans 1980: 836–45;
Benedictow 2002: 102–5, 354–5, see especially Table 2A showing all known plague
epidemics in Norway, England, Northern Germany and the Netherlands in the period
1348–1500 organized so as to facilitate comparison and discussion of territorial origin.
Also see the references on this subject cited just above.
32
Mansa 1873: 92–100.
33
Sticker 1908: 8; Steffensen 1974: 47–50.
34
Mansa 1873: 99.
35
36
The Shorter Oxford English Dictionary, vol. 2, p. 2109 gives the following defini-
tion “staple:” “A town or place appointed by royal authority, in which there was a body
of merchants having the exclusive right of purchase of certain classes of goods destined
for export; also the body of merchants so privileged.”
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Thus, 1402–4 were years with unusually few outbreaks of plague in

Europe and they occurred far away from the northerly parts of Europe
and commercial centres that could serve as the point of departure for
transportation of plague by ship to Iceland. These findings permit a
secure conclusion. No doubt there was a serious or severe epidemic in
Iceland in the years 1402–4, but plague in any form based on the con-
tagion Yersinia pestis appears to be excluded: there was no plague epi-
demic in any of the countries or regions with shipping activity with
Iceland whence it could have been transported there. Another point
which excludes primary pneumonic plague is the long duration of an
epidemic which requires continuous and rapid spread in such a tiny
population (probably 30,000–40,000 inhabitants37), and this duration
would by far be the longest on the record.
At the time, Iceland was a long voyage from any port in the northerly
parts of Europe. The voyage from western Norway to Iceland would
under favourable circumstances and with suitable wind usually take
a couple weeks of sailing. However, ships from Bergen or Nidaros/
Trondheim would first sail along the coast approximately to the north-
western point of Stad, which would normally take about five days,
before they could turn and with an easterly wind sail westwards to
Iceland.38 Waiting periods for useful winds could easily take much
more time than the actual sailing.39 This would very much be the case
for ships waiting for the easterly winds necessary for sailing west-
wards to Iceland, since Norway is situated in the so-called west wind
belt which is dominated by westerly winds. In the twentieth century,
easterly winds constituted only 2.2 per cent of all wind measure-
ments in the sailing season 1 April–30 September40 in western Norway.41
Obviously, any ship with primary pneumonic plague on board among
the cramped conditions for crew and passengers after cargo had
been given strong priority would be rapidly heading for disaster.
37
See below, fn. 68.
38
Helle 1982: 68. Cf. Steen 1934: 227.
39
Steen 1942: 306.
40
The maximum sailing season is given in the important Norwegian source
Kongespeilet [The King’s Mirror] written around 1250. Here I have used the recognized
translation Kongespeilet 1947: 53, 55.
41
Since the prevailing distribution of wind direction is heavily affected by the direc-
tion of the earth’s rotation, the distribution of wind directions has probably not varied
greatly over historical time. The crude data of all wind-force measurements registered
by the wind-gauge stations in Bergen are published by the Norwegian Meteorological
Institute: www.met.no
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Since no epidemic of primary pneumonic plague has been identified

in Norwegian sources, and in the year in question (1402) not even a
plague epidemic, Steffensen’s theory is only a speculative flight of
imagination.
In the case of the supposed plague epidemic of 1494–5, the situation
is much the same. Karlsson has not attempted to identify the provenance
of the contagion and passes in silence by the problem of whence
plague contagion could have been transported to Iceland. In the mean-
time, shipping activities in northern Europe had increased greatly.
Although the small island of Iceland with its tiny population situated
in the middle of the North Atlantic Ocean on the northwestern out-
skirts of Christendom was a destination with limited attraction, it was
by now less isolated and to some extent linked to northern Europe
through trade in stockfish. At the time, English interest in fisheries in
Icelandic waters and commercial interests in the island had been
sharply reduced, due largely to strong efforts by Hanseatic cities to
drive the English away and assert their primacy and the importance of
the staple of stockfish in Bergen. By the end of the fifteenth century,
Iceland was apparently quite regularly visited by a ship sent there by the
commander of the King’s Mansion in Bergen in order to collect the
royal taxes, and stockfish may at least occasionally also have been pur-
chased in order to fill up the ship and earn some extra income. This
pattern can be discerned in a sprinkling of fifteenth-century sources
and is confirmed by the records of Bergenhus Castle, the new royal
castle in Bergen, which are extant from 1514, and where also the occa-
sional Icelandic ship is mentioned.42 The sources reveal that Iceland at
this time had some regular commercial contacts with Norway and was
now more exposed to the importation of contagion than at the begin-
ning of the century.
This puts the epidemics of 1494–5 in a somewhat different light.
However, as can be seen from Table 2A and the comprehensive com-
ments in my Norwegian plague history, there was no plague epidemic
in these years in Norway, England, Northern Germany or in the coastal
commercial cities of the Netherlands.43 In 1494, epidemics are men-
tioned in Gouda and Guelders as typical localized outbreaks and in
inland cities without shipping contacts or commercial connections
42
Norske Regnskaber og Jordebøger. See the very good index.
43
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with Norway or Iceland.44 Gouda and Guelders are the only places
where there may have been outbreaks of plague this year.45
Nonetheless, Steffensen asserts again that the contagion that trig-
gered the purported Icelandic plague epidemic was imported from
England. This conclusion is seemingly the outcome of a process of
elimination. He admits that plague is not mentioned in “Scandinavia or
Denmark” in 1494. He has again consulted Sticker, who in the crucial
year of 1494 in the whole of Europe has registered plague only in
Nuremberg, and in 1495 more or less probable or possible plague epi-
demics in Landshut (Bavaria), Erfurt and in Lower Austria.46 Since
Steffensen does not specify these localities he can state rather inaccu-
rately that plague “is mentioned in many German towns.”47 Obviously,
the contagion that unleashed the Icelandic epidemic could not have
originated in any of these localities which were not Hanseatic commer-
cial cities on the North Sea or Baltic Sea. Since Sticker cannot help him
with a plague epidemic in England, not even by a slip of the pen,
Steffensen must look elsewhere for support of his theory of provenance.
He now mentions that he has consulted Shrewsbury’s recent mono-
graph, thus admitting that he knows it, but was confronted with the
fact that Shrewsbury does not consider that there has been any pesti-
lence in England in the last decade of the 15th century.48
Since he is not willing to draw the scholarly conclusion that there
was no plague epidemic either in England (or anywhere in the British
Isles) or elsewhere in northwestern or northern Europe that could
have served as an origin of the contagion which was transported to
Iceland in 1494, he looks elsewhere for support. He turns to Creighton’s
monograph of 1891, A History of Epidemics in Britain, where “minor
44
Noordergraaf and Valk 1996: 225; Blockmans 1980: 854.
45
In the following year, 1495, there appears to have been a plague epidemic in
southeastern Sweden, as the convent of Vadstena and the city of Stockholm on the
Baltic Sea is reported in contemporary chronicles as being seriously visited by pesti-
lence. Moseng 2006: 314–5. Since an outbreak of plague in Sweden in 1495 cannot be
the origin of plague in Iceland in 1494 and Sweden had no contact with Iceland by ship,
this epidemic is not significant in the present context. It is also noteworthy that eastern
Sweden was exposed to importation of plague across the Baltic Sea and had, like
Denmark, a different temporal rhythm of plague epidemics than Norway which im-
ported plague from England and northwestern Europe more generally, but never from
Sweden or Denmark.
46
Sticker 1908: 87.
47
48
Shrewsbury 1970: 149, 155.
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epidemics are mentioned in Oxford 1486, 1491 and 1493, and it

appears that the pestilence was close to Edinburgh in March 1493.”49
Although Creighton does not use the term “plague epidemics,” but only
the unspecific term “epidemics,” this statement is taken to constitute
justification for an unqualified assertion to the effect that Shrewsbury
took no interest in minor plague epidemics and “presumably means
only large-scale epidemics.” Every reader of Shrewsbury’s highly
detailed work will know that this assumption is groundless: no epi-
demic is too small to escape his acute interest, neither can Shrewsbury’s
numerous references to and detailed knowledge of Creighton’s work
escape notice. In fact, Steffensen’s assertion in relation to Shrewsbury
work is at variance with Shrewsbury’s presentation of his research pro-
gram on fifteenth century plague epidemics: “As this work is primarily
a history of bubonic plague, an attempt must now be made to pinpoint
the possible outbreaks of that disease in the British Isles during this
century,”50 making it clear that his objective is to identify every possible
outbreak of plague. This does not exclude the possibility that he over-
looked epidemics, especially local outbreaks.51 Scrutiny of the sources
or research literature for more information is always warranted but
Steffensen did not succeed in identifying any plague epidemic and did
not accept the consequences.
The reason Shrewsbury does not mention the epidemics in Oxford
in these years is that he did not find any evidence to the effect that they
were plague. In fact, Shrewsbury has not registered a single epidemic of
plague in England “after November 1480 until an epidemic erupted at
Oxford in 1499” which he considers a “doubtful exception.” Thus,
Shrewsbury is clear in his view that in the sources there is no indication
of plague in England in the period comprising the epidemics in Oxford
and the purported Icelandic plague epidemic. It can also be shown that
he was certainly not averse to mentioning small possible outbreaks of
plague in Oxford.52
J. Hatcher and P. Slack, prominent English scholars who, in impor-
tant subsequent studies of plague in England, have fine-combed the
sources for epidemics, including the sources relating to the last two
decades of the fifteenth century, did not find any credible information
49
Creighton 1891: 283; Steffensen 1974: 53.
50
51
See Gottfried 1978: 238–40.
52
See Shrewsbury 1971: 149.
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to the effect that the small epidemics in Oxford mentioned by Creighton

were plague.53 The reason may quite safely be assumed to be that there
is no such evidence. Another insurmountable problem is how conta-
gion from this small inland outbreak of an epidemic disease should
have been moved to Iceland, as the continuous lines of communication
presumed by such an event appear to be completely unknown to either
contemporaries or to modern historians. Another insurmountable
problem is that even the last mentioned epidemic in Oxford occurred
in 1493 and cannot be linked to the outbreak of an epidemic in Iceland
1494.
Steffensen appears to assume that he can brush aside Shrewsbury’s
recent work, written by a modern bacteriologist, and substitute it with
Creighton’s proto-scientific work of 1891. Creighton’s monograph is, as
noted above, written according to the spirit of an ardent protagonist
and defender of miasmatic epidemiological theory in the face of the
rise of the new science of bacteriology. This means that Creighton
denied that each epidemic disease was caused by a specific microbio-
logical agent and believed instead that miasma could take on various
forms and could develop into plague from other manifestations of
miasmatic disease (i.e., other epidemic diseases), especially from
typhus and dysentery; he also claimed that plague was due to a poison
emanating from putrescent corpses.54 According to miasmatic theory,
an outbreak of any epidemic disease could therefore be of interest to a
study of plague since it could develop into plague. This is also the rea-
son for Steffensen’s sudden use of the term “pestilence” in the citations
above. It reflects the miasmatic assumptions that have now been
inserted at the core of his argument, although nothing is explicitly said
about this extraordinary turn of his argument away from modern sci-
entific bacteriological and epidemiological premises of analysis to
untenable proto-scientific miasmatic medical theory. Besides the fact
that Creighton has not suggested that the epidemics in Oxford were
plague, it must be emphasized that Creighton does not assert that there
was an epidemic at Oxford or anywhere else in England in 1494.
Nonetheless, Steffensen sticks to his theory, although it is untrue that
Shrewsbury only took interest in major plague epidemics and ignored
minor epidemics, so that plague could have been imported from
53
Hatcher 1977/1987: 17–8; Slack 1985: 53–65.
54
See, e.g., Hirst 1953: 74–5, 87, 89, 93–4, 285; Shrewsbury 1971: 150.
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England to Iceland in 1494 in connection with some minor outbreak

of plague which Shrewsbury ignored, Creighton did not know, and
which Hatcher and Slack overlooked. According to all accumulated
scholarly knowledge on English plague history no plague contagion
could have been transported from England to Iceland in 1494.
Steffensen also mentions a possible plague epidemic “close to
Edinburgh” in 1493, referring again to Creighton as his source.
Shrewsbury takes seriously the possibility of an outbreak of plague in
Edinburgh and outlying townships in 1493 which led to the isolation of
the town, but thinks that it probably was an epidemic of typhus. He
concludes therefore his chapter on plague in Scotland in the fifteenth
century by stating: “There does not seem to be any outbreak of epi-
demic disease in Scotland that presents any circumstantial evidence
for its identification as an outbreak of bubonic plague, with the doubt-
ful exception of 1499.”55 Significantly, this epidemic did not spread to
any other place in Scotland, which makes it a very local outbreak of
whatever disease it might have been. Furthermore, an epidemic out-
break in 1493 is out of chronological co-ordination and cannot serve
even as a hypothetical origin for the Icelandic epidemic. Edinburgh
was not a commercial shipping centre, and it is rather unsurprising
that it had no known connection by ship with Norway, and certainly
not with Iceland. Again, it is not possible to construct any case for
transportation of plague contagion from Scotland to Iceland in 1494.
Thus it is not possible to adduce empirical support for the theory
that the epidemic outbreak in Iceland in 1494 was primary pneumonic
plague or bubonic plague for that matter, since there was no area or city
which was visited by plague whence plague could have been shipped to
Iceland. Undoubtedly this epidemic in Iceland was a serious outbreak
of a contagious disease or multiple contagious diseases taking a high
toll of lives. One should take note that there are numerous accounts in
the Icelandic annals of serious or severe epidemics, including accounts
that pre-date the advent of plague in Europe and also subsequent epi-
demics that typically are out of rhythm with known European plague
epidemics. Some examples may be useful: in 1292, “Came such a big
disease over all the country […] and caused great mortality”; in 1306,
“Big epidemic in Iceland and high mortality in the south of the coun-
try”; in 1309, “Big killing disease in the north of the country”; in 1310,
“Killing disease and mortality in all the Vestfjord area and the
55
Shrewsbury 1971: 151, 155.
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Southerners’ area and boil disease”; or in 1380 and 1382: “Huge boil
disease all around the country and great mortality […] disease over all
the country and huge mortality.”56
Thus, also 1494 was a year with particularly few plague epidemics
in Europe and they occurred far away from the northerly parts of
Europe and from commercial sea ports that could serve as a point of
departure for transportation of plague contagion by ship to Iceland.
Steffensen’s assertion that plague contagion came from England has
been shown to have no evidential underpinning, essentially it is an
arbitrary assertion, and likewise not a single plague epidemic was reg-
istered in these years in Norway. Again, the intensive and comprehen-
sive discussion permits a clear conclusion: no doubt there was a serious
or severe epidemic in Iceland in the years 1494–5, but it appears impos-
sible that it could have been due to plague in any form based on the
contagion Yersinia pestis.
Steffensen sees the problem of provenance clearly and appreciates
the fact that positive identification of at least one case of plague in one
sea port with at least some evidential support for possible shipping to
Iceland is crucial to instil his theory with any (level of) tenability, how-
ever low. However, he cannot come to terms with the the complete lack
of supporting evidence on both points for both epidemics.
Karlsson has chosen the option of passing the problem by in silence,
although this undermines the very foundations of his theory, quite
possibly because he recognizes that there is no supporting evidence.
This exhaustive discussion of a possible provenance of plague conta-
gion (Yersinia pestis) for the purported plague epidemics in Iceland in
the years 1402–4 and 1494–5 has been completely negative. This find-
ing constitutes a sufficient condition for characterizing the theory as
materially untenable and for the conclusion that it must be rejected.
This does not mean that there cannot be other independent and suffi-
cient conditions for rejecting the theory.
Pure Epidemics of Primary Pneumonic Plague: Fact or Fiction?
A thorough and for all practical purposes complete presentation of the

medical and epidemiological studies of primary pneumonic plague is
presented in my thesis in order to provide the broadest possible basis
56
Annales Islandici 1888: 71, 53, cf. 75, 364. My translation from Icelandic Norse.
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for my discussion of the nature of the late medieval plague epidem-

ics in the Nordic countries. It was also motivated more specifically
by my desire to provide a background for discussion of Steffensen’s
paper,57 since his theory of epidemics of primary pneumonic plague
in Iceland is not supported by a single reference to any medical or
epidemiological study of primary pneumonic plague. Karlsson who
defends his theory intensively fails to include any reference in his paper
to a primary study of pneumonic plague or to the broad summaries of
such studies provided in the standard works on plague, not even to
K. Meyer’s brief and succinct paper. However, according to the meth-
odological tenets of medical and historical science, their theory of the
nature of these Icelandic epidemics as being primary pneumonic plague
or some mutant variant of this disease can only be adequately discussed
in relation to modern medical and epidemiological knowledge on this
modality of plague, implemented in the form of a systematic compari-
son between historical data and modern data. The better and more
comprehensive the correspondence or correlation between modern
medical data and historical data, the more tenable the inference of the
identity as primary pneumonic plague.
Fruitful discussion requires a satisfactory empirical knowledge of
the medical characteristics, epidemiological structures, lethality and
demographic effects (population mortality) of primary pneumonic
plague. Since Karlsson denies that there were any rats in Iceland, he
is obliged to, launch a theory of pure epidemics of primary pneu-
monic plague, which requires that he consistently avoids the medical
literature on primary pneumonic plague and instead makes his case
depending entirely on an assertion in a review paper by Morris. This
assertion occurs in a passage where Morris scathingly and disparag-
ingly attacks Shrewsbury for denying the existence of this form of
plague:
What is the cause of Shrewsbury’s myopia?58 Perhaps it came upon him at
the moment when (on page 6) he delivered himself of the dictum “pneu-
monic plague cannot occur in the absence of the bubonic form and it
cannot persist as an independent form of plague.” This is untrue […]. The
Manchurian epidemic was indeed exclusively pneumonic, as was the
slightly less destructive outbreak of 1920–1; […] Wu Lien-Teh’s classic
57
Benedictow 1993/1996: 25–31, 214–27.
58
“Myopia” means shortsightedness in a medical sense or figuratively narrow-
mindedness.
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treatise on pneumonic plague is significantly absent from Shrewsbury’s

very extensive bibliography.59
This basic idea and crucial premise of Morris’s theory of the nature of
plague in England and Karlsson’s theory of plague in Iceland, the notion
of pure epidemics of primary pneumonic plague, can usefully be
addressed first.
Theoretically, pure epidemics of primary pneumonic plague are pos-
sible in the technical meaning that they could start de novo from an
original case of primary infection: hunters could, for instance, be
infected by droplet infection when skinning or cutting up a sick animal
with plague septicaemia; American veterinary personnel have con-
tracted primary pneumonic plague directly from pet cats which had
inhaled contaminated droplets in the process of killing rodents with
plague septicaemia. These cases relate to a rodent basis in the form of
a plague reservoir where plague circulates continuously, which is
excluded in the case of Karlsson’s Icelandic theory. Furthermore, these
very few cases have never caused spread to any other person, thus, they
have never given rise to an endemic development (with possible conse-
quent epidemic forms).60
Morris refers to Wu Lien-Teh’s monograph on primary pneumonic
plague for empirical support of the existence of pure epidemics of
primary pneumonic plague, and Karlsson does so indirectly by cit-
ing parts of the citation including the explicit reference to this work.
However, Wu Lien-Teh states the contrary unequivocally:
It is generally agreed that the pneumonic form of plague is not directly
traceable to the epizootics [i.e., does not originate by cross-infection with
plague-infected droplets from rodent to man] but arises from human
cases of bubonic plague with secondary lung involvement.61
Wu Lien-Teh states here emphatically, and repeatedly, that primary
pneumonic plague develops only from cases of secondary pneumonic
plague, i.e., human victims of bubonic plague who have developed
septicaemia. He argues that the term ‘pure epidemic of pneumonic
plague’ “should be avoided as it is misleading as far as the origin of
the outbreaks is concerned.”62 This puts Karlsson’s theory of pure
59
Morris 1971: 208.
60
Benedictow 1993/1996a: 215–9.
61
Wu Lien-Teh 1926: 162–4. Wu Lien-Teh, Chun, Pollitzer 1934: 83.
62
Wu Lien-Teh 1936b: 418–9.
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epidemics of pneumonic plague in Iceland in perspective, disclosing in

another way the arbitrary nature of his theory and its lack of empirical
underpinning in primary studies on pneumonic plague. It also puts in
perspective the fictitious support Karlsson draws from Morris who
insists that the Manchurian epidemics were pure epidemics of primary
pneumonic plague without basis in bubonic plague and incorrectly
refers to Wu Lien-Teh’s monograph for empirical support.63
The arguments on this point can now be summed up: researchers
have not succeeded in identifying a single epidemic of pure primary
pneumonic plague. If empirical evidence is for methodological reasons
considered essential for establishing factual data with any level of valid-
ity or tenability that can be used for construction of explanatory theo-
ries, epidemics of primary pneumonic plague do not develop de novo.
There is no such thing as pure epidemics of pneumonic plague, and all
assertions to the contrary are arbitrary.64
Since there is no such thing as a pure epidemic of primary pneu-
monic plague, there cannot have been pure epidemics of primary
pneumonic plague in Iceland. According to ordinary methodological
considerations, the discussion of this point has produced another
sufficient independent condition for rejecting Karlsson’s theory.
Primary Pneumonic Plague in Manchuria: A Model for Iceland?
According to Steffensen and Karlsson, the Icelandic epidemics were

large-scale, sweeping away a large part or even most of the Icelandic
population. This view should be seen in the light of the fact that only
one fairly large epidemic of primary pneumonic plague has so far been
identified with certainty in the history of plague, namely the epidemic
of 1910–11 in Manchuria and adjacent regions that took around
60,000 lives, with 10,000 deaths occurring in the Russian Vladivostok
area. This is by far the largest epidemic of this modality of plague ever
recorded, and was followed by the second largest epidemic in the
same area a decade later. The first of these epidemics are cited enthusi-
astically by protagonists of the importance of large-scale epidemics of
63
Morris 1971: 208–9.
64
See especially Wu Lien-Teh 1926: 162–95; Wu Lien-Teh 1936b: 401–3.
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primary pneumonic plague, also by Steffensen and Karlsson. This is

only possible because they avoid taking into account:
(1) the tiny rate of population mortality in these epidemics which has
no explanatory potential for the Icelandic case;
(2) the exceptional circumstances of these two epidemics;
(3) the medical and epidemiological evidence provided by scholarly
studies of primary pneumonic plague when it does not suit their
case.
A brief summary here may therefore be of use.
A fresh presentation of the central structural circumstances that
gave these two Manchurian epidemics of primary pneumonic plague
their exceptional dynamics is needed in order to permit a concrete
comparison of basic and epidemiologically relevant social structures
between Manchuria at the beginning of the twentieth century and late
medieval Iceland (or Europe more generally):
(1) At the time, Manchuria’s population underwent exceptional
growth through the immigration of adult males from China for work,
and increased from 12.7 million according to the Chinese Census of
1912 to 22 million in 1922.65 The great majority of the Manchurian
population was Chinese coolies working in the mines and along the
rivers Sungari and Amur. Some 10,000 hunted large rodents called
tarabagans (marmots) for their valuable fur, and since plague infection
circulated among these rodents, hunting was the origin of quite fre-
quent cases of bubonic plague that were the origin also of the primary
pneumonic epidemics. This means that the social structure and the age
and gender dimensions of the population were extremely skewed and
entirely unrepresentative of any normal population. When the epi-
demic of 1910–11 broke out, there was no anti-epidemic organization
which could combat it. When the second epidemic broke out in 1921,
an organization had been built to deal with such an event and thus
much better records are available which provide more detailed knowl-
edge also of the population’s social composition and its extremely
skewed character compared with normal populations: for instance,
among the patients at the hospital in Harbin there were 1139 labourers
out of a total of 1252 patients (91 per cent), 67 women as against 1243
65
Wu Lien-Teh 1922–3: 262.
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males (5 per cent), and 21 children of ages 0–10 constituting 1.67 per
cent of the patients.66
The immense inrush of poor migrant workers created a gigantic
market for miserable accommodation. They stayed mostly in incredi-
bly overcrowded inns and lodging houses of a kind completely unheard
of in normal populations whether in Iceland or elsewhere in medieval
Europe:
The accommodation in both types of inns is based upon much the same
plan. Two, and sometimes three, tiers of berths for the lodgers are present,
there being just room enough between the tiers for a man to sit up […].
Dr Ch’uan visited some of these inns in the winter. His report showed the
conditions to be bad in the extreme: “in one hut, 15 ft. square and 12 ft.
high [20.9 sq. metres or 76.4 cu. metres], there were packed in three tiers
of berths, one above the other, more than 40 people,” thus, each having
at his disposal less than 1.9 cu. metre of space. For protection against
the cold in the winters, when the temperature “as a rule reaches −30°C
to −40°C,” the lodging-houses were constructed either entirely under-
ground or at least partly underground. The windows were closed during
the winters, and “even in May the rooms were ill-ventilated and stuffy.”
“The men eat, sleep and very often cook in the same room. They sleep in
rows with the head against the wall and the feet towards the central pas-
sage. There is no partition between adjoining berths so that they can eas-
ily breathe and cough into each other’s faces.67
These men were living in incredible density in extremely ill-ventilated
housing, breathing, sneezing and coughing in the immediate proxim-
ity of the face of the next man. For a very large proportion of the
population, the social circumstances were extreme, in the sense of
extremely favourable to propagation of disease by droplet infection,
much more favourable than in the case of any normal medieval popu-
lation. The contrast to Iceland is extreme: an isolated island society
with slight contact abroad, with very sparsely and highly dispersed set-
tlements and a largely stable population distributed on (probably)
5000–6000 detached tenancies or free holdings.68 The inhabitants were
66
Wu Lien-The 1926: 82; Chun 1936: 320–1. The change in the total number of
patients from 1252 to 1310 in the information on the gender incidence is due to a cat-
egory of 60 persons with unknown age which means that the total number of patients
actually was 1312, but these inaccuracies do not significantly affect the estimates.
67
Wu Lien-Teh 1913: 248–9.
68
Benedictow 1996b: 182–4; Benedictow 2003: 34; Orrman 2003: 438. According to
Orrman, the maximum number of peasant holdings in operation in Iceland at the time
was 3800–4500, but according Jón V. Sigurðsson 5000–6000. In my view, Orrman’s use
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overwhelmingly making their living by subsistence economy, mostly

extensive domestic husbandry more or less in combination with
some fishing, gathering and small-scale hunting, which means that the
agricultural units needed large territories and the farmsteads were
greatly dispersed. There was, consequently, relatively little social
exchange and commercial contact between these constituent parts
of the Icelandic population, quite likely less than among any other
European population.
(2) The railway played a pivotal dynamic and entirely unmedieval
role in the process of disseminating the epidemic: it was first spread
from Manchouli69 “along the railroad, westwards into Siberia again and
eastwards into China” and “the Chinese Eastern Railway conveyed the
infection broadcast.”70 Because primary pneumonic plague is spread by
interhuman dissemination, Wu Lien-Teh, points out that “such spread
will be slow in sparsely populated territories […] an epidemic will
cover wide distances with almost lightning rapidity as soon as modern
means of communication are available.”71 The last observation reflects
the process of dissemination in the Manchurian epidemics and ought
to put the dynamics of the Manchurian epidemics in an instructive
perspective, particularly in relation to medieval Iceland.
(3) The epidemic ran its course from April to the end of 1910 with-
out significant countermeasures. On Christmas Eve, the Cambridge-
trained Chinese physician Wu Lien-Teh arrived in the provincial
capital of Harbin under orders from the Imperial administration to
of these figures reflects incomplete source-criticism: the actual figure must be higher
and Jón Sigurðsson’s estimate seems more credible. There is no evidence on contempo-
rary household size and thus on household multiplier, except some indications that
multiple households were not unusual. The Icelandic Census of 1703 shows an average
household size of 6.5 persons. If this can be taken as fairly representative also of early
fourteenth-century household structure, and in the meantime there had been little
change in the economic basis or structures regulating population size according to
Malthusian principles, Jón Sigurðsson’s estimate indicates a population size of
30–40,000. It is highly unlikely that medieval population was at any time larger than
recorded by the Census of 1703, namely 50,400 inhabitants, which also is the figure
suggested by Orrman, implying a much higher average household size than that found
by Jón Sigurðsson. See the discussion in Benedictow 1996b: 182–4.
69
Situated in northern Manchuria at the junction of the Chinese Eastern Railway
and the Trans-Siberian Railway.
70
Wu Lien-Teh 1926: 71; Wu Lien-Teh 1936a: 32. The Manchurian Plague Prevention
Service was established in 1912. Manchurian Plague Prevention Service. Memorial
Volume. 1934.
71
Wu Lien-Teh 1926: 182–3, cf. 74.
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take charge of combating of the epidemic. One should recognize that

what this excellent scholar could achieve was quite limited. At the time,
very little was known about primary pneumonic plague. He had at his
disposal a minimal sanitary administration or medical staff which was
responsible for a vast region with c. 12 million inhabitants spread over
939,000 sq. km (363,000 sq. miles), more than six times the size of
England and Wales, with the possible support of only a rudimentary
Chinese Imperial administration and with military occupation of size-
able areas by Russian and Japanese forces.72 Wu Lien-Teh had at his
disposal only the most rudimentary medical facilities, a situation that
was much improved only after the establishment of the Manchurian
Plague Prevention Service in 1912 with him as director and the appro-
priation of substantial funds for hospitals, laboratories and staff.73
Importantly, Wu Lien-Teh does not in any of his copious and detailed
writings on the Manchurian epidemic make any claim to the effect that
his actions had significant effect on the further course of this epidemic.
Morris’s claim to the contrary on his behalf is groundless. Nonetheless,
by April 1911, the epidemic had faded away.
The Spontaneous Decline of Epidemics of Primary

Pneumonic Plague
Wu Lien-Teh, who led the campaigns against both Manchurian epi-

demics of primary pneumonic plague, has written most of the medical
and epidemiological studies on this disease, including the only mono-
graph, a fact that also reflects the relative rarity of this disease. He has
clear opinions on the reasons or mechanisms causing the decline: the
main reason for the fading away of the epidemic was not his personal
efforts but the characteristic tendency of epidemics of primary pneu-
monic plague to undergo “spontaneous decline.”74 In a later work, Wu
Lien-Teh relates that when he first came to Harbin, “many of the inhab-
itants with whom I conversed informed me that this epidemic was quite
an ordinary visitation, to which they had been accustomed. It never
killed many, and would stop of itself, if no attention were paid to it.”75
72
Wu Lien-Teh 1913, 1926.
73
Wu Lien-Teh 1934a: 1–3.
74
Wu Lien-Teh 1926: 188–92; Wu Lien-Teh, Chun, Pollitzer 1934: 85–6.
75
Wu Lien-Teh 1934b: 16.
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Obviously, something new had happened that gave the outbreak of pri-
mary pneumonic plague much enhanced powers of spread, namely the
immense influx of coolies living in exceptional density in the lodging
houses or inns, the extreme cold that kept them indoors, and the dis-
seminative effects of the railway. Nonetheless, also in the new condi-
tions with much strengthened epidemic dynamics and higher rates of
spread and mortality the disease’s tendency to self-limitation and spon-
taneous decline still prevailed.
The fact that spontaneous decline can be such a prominent feature
of epidemics of primary pneumonic plague despite exceptionally
favourable conditions for respiratory transmission compared with the
medieval social scene explains why population mortality in much the
largest of all known epidemics of primary pneumonic plague was only
a minute fraction of the rates ordinarily wrought on populations by
medieval plague epidemics. The Manchurian epidemic of 1910–11
claimed about 50,000 lives in Manchuria, which means that popula-
tion mortality was only a tiny 0.4 per cent, not at all compatible with
or comparable to the mortality rates assumed by Steffensen and
Karlsson for the Icelandic epidemics under discussion or by Morris for
England.
Since Karlsson had read parts of my doctoral thesis, he saw the threat
that these facts presented to his theory and argues that the same prob-
lem, or “riddle” as he calls it, of minimal mortality also prevailed in the
bubonic plague epidemics in India around the turn of the previous
century, and asserts that this must have escaped my notice.76 That is not
correct. As pointed out above, the mortality in the Indian epidemics of
bubonic plague was small because they were from the outset combated
intensely with efficient anti-epidemic countermeasures, which con-
spicuously was not the case with the Manchurian epidemic of primary
plague of 1910–11 or with the Black Death or subsequent plague
epidemics.77
If Wu Lien-Teh’s observation of a marked tendency of self-limitation
and spontaneous decline of epidemics of primary pneumonic plague is
correct, it implies that it is a characteristic feature of such epidemics to
be small. This proposition can be tested by collecting and collating all
evidence on all known epidemics of this mode of plague, a task Karlsson
76
Karlsson 1996: 283.
77
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neglected. This material makes it clear that the two Manchurian epi-
demics are the only instances of fairly large epidemics of primary pneu-
monic plague, and that even they caused miniscule population mortality
rates. The corpus of scholarly studies on primary pneumonic plague
contains only one probable and one possible instance of epidemics des-
ignated primary pneumonic plague (other than the two in Manchuria)
with as many as one thousand cases: (1) in 1905, an epidemic with
around 1000 cases occurred, according to Wu Lien-Teh, in the Bukeëf
Horde of the Kirghiz Steppes of the (Imperial Russian) Astrakhan
Government (“guberniya”); however, according to Klimenko, there
were 659 cases with 621 deaths, which means that the epidemic was
considerably smaller, included about190 bubonic cases,78 and should
rather be designated a mixed epidemic. In 1920, 1056 pneumonic cases
were registered in the northern Punjab province of India.79 Scholars
have registered a small number of epidemics designated primary pneu-
monic plague with over one hundred cases, the largest comprising 416
cases.80 Thus, the overwhelming majority of known outbreaks of epi-
demics designated primary pneumonic plague are quite small or even
tiny, most of them restricted to the social level of household, relatives
or neighbours, the great majority of outbreaks comprising from a cou-
ple of cases to a few tens of victims. This is a general feature covering all
areas where epidemics designated primary pneumonic plague have
been medically verified, whether in Russia, Central Asia, India, China,
Manchuria, Egypt, Madagascar, Vietnam or Indonesia, or elsewhere.81
Arguably, this could be taken to mean that primary pneumonic plague
in the overwhelming majority of outbreaks assumes an endemic char-
acter, becoming extinguished without having developed an epidemic
form comprising a significant number of cases.
Similarly, it appears impossible to identify any certain or likely his-
torical epidemic of primary pneumonic plague. Sticker, who was an
impressive pioneer in the field of plague history, attempted to collect all
78
The estimate is based on assumptions of a 100 per cent lethality rate in cases of
primary pneumonic plague and 80 per cent in cases of bubonic plague.
79
Wu Lien-Teh 1913–4: 244; idem, 1926: 56; Klimenko 1910: 660; Wu Lien-Teh
1927–8: 58.
80
Klimenko 1910: 660. Cf. Wu Lien-Teh 1913–4: 244.
81
Studies presenting epidemics of primary pneumonic plague include Klimenko
1910: 657–63; Wu Lien-Teh 1913: 237–52; Wu Lien-Teh 1926: 9–99; Wu Lien-Teh
1927–8: 55–92; Tieh, Landauer, Miyagawa et al. 1948: 52–8; Pollitzer and Li 1943: 212–
6; Brygoo 1966: 51–2; Trong, Nhu and Marshall 1967: 93–7; Narkevich, Onishchenko,
Naumov et al. 1991: 32.
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relevant historical evidence on pneumonic plague, but managed to find

only a few interesting possible cases of such epidemics, six before 1800.
Importantly, he cautiously designates them as being characterized by
“predominant [“vorherrschende”] lung disease,” which presumably
should be taken to mean that, in his view, they were mixed epidemics
that also included significant proportions of bubonic cases.82 One
should also note that he does not (because the sources will not permit
it) differentiate between secondary and primary pneumonic plague.83
Wu Lien-Teh, who took a strong interest in plague history, succeeded
in adding a few epidemics to the list, but also in his case all epidemics
are mixed.84 In his excellent study of plague and other epidemic dis-
eases in Early Modern Central Europe (1560–640), E.A. Eckert dis-
cusses some evidence based on parish registers relating to plague
epidemics in seventeen communities in southern central Europe and
the Rhenish region in the years 1563–4. The clinical evidence provided
by contemporaries does not discern between secondary and primary
pneumonic plague, but the fact that 11 of 17 communal epidemics
reached their peaks of burials in the winter months merits attention.
However, the author concludes his discussion by stating that these and
other outbreaks of winter epidemics probably were mixed epidemics,
pointing to the Madagascan epidemics for an analogous model.85 In my
monograph on the Black Death, doing my very best to collect and col-
late all relevant studies for the whole of Europe, I similarly found no
evidence implying epidemics of primary pneumonic plague, only two
possible cases of mixed epidemics, namely in Avignon and only (just)
possibly in Novgorod. And this outcome was strongly confirmed by the
seasonality and pattern of spread of the Black Death.86
Despite much effort, it has so far not been possible to identify a likely
historical case (before c. 1850) of an epidemic of primary pneumonic
plague. The notion of pure epidemics of primary pneumonic plague is,
as shown above, fictitious, an epidemic of this type has never been
82
Mixed epidemics comprising (for social and cultural reasons) an increased inci-
dence or level of pneumonic plague have been studied by modern scholars in
Madagascar 1924–40 (20 per cent), Upper Egypt 1904–22 (31 per cent), Java (4–8 per
cent) and episodically in Vietnam. Brygoo 1966: 45–7; Wu Lien-Teh 1926: 33, 23;
Trong, Nhu and Marshall 1967: 93–7.
83
Sticker 1910: 246.
84
85
Eckert 1996: 83, 85–6. For the Madagascan plague epidemics, see fine and com-
prehensive overview by Brygoo 1966.
86
Benedictow 2004: 214, 233–41, 238–9.
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observed in the research history of plague. Steffensen’s and Karlsson’s

assertions that there were epidemics of primary pneumonic plague or
pure epidemics of primary plague in Iceland and Karlsson’s view that
that the Black Death in general was primary pneumonic plague, are
without empirical support. This may explain that there is no indication
in Karlsson’s paper of any effort to obtain relevant information on the
matter. This discussion has established another independent sufficient
condition for rejecting their assertions.
The epidemiological effects that could be expected if Wu Lien-Teh’s
observation is correct, that the course of epidemics of primary pneu-
monic plague are characterized by “spontaneous decline,” have now
been tested on the complete record of registrations of epidemics of
this modality of plague and the outcome has been found to conform
entirely to his prediction: generally, outbreaks in normal populations
are quite small or tiny, rarely exceeding a hundred cases. Neither in the
past nor in recent history is there any instance in the records of an
epidemic of primary pneumonic plague in a normal population com-
prising the number of cases (mortality) or sweeping away the propor-
tion of the population (population mortality) corresponding to
Steffensen’s and Karlsson’s assertions as to the mortality effects of the
Icelandic epidemics of 1402–4 and 1494–5, and by very large margins.
This outcome of the discussion of this epidemiological aspect, the
highly limited powers of spread of primary pneumonic plague, suffices
as another independent sufficient condition for rejecting Steffensen’s
and Karlsson’s theory.
It would, however, be unsatisfactory to leave this subject without iden-

tifying the main reasons for the three very important characteristic epi-
demiological features of epidemics of primary pneumonic plague,
namely to undergo “spontaneous decline,” be small or tiny, and to give
rise to a relatively small number of outbreaks—three epidemiological
manifestations of the disease that are, presumably, closely causally
linked. There are three main reasons:
(1A) Contrary to what is asserted surprisingly often, primary pneu-
monic plague is not strongly contagious and does not easily
“recruit” new infective agents who assure the continuation and
dynamic development of the epidemic process, except, as under-
scored above, under exceptional social circumstances of extreme
overcrowding. Again, in the words of Wu Lien-Teh:
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Inasmuch as, in our opinion, an overwhelming majority of cases

receive infection through being in the direct range of a cough, we
wish to lay stress upon overcrowding,
and he goes on to illustrate the point:
At Dalinor mines, though the population consisted of 4,000
Chinese and 2,000 Russians, the 1921 epidemic claimed only four
Russians out of a total mortality of 1,017. The Russians were better
housed on level ground, while the Chinese lived in crowded semi-
underground dwellings.87
The crucial importance of close physical proximity is still the pre-
vailing view. The American scholar J.D. Poland makes this point:
Primary plague pneumonia occurs primarily in persons in close
and prolonged contact with another person with pneumonic
plague. Hence, respiratory transmission occurs most frequently to
medical personnel or household contacts who are directly involved
with the care of the patient.88
(1B) Presumably, this feature is at least to a large extent due to the fact
that plague is a bacterial disease and bacteria, being hundreds of
times larger than viruses, need much larger and heavier droplets
for aerial transportation and will, consequently, normally move
much shorter distances through the air. Hirst summarizes recent
research showing that
droplets of sputum ejected from the mouth tend to fall rapidly
towards the ground and that, even when people cough, a surpris-
ingly small number of bacterial colonies develop on culture plates
placed only a foot directly opposite the mouth.
This corresponds well with the fact that
most patients give a history of association with a previous case for
a period of hours, or even days.89
(2) Another crucial reason for the weak powers of transmission and
dissemination of primary pneumonic plague is that this disease
is an extraordinarily fast killer, leaving little time for interhuman
spread. In 1921, in Harbin (Manchuria) mean duration of the
87
Wu Lien-Teh 1926: 180–1, 298–302.
88
Poland 1983: 1230. See also Meyer 1961: 252.
89
Hirst 1953: 226–7.
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disease in 1,128 patients was 1.8 days.90 This characteristic is con-

firmed by observations made during smaller epidemics, for
instance, during an epidemic in Vietnam in 1915 comprising
twenty-four persons including three medical personnel, all of
whom died. It was documented that “death occurred within
forty-eight hours of the onset of primary symptoms,” which must
be taken as a more inaccurate way of expressing an identical
observation. Also in a study of another plague epidemic of about
the same size in Vietnam in 1941 it was documented that all cases
were dead within forty-eight hours of the onset of the symp-
toms.91 Importantly, it takes, on average, twenty-four hours before
the contagious cough with bloody expectoration develops, which
leaves only 0.8 day for transmission.92 Also this clinical feature
explains why outbreaks of this disease normally comprise only a
small number of cases and will tend to be quite easily extin-
guished in the incipient or early endemic phase or, quite rarely,
early in the epidemic process. Arguably, this clinical feature also
represents an independent sufficient cause.
(3) However, the causation of “spontaneous decline” is more com-
plicated; it results from the combined effect of three usual clinical
forms of the disease that do not (or only slightly) lead to develop-
ment of the cough with bloody expectoration which is the prin-
cipal vehicle of dissemination of primary pneumonic plague:
(3A) As suggested by the extremely rapid course and brief dura-
tion of the disease, one such form is quite a frequent inci-
dence of a fulminant course of ordinary cases of primary
pneumonic plague leading to the rapid demise of the patient
before the contagious cough with bloody sputum has had
time to develop.
(3B) When larger droplets are inhaled (and as pointed out above,
this will quite often be the case, see 1B), they tend to impinge
on the upper parts of the respiratory tract where they infect
the tonsillar region, causing pharyngeal and primary septi-
caemic plague with extremely rapid death of the patients
who will not become contagious since the droplets are not
90
Chun 1936: 318–9.
91
Trong, Nhu and Marshall 1967: 93.
92
Wu Lien-Teh 1922–3: 274; Wu Lien-Teh 1926: 297; Wu Lien-Teh, Chun, and
Pollitzer 1934: 80.
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deposited in the lungs and cannot give rise to the cough

with bloody sputum.
(3C) Wu Lien-Teh stresses in particular the importance of a
third type of fulminant case called pulmonary plague. Dis-
section of lungs of such cases did not show the
usual pneumonic foci [which produce the cough with bloody
sputum: my insertion] but presented—though undoubtedly
infected through the respiratory tract—only hyperaemic93
and oedematous94 changes in the lungs as well as marked
septicaemic features. We designated these cases pulmonary
plague because, though they were anatomically similar to
the septicaemic cases encountered in bubonic plague, they
were etiologically different from them, the infection having
entered through the respiratory tract.
Conspicuously, the incidence of pulmonary plague increased sharply
towards the end of the epidemics, while pneumonic cases, i.e. cases
with pneumonic foci in the lungs (which give rise to the cough with
bloody sputum), became relatively scarce. In Wu Lien-Teh’s opinion,
these cases were probably
due to an enhanced virulence of the B. pestis developing through passage
from lung to lung. We assumed that through such repeated passages the
invading organism finally became so virulent as to cause mainly pulmo-
nary cases. These—though very fatally infected—are comparatively little
infectious, because the disease runs a rapid course. As a consequence, the
principal medium of infection, namely, the sputum, is absent. In other
words, our post-mortem findings at the end of the 1920–1 outbreak give
a scientific reason in favour of a spontaneous decline of pneumonic-
plague epidemics […].
Being thus rendered less infectious, the “spontaneous decline” of the
epidemic, even in foci unattended by sanitary organizations, might be
easily explained.95
R. Pollitzer, who was among the medical staff working in the epidemic of
1920–1 and made “a fairly large number of postmortems on lung pest
victims,” later confirmed that he made exactly the same observations as
93
Denoting hyperaemia: an excess of blood in a part, engorgement.
94
Pertaining to, or of the nature of, oedema, affected by oedema. Oedema: the pres-
ence of abnormally large amounts of fluid in the intercellular tissue spaces of the body,
usually applied to demonstrable accumulation of excessive fluid in the subcutaneous
tissues.
95
Wu Lien-Teh 1926: 189–92; Wu Lien-Teh, Chun, Pollitzer 1934: 86; Wu Lien-Teh
1936b: 420–1.
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Wu Lien-Teh. Importantly, this was also the case with respect to the
rhythm of developments, that
dead bodies showing no pneumonic foci were mainly met with at the end
of the epidemic. It was therefore tempting to assume that there might be
a causal connection between the preponderance of this “non-pneumonic”
form of lung pest and the decline of the outbreak.96
In 1942, Pollitzer and Li conducted a complete investigation of an out-
break of quite a usual size of primary pneumonic plague, comprising
sixteen cases, which had taken place in a district in North Hunan
(China). They made the following observations:
(1) “The last patient in each of the two first affected families had no
more bloody sputum.”
(2) “In five of the six instances where the infection was carried from
these two households into other families, no further spread took
place, evidently because the secondary victims had no bloody spu-
tum, in three instances even no cough.”
(3) “Further inquiries showed that infection never resulted from con-
tact with patients having neither bloody sputum nor cough. In
only two out of fifteen instances was infection due to contact with
patients having cough but no bloody sputum.”
(4) Of particular importance in the present context are the following
assertions:
(a) the outbreak came to an end before measures taken by us could
have any effect: (b) this decline took place during a rainy spell, when
the temperature was comparatively low.
The first point of the last citation confirms the spontaneous decline at
an early stage that characterizes outbreaks of primary pneumonic
plague in which no countermeasures are applied, the second point is of
relevance to some extraordinary assertions by Steffensen and Karlsson
as to the importance of the climate in Iceland (see below). Pollitzer and
Li make the following general conclusion:
More or less rapid evolution of a “non-pneumonic” type of lung pest,
characterized by absence of the usual vehicle of infection, the bloody
sputum, and often also of cough, appears to be of causal importance in
the decline of pneumonic plague epidemics.97
96
Pollitzer and Li 1943: 215.
97
Pollitzer and Li 1943: 212–6.
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Outbreaks of primary pneumonic plague have been shown above to be

generally small or tiny, comprising only a paltry fraction of the number
of cases or level of population mortality envisaged by Steffensen and
Karlsson. The medical and epidemiological reason for this feature
are also clear: the high frequency of various types of fulminant non-
contagious forms that do not contribute to further dissemination of the
epidemic and therefore break the chain of transmission. Most impor-
tant among these forms is the appearance at an early stage of outbreaks
of a strong increase in the incidence of cases of pulmonary plague that
leads to a rapid decline and disappearance of the epidemics, a phenom-
enon designated “spontaneous decline.” These non-contagious forms
arise from a combination of the virulence and size of the plague bacte-
rium and the mode of respiratory transmission. Thus, they constitute a
basic property and characteristic feature of this modality of plague
which mould all known outbreaks in the past and in modern times into
clearly defined medical, epidemiological and demographic patterns.
These patterns diverge radically and decisively from the patterns
envisaged by Steffensen’s theory that the two Icelandic epidemics of
1402–4 and 1494–5 were primary pneumonic plague and Karlsson’s
theory to the effect that these two Icelandic epidemics were pure epi-
demics of primary pneumonic plague and that this was a general fea-
ture of the Black Death in Europe. Their theories are incompatible with
the corpus of knowledge of the medical and epidemiological causes of
the rise and course of the outbreaks of primary pneumonic plague.
This explains also why there is no epidemic of primary pneumonic
plague on the record with a duration of two or three years as in the case
of the Icelandic epidemics of 1402–4 and 1494–5: the clear and system-
atic tendency of spontaneous decline would prevent this from happen-
ing. Thus also the duration of the Icelandic epidemics is a strong
argument against their being primary pneumonic plague; that the
notion of pure epidemics of primary pneumonic plague is fictitious is
another matter.
Finally, I would also like to point out that in the plague history of
Norway from 1348–654, covering more than thirty waves of bubonic-
plague epidemics, there is not a single instance of an epidemic that
lasted so long in the same region, which is also a strong argument
against this Icelandic epidemic having been bubonic plague.98
98
Benedictow 2002.
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The Icelandic Climatic Theory of Primary Pneumonic Plague
Steffensen, who bases his theory on the hypothesis that the supposed
Icelandic plague epidemics started from bubonic plague victims who
developed secondary pneumonia, accepts the fact that there were rats
in Iceland and thus avoids the impossibilities and absurdities of
Karlsson’s theory as to the origin of epidemics of pure primary pneu-
monic plague. However, he cannot avoid the issue of the excep-
tional powers of spread that are not observed anywhere else, and must
construct a unique Icelandic case based on assumptions of climate.
Steffensen argues that
bacteria harboured in the mucus of the respiratory tract derive from it
some protection against dryness. In damp and cold air, such drops of
moisture can preserve living bacteria for months on end, especially if
there is frost. Under Icelandic conditions, therefore, it is quite possible
for living plague bacteria to remain in tiny drops of moisture on, for
example, bedclothes and personal clothing, long after the patient’s death,
and for drops to be stirred up again and carried down into the lungs of
the person, for example, who is about to bury the body […] there is,
therefore, no apparent biological reason why an epidemic of primary
pneumonic plague could not have occurred in Iceland.99
Steffensen does not consider this statement a composite working
hypothesis constituted by several hypothetical elements each depend-
ent on empirical support or corroboration for its viability. In his
understanding of scholarly or scientific work the mere proposal of a
hypothesis confers tenability on it without empirical support or refer-
ences to research literature. This is obviously fallacious. The research
literature on primary pneumonic plague contains no support, not even
a unique case or sporadic case histories of this type of dissemination.
No case has been observed of a person who has contracted primary
pneumonic plague from plague-contaminated droplets in clothing or
bedclothes left by patients at any time or in any climatic zone. This
might constitute a pure epidemic of primary pneumonic plague which,
as shown above, has never been observed or ascertained in any schol-
arly study of this disease. “Damp and cold air” is very far from being a
unique Icelandic type of climate, as the circumstances of the epidemic
of primary pneumonic plague studied by Pollitzer and Li in Hunan
Province show (see above). The coasts of western and northern Norway
99
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are also characterized by “damp and cold” climate for a large part of the
year, but no epidemic of primary pneumonic plague can be ascertained
from the sources; all Norwegian plague epidemics conform to the pat-
tern of spread and seasonality of bubonic plague.
There is also another crucial point that Steffensen has failed to con-
sider and which undermines or even invalidates his theory, namely, the
effect of extraneous conditions on the virulence of plague bacteria. As
stated by Pollitzer and Meyer:
it is generally agreed that, although […] plague-contaminated objects
may remain infected for some time, the chances of their proving infec-
tive, thus becoming responsible for the spread of the disease, are usually
remote. Plague […] in its pneumonic form […] is almost always the
result of a direct infection contracted in the immediate vicinity of patients
suffering from secondary or primary lung involvement.100
Similarly, Wu Lien-Teh states specifically in relation to primary pneu-
monic plague that:
the unsuitability of the plague bacillus for prolonged existence as a sapro-
phyte and the unlikelihood of rodent or man contracting direct infection
from contaminated inanimate objects, rule out the free existence of the
causative organism as a means for preservation of the disease.101
This quotation is also given in my doctoral thesis102 in the discussion of
this matter, however, to no avail, as Karlsson simply ignores it.
Steffensen argues his case for primary pneumonic plague in Iceland
in terms of what is possible under particular Icelandic climatic condi-
tions: his concluding sentence is couched in the formal language of
hypothesis formation. But he has built a model which cannot be tested,
because no Icelandic material is available that allows the identification
of the form of plague or epidemic disease afflicting the population. For
this situation the following methodical rule applies: the inability to test
an explanatory model does not invalidate it, but does render it useless
as a scientific hypothesis. The justification for constructing this explan-
atory hypothesis, model or working hypothesis would have been
strengthened if at least a sprinkling of this type of endemic cases had
been observed elsewhere. But Steffensen’s is based on pure specula-
tion, it has no evidentiary basis, no validity, no tenability. Its use in the
100
Pollitzer and Meyer 1961: 434–5.
101
Wu Lien-Teh 1936a: xxviii.
102
Benedictow 1993/1996: 216.
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construction of an alternative theory of plague in Iceland can only

serve to undermine the theory, and claims that such a theory of
plague is superior to other empirically supported theories are obviously
invalid.103
Conspicuously, later in his paper, Steffensen argues that the clinical
elements in the account of the Lawman’s Annal on the Black Death in
Bergen in 1349 show that it was an epidemic of primary pneumonic
plague, an argument that will be addressed below and shown to be
untenable. Here the following point shall be made: by turning to
Norway, Steffensen greatly extends the scope of climatic conditions
that allow large-scale epidemics of pneumonic plague. Whilst he origi-
nally stresses the uniqueness of the Icelandic climate, making a claim
for Iceland as a unique case, the extreme weakness of his case has led
him to a line of climatic argument which includes a much wider range
of territorial relevance, covering quite large parts of northerly Europe
including northern England and Scotland. This makes the rarity of epi-
demics of primary pneumonic plague, if indeed any occurred, even
more hard to explain, as no such epidemic, as mentioned above, has
been confirmed in any pre-industrial society.
Steffensen’s and Karlsson’s assertions are without empirical medical
or epidemiological support in the most accurate meaning of the terms.
It has been possible to identify several independent sufficient causes for
rejecting their theories.
Mortality Rate of the Purported Plague Epidemics in Iceland
Karlsson makes two central assertions with respect to the mortality

caused by the Icelandic epidemics: (1) that the mortality rate in the
epidemic of 1402–4 was 60 per cent and in the next epidemic of
1494–5 it was 53 per cent, and (2) that these mortality rates constitute
definite proof that the epidemics were primary pneumonic plague.104
The massively documented fact is that no epidemic of primary pneu-
monic plague is known which has caused a population mortality
exceeding 1 per cent. This is the case for very concrete and strong
103
Benedictow 1993/1996: 223–5.
104
Karlsson 1996: 268–76. In the second case, Karlsson quite arbitrarily moderates
his mortality estimate for the second epidemic to 30–50 per cent, since he recognizes
that the evidence is very poor to put it mildly.
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medical and epidemiological reasons. A level of population mortality

of 60 per cent thus constitutes certain proof that the Icelandic epidem-
ics must have been a different disease or conjunction of diseases.
However, Karlsson’s estimates of mortality must be rejected. The
texts of the Icelandic annalists or chroniclers on which these estimates
are based are cited in English translation in Appendix 2. The sugges-
tion that medieval chroniclers provide accurate information on distri-
bution, mortality rates and areas affected cannot be taken seriously,
as shown repeatedly above and again below.105 Hatcher disregards the
“overwrought imaginings and hopelessly inaccurate quantification of
the chroniclers.”106 Just to take a couple of illustrating examples of the
nonsense of figures in Icelandic annals: in the Annal of Skálholt, it is
related that in 1305 that King Håkon V of Norway went to war with
Sweden with an army of 40,000 warriors, which is without any basis in
the known facts on Norwegian military manpower at the time, to put it
mildly. Compared with England’s contemporary population of around
six million, it would correspond to an assertion that the king of England
went to war with 700,000 warriors. The Lawman’s Annal asserts that
only fourteen persons survived the Black Death in London.107 Instead,
as Hatcher states, “advances in knowledge and technique have enabled
us to proceed […] to a position where the majority of historians are
agreed upon a reasonably narrow range of probabilities.” Only mortal-
ity figures based on population records that can be examined and eval-
uated according to the principles of demography are used in my
monograph on the Black Death.108 Chroniclers’ assertions cannot be
accepted, especially their assertions of numerical and demographic
data, if source-criticism cannot be applied and the possible tenability
at any level can be ascertained by independent material evidence.
In this perspective it could be of interest that there are numerous
105
See, for instance, above: 78–84, 219–22, below: 589–92.
106
Hatcher 1977/78: 21.
107
Islandske Annaler 1888: 200, 275.
108
One partial exception is the chronicle of Giovanni Villani. which can be consid-
ered usable, because it can be shown that he takes real interest in collecting statistical
information on his beloved city of Florence and that the city’s authorities produced
statistically usable population registers, for instance of taxable householders, that he
has real competence with regard to statistical data, that his estimates are based on em-
pirical material of various kinds, and because his estimate of mortality in the Black
Death can be tested against various types of population records. His approach is proto-
scientific, reflecting his central background in the Early Renaissance in Florence, and
therefore contains valuable empirical and statistical material.
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demographic studies showing that epidemics of bubonic plague pro-

duce mortality rates at the level of 60 per cent.109
Karlsson does not mention that Steffensen, on the basis of the same
sources, conjectures a population mortality of one-third,110 about half
of Karlsson’s estimate. Since Steffensen honestly characterizes his esti-
mate as a conjecture, i.e., a guess or guesstimate, the margins of error
are obviously huge. Thus, Karlsson asserts that he has found solid
ground for an accurate mortality estimate on the basis of sources that
Steffensen thinks permit only a conjecture or qualified guess of a much
lower level of population loss. This puts in perspective Karlsson’s con-
tention that the margin of error could be a ludicrously low 10 per cent
and the fact that this has been accepted by the editors and consultant(s)
of the Journal of Medieval History.111 The difference between Steffensen’s
and Karlsson’s estimates is 100 per cent, representing a corresponding
margin of error.
Karlsson incredibly maintains that the annals’ indication of area
affected, distribution and level of mortality rates are accurate within
margins of a couple of per cent, which soundly beats the margins of
error associated with modern population censuses based on statistical
data systematically collected by trained personnel. In view of the fact
that margins of uncertainty associated with the various elements that
constitute estimates relate multiplicatively to each other, the margins of
error are much higher. Any scholarly critical examination of the annals
and other evidence cited by Karlsson will demonstrate the justification
for at least a modicum of prudence as shown by Steffensen. In my opin-
ion, they permit no useful quantification of a specific mortality rate at
all, only the impression of serious and locally also severe mortality (see
below, Appendix 2).
This perspective is corroborated in the most recent evaluation of
population losses in the two fifteenth-century epidemics based on
agrarian studies relating to northern and eastern Iceland where it is
stated that they indicate
a limited abandonment of farms in 1420–50 and 1495–1550 when some
20–25 per cent of the farms were deserted. The effect was particu-
larly notable on the coast but it was temporary and probably caused by
109
110
111
Karlsson 1996: 276.
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outbreaks of plague in 1402–4 and 1494–5. In the fifteenth century cli-

matic deterioration should also be taken into account, the westernmost
parts of Iceland, on the other hand, saw population growth and settle-
ment expansion from about 1300 and show no signs of recession at all in
the three following centuries.112
Clearly, Karlsson’s “estimates” fly in the face of the sources and empiri-
cal studies on settlement developments. The settlement studies suggest
a population loss which is much lower; this shows that Karlsson’s “esti-
mates” are wildly exaggerated, the predictable outcome of a basically
arbitrary approach. Mortality at the level of 15–20 per cent can be
caused by a number of epidemic diseases or conjunction of more or
less concomitantly spreading epidemic diseases, especially in the epi-
demiological circumstances characterizing Iceland at the time.113
Summary: Why There Never Was a Plague Epidemic in Iceland
The presentation of the characteristic medical and epidemiological

features of primary pneumonic plague based on the complete corpus of
relevant research constitutes a broad basis for comments on Morris’s
alternative theory of late medieval plague as being primary pneumonic
plague and on Karlsson’s use of this theory in his paper on the epidem-
ics that ravaged Iceland in 1402–4 and 1494–5. It has been shown that
their assertions are unfounded and erroneous on the following main
points:
(1) There is no such thing as pure epidemics of primary pneumonic
plague, i.e., independent of an infected murine basis. No case of an
epidemic of pure primary pneumonic plague has been identified
in the entire corpus of historical studies of plague. All assertions to
the contrary are empirically unfounded and arbitrary.
(2) Since there were no rats in Iceland, according to Karlsson, no epi-
demic of plague of any kind could have arisen in the island, pure
or not.
(3) It is not correct that assertions in the sources to the effect that
plague victims typically died in the course of three days of illness
are indicative of primary pneumonic plague. The average duration
112
Vahtola 2003: 575–6.
113
Cf. Cliff and Haggett 1985; McArthur 1968.
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of the course of primary pneumonic plague is 1.8 days, and patients

normally die within 48 hours. One would also expect that the fre-
quent incidence of even much shorter fulminant cases would
attract attention by their frightening character and tend to acquire
prominence in contemporary accounts. Three days are within the
normal range of the course of illness of bubonic plague, namely
three to five days,114 and an average duration of plague disease
within this range is therefore a clear indication of bubonic
plague.115
(4) It is not correct that all victims of primary pneumonic plague
develop infectious cough with bloody expectoration. On the con-
trary, epidemics of primary pneumonic plague are characterized
by large and increasing proportions of cases of several clinical
types which do not cause development of a cough with bloody
expectoration in the diseased, who therefore do not pass on the
infection.
114
Chun 1936: 313. Above: 279–80.
115
Morris 1971: 206–7, maintains erroneously that the average duration of cases of
primary pneumonic plague is three days and of cases of bubonic plague is five days.
Since he does not support his view with a footnote, the basis or source of this asser-
tion cannot be ascertained and examined. He refers to Gui de Chauliac’s account of the
Black Death in Avignon where this contemporary observer discerns between a first
phase, in which the course of illness lasted three days, and a second phase where it
lasted five days, as proof that the first phase was primary pneumonic plague. However,
this is not evidence to this effect, since both indications of duration of illness are
within the normal range of bubonic plague. Since cough and bloody expectoration of
secondary pneumonic plague cases normally constitute a significant but variable pro-
portion of cases of bubonic plague, there cannot have been any phase without a notice-
able incidence of this clinical feature, but there can have been substantial variation or
change in the incidence. It is also not correct, as Morris contends or implies, that
primary pneumonic plague can be the origin of epidemics of bubonic plague; the in-
correctness of this assertion is demonstrated by the experience in the Manchurian
epidemics. Although there were 50,000 cases in Manchuria itself and the dwellings
of the Chinese coolies that constituted the great majority of cases swarmed with fleas
and other blood-sucking parasites, bubonic cases that could have been caused by fleas
infected by pneumonic cases were extremely few and isolated and only one case can be
considered quite certain; in the words of Wu Lien-Teh: “practical experience has shown
that pneumonic plague rarely caused the bubonic form,” and “Not so much the exist-
ence as the rarity of such cases calls for comment.” 1926: 186–7. The first phase of
plague in Avignon was, therefore, probably a mixed epidemic in which the primary
pneumonic part faded away due to the characteristic “spontaneous decline” of this mo-
dality of epidemic plague and a more usual epidemic of bubonic plague emerged.
Benedictow 2004: 236–8. No instance of a primary plague epidemic that develops into
a bubonic plague epidemic has ever been recorded.
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(5) It is therefore not correct that epidemics of primary pneumonic

plague have great powers of spread. On the contrary, epidemics of
primary pneumonic plague are characterized by low diffusibility
and “spontaneous decline.” Outbreaks of primary pneumonic
plague are small or tiny, population mortality rates are consistently
minuscule, and even the largest epidemic of this type, the first
Manchurian epidemic of 1910–11, occasioned a population mor-
tality rate of only 0.4 per cent. Mortality rates of the size asserted
by Morris for England and by Karlsson (and Steffensen) for the
Icelandic epidemics of 1402–4 and 1494–5 are unknown in the
complete corpus of research on primary pneumonic plague, and
by wide margins. Their assertions to the effect that the English or
the Icelandic epidemics swept away large parts of the respective
populations are powerful arguments against the notion that they
could have been primary pneumonic plague.
(6) No epidemic of primary pneumonic plague or of bubonic plague
has been identified in the northerly parts of Europe 1402 or 1494,
the years when the two epidemics broke out in Iceland or in the
preceding years. There is therefore no way plague contagion in any
form could have been transported to Iceland in these years.
(7) Karlsson’s theory of a mutant version of plague disease specifi-
cally designed to suit his arguments is arbitrary, and it is also falla-
cious, since it is not developed according to the requirements of
evolutionary theory and the obligation to uncover and present the
mechanisms of selection. The territorial origin of a specific mutant
version of primary pneumonic plague of the purported Icelandic
epidemics is a crucial question left unanswered; its origin is also
therefore arbitrary. Also unexplained is the crucial question of
whether the same mutant strain really could have arisen twice, or
where on earth it took refuge in the meantime. No such mutant
strain has been identified by modern DNA studies of genetic mate-
rial taken from plague graves. All of these crucial assertions by
Stephenson and Karlsson are arbitrary and untenable.
According to the normal methodological and empirical considerations
and assumptions of scholarly work, these seven medical and epidemio-
logical points settle the case, as they contain as many independent suf-
ficient grounds for invalidating the theory. There never was a plague
epidemic without rats in Iceland. There never was a plague epidemic in
Iceland.
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Was the Black Death in Bergen (Norway) 1349 Primary

Pneumonic Plague?
Karlsson states explicitly, as mentioned above, that the central objective

of his paper is to defend Steffensen’s paper against my criticism of it and
his theory that plague in Iceland was primary pneumonic plague. He is
especially outraged at my criticism of Steffensen’s presentation and
analysis of the clinical description of plague cases given in the Lawman’s
Annal’s account of the Black Death in Bergen in 1349 and of his conclu-
sion that it describes an epidemic of primary pneumonic plague. This
account and another given in the so-called Fragment of the Annal of
Skálholt, which is closely related but not identical,116 are normally and
reasonably assumed to be based on accounts of two prominent Icelandic
prelates who stayed in Bergen at the time of the Black Death and
returned in 1350 and 1351, respectively.117 However, other Icelanders
who returned, some quite likely in 1350,118 may have added independ-
ent information. Karlsson aggressively defends Steffensen’s views;
I consider some of his arguments personally offensive, but will refrain
from commenting on them, as the facts speak for themselves clearly
and loudly.
One should note that there are crucial problems not only with regard
to the interpretation of the clinical descriptions of the Black Death in
Norway provided by these Icelandic chronicles. Tacitly, Steffensen
assumes that it is unproblematic to use the Lawman’s Annal’s account
of the Black Death in Bergen in 1349 for the purpose of corroborating
his views on the nature of the epidemics that spread in Iceland in
1402–4 and 1494–5 as primary pneumonic plague (see Appendix 2).
This inevitably implies, as pointed out above, a sudden abandonment
of his argument of the specificity of Icelandic climate as a necessary
condition for the spread of large-scale epidemics of primary pneu-
116
Islandske Annaler 1888: 224: “þat uar kyn sottarinnar at menn lifdu iij dægr med
hardan stinga þa toku menn blodspyu ok for þar med onndin.” The text is cited without
indicating the expansion of abbreviations. Cf. below: 551 and fn. 151.
117
Benedictow 2006: 88, 101–2.
118
In the Lawman’s Annal it is mentioned that Thorlak’s ship at quay in Bergen was
ready to leave for Iceland with a number of named Icelanders on board, but was so
severely hit by the Black Death that it was prevented from putting to sea. Quite likely,
this ship returned to Iceland in the shipping season of 1350 with survivors and other
passengers and crew members on board who had their own stories to tell. Benedictow
2002: 67–72.
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monic plague. In addition, his approach is problematic in several other

important respects that he does not address:
(1) The Icelandic annals give no clinical information about the two
purported fifteenth-century epidemics of primary pneumonic
plague. Consequently, there is no basis for valid comparison with
the Black Death in Bergen or elsewhere, they are not in pari mate-
ria. Steffensen’s use of comparative analysis is fallacious.
(2) Steffensen gives a highly problematic translation of a crucial part
of the text which in a decisive way seemingly strengthens his case.
This can be demonstrated by citing both the original text from the
Lawman’s Annal,119 as I did in my thesis,120 and Steffensen’s and my
translations, italics showing the crucial bit of contested translation
relating to the two original Norse words “hordum stinga,” with the
basic meaning of sharp, pricking, painful sting (literally “hard
sting”), which is here associated with the clinical manifestations of
the Black Death in Bergen.
– Benedictow:
The disease was such that men did not live for more than a day or
two with sharp pangs of pain, then they began to vomit blood, and
then they expired.
– Steffensen:
The nature of the sickness was such that men lived not more than
one day or two, with great pleuritic pain, whereupon they began to
vomit blood and then the spirit passed on its way.
Steffensen uses the medical word “pleuritic” in his translation,

although no word with this meaning occurs in the source. To add
one or more crucial words to the translation of a text, without
making it clear to the reader and providing a persuasive reason for
it, violates one of the basic methodological conventions of histori-
cal science. Conceivably, it could be a matter of interpretation or
connotations, but then, according to the conventional principles
119
Islandske Annaler 1888: 275–6: “þat var kyn sottarinnar at menn lifdu eige meirr
en eitt dægr edr tuo. med hordum stinga. eftir þat sætte at blod spyiu ok for þar ondin
med sinn vegh.” The text is cited without indicating expansion of abbreviations.
120
The text is almost identical with the text of the Fragment of the Annal of Skálholt;
see above: fn. 116, and below: 551 and fn. 151.
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of historical methodology and source-criticism, the reason should

be explained and discussed openly, and not, as in this case, intro-
duced tacitly or covertly. I simply cannot understand how Karlsson
or other Icelandic scholars can defend this procedure. It is pre-
cisely the addition of the medical term “pleuritic” which permits
him to identify the Black Death in Norway as an epidemic of pri-
mary pneumonic plague. He believes that he can assert that pri-
mary pneumonic plague is directly and normally associated with
great pleuritic pain without any reference to the medical literature
on primary pneumonic plague which confirms or supports that
this is the case.
(3) Steffensen and Karlsson do not consider it necessary to base asser-
tions regarding the clinical and medical manifestations of (primary
pneumonic) plague on the primary research literature or the stan-
dard textbooks on plague. Their unflinching confidence in their
assertions that cases of primary pneumonic plague are clinically
characterized by “great pleuritic pain” stand completely unsup-
ported by any reference to the medical literature on primary pneu-
monic plague. As such, these assertions are arbitrary according to
the standard conventions of methodology of historical, social and
medical sciences. If empirical facts count, the medical research lit-
erature on primary pneumonic plague should be consulted. In his
excellent treatise on primary pneumonic plague, the only mono-
graph on this disease, Wu Lien-Teh discusses relevant points in
this connection at some length. He does not state that cases of pri-
mary pneumonic plague are characterized by “great pleuritic pain.”
He points out that there may initially be “no pain in the chest, only
a feeling of constriction when breathing and coughing” and that
“later on, these pains are usually more marked,” but that the pain is
“never so severe as in ordinary pneumonia.”121 Thus, according to
Wu Lien-Teh, some pain, but not great pain, is characteristic of
cases in advanced stages of primary pneumonic plague. However,
importantly, this element of pain is not associated with pleuritic
pain caused by inflammation of the pleura, the membrane of the
thorax and lungs. This description, some pain but not pleuritic
pain, conforms and accords with other relevant comments. He
underlines also that in cases of primary pneumonic plague there is
121
1926: 255, 259.
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a “marked disproportion” between slight lung changes and serious

general signs (of illness) which is “of great diagnostic value.” The
crucial point is that pleurisy is characterized by “inflammation of
the delicate membrane of the thorax and the lungs, causing severe
pain in the chest or sides,” which is not a characteristic clinical fea-
ture of primary pneumonic plague.122 Instead, Wu Lien-Teh associ-
ates the small elements of pain in primary pneumonic plague with
dyspnœa (difficulty of breathing) caused primarily by “the action
of plague endotoxins upon the respiration” and “changed blood
circulation.”123
In the most important general standard work on plague which is co-
authored by Wu Lien-Teh, Chun, Pollitzer and C.Y. Wu, undoubtedly
the most competent group of experts on primary pneumonic plague
ever to come together on the same plague-related project, Chun, who
wrote the part on clinical manifestations, states: “The patient complains
of pain and a restricted feeling in the chest, but this is not severe […]
he appears to suffer little,” and goes on to summarize the point clearly
and unambiguously:
There is not much pain in connection with plague pneumonia in contrast
to ordinary pneumonia, though a few exceptions were observed.124
Chun stresses also, in accordance with Wu Lien-Teh’s description, that
the “physical signs in the lungs are often slight, even in cases well
advanced in the disease,” which, as pointed out, contrasts sharply with
the condition of pleurisy. These statements by Chun must be assumed
to have been accepted as adequate by his co-authors and are compatible
with Wu Lien-Teh’s statements.
This is confirmed by Pollitzer who in his own general standard work
on plague of 1954 explicitly agrees with Chun’s views on these points,
and even cites him quite extensively.125 As shown above, Pollitzer had a
leading role in the combat of the second Manchurian epidemic of pri-
mary pneumonic plague and also performed numerous autopsies. He
also carried out studies of later outbreaks of this disease. The fact that
there are rare victims of pneumonic plague who suffer considerable
pain cannot be assigned significance in this context in connection with
122
Oxford Advanced Learner’s Dictionary of Current English 1989: 950.
123
124
Chun 1936: 318–20.
125
Pollitzer 1954: 441–2.
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the quite generalized accounts of the Icelandic annals. Furthermore,

this pain does not at all accord with the character of the two Icelandic
scholars’ assertion with regard to “great pleuritic pain.” The slight sig-
nificance of pain associated with lungs or the chest in normal cases of
primary pneumonic plague finds also an indirect expression in the fact
that several of the leading standard works on plague do not mention
this subject at all, presumably because it is not a significant clinical fea-
ture.126 Consequently, Steffensen’s addition of the word “pleuritic” and
Karlsson’s defence of this addition are not only flagrant breaches of the
basic principles of source-criticism and scholarly work, but their inter-
pretations that this pain indicates the presence of primary pneumonic
plague are factually wrong according to the corpus of primary studies
on primary pneumonic plague and the summaries given in standard
works.
I do not understand on what grounds Karlsson accuses me of not
recognizing that “stinga” can refer also to strong pleuritic pain caused,
for instance, by pneumonic tuberculosis or pneumonia.127 My point is
that the clinical picture of primary pneumonic plague is not character-
ized by great pleuritic pain or sharp pain in the lungs or chest more
generally, and that the term “hordum stinga” for this reason cannot
refer to primary pneumonic plague and “great pleuritic pain” caused by
this disease. “Stinga” just means “sharp pain,” and can refer to such pain
in any part of the body. It is the same word as the English “sting” and
has in medieval Norse much the same meaning as in modern English.
Sting or “stinga” can be felt any place on the body that is stung by an
insect, for example. Karlsson mentions a source that refers to “stinga”
“under the arm,” which certainly could refer to a plague bubo in the
second most usual site, namely an axilla. However, since the source is
earlier than the arrival of the Black Death in Europe, this cannot be
the case. Instead, this source reflects the elementary fact that infections
of almost any origin can in special circumstances be drained through a
lymph tract to one of the sites of clusters of lymph nodes and can there
give rise to sharply painful or intensely tender swollen lymph-nodes of
the type called bubo or boil. It is the epidemic incidence of swollen
lymph-nodes in the form of buboes that is a defining feature of bubonic
plague.128 Clearly, according to the principles of source-criticism, only
126
See for instance Hirst 1953, Langen and Lichtenstein 1936.
127
Karlsson 1996: 281.
128
Above: 203–05.
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the use of the word “stinga” in sources produced after the arrival of the
Black Death or subsequent plague epidemics can be of value for under-
standing the meaning and connotations of this word associated with
plague disease. Karlsson has found only one instance, which occurs in
a fifteenth-century Icelandic manuscript in a text about the treatment
of plague which refers to “stinga” with “extreme pain and a boil/bubo.”
Karlsson passes easily, even hastily, by it and prefers to emphasize the
significance of the few pre-plague uses of the word.129 However, this is
strong evidence to the effect that extreme pain is associated with the
buboes of bubonic plague and that the word “stinga” at the time was
considered suitable in Iceland for the description of the pain in plague
buboes.
Karlsson is extremely critical of my translation of “hordum stinga”
with an expression using the plural form “pangs” of pain when the
original is in the singular form. He accuses me of making a deliberate
mistranslation in order to construct a false basis for a theory that this
pain could be associated with other parts of the body than the lungs
and, thus, that the clinical descriptions of the Icelandic annals could
reflect bubonic plague.130 I am not a native speaker of English, but a
foreigner who has worked hard to achieve a usable knowledge of aca-
demic English for the purpose of communicating with the interna-
tional community of scholars in the field of the history of disease and
demography. I may not make accurate translations in all contexts which
successfully incorporate the right connotations and nuances whatever
my ambition and endeavours. However, the point for me in using the
plural form was to indicate continuous sharp pain in order to avoid
what I assumed would be the implication in English of using the singu-
lar form, namely that there was one sharp pang of pain which then
disappeared. Notably Cohn, who is an (American) English speaker,
uses the same plural form of the term when describing the type of pain
associated with plague buboes, namely “sharp pangs.”131 However, some
central points still await full clarification. Now for the hard evidence.
Steffensen and Karlsson ignore standard medical works on plague,
although the crucial question of whether or not the descriptions pro-
vided by the Icelandic annals of the clinical manifestations of the Black
Death in Bergen in 1349 is compatible with primary pneumonic plague
129
Karlsson 1996: 282.
130
Ibid.
131
Cohn 2002: 24.
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or bubonic plague and buboes can only be decided according to the

information provided there. It has been shown that the expression
“hordum stinga” cannot relate to pleuritic pain in cases of primary
pneumonic plague, and Steffensen’s and Karlsson’s assertions to this
effect are arbitrary and untenable. However, it remains to be seen
whether or not the standard works on plague which summarize the
great mass of clinical evidence on bubonic plague confirm my opinion
that plague buboes are extremely painful in a way that corresponds
with the clinical descriptions given in the Icelandic annals on the Black
Death in Bergen 1349 and can be responsibly translated by “sharp
pangs of pain” indicating repeated or continuous sharp pain as a nor-
mal clinical manifestation. The following citations are arranged accord-
ing to the chronology of modern scientific standard works on plague
and represent to my knowledge a complete and therefore also a repre-
sentative collection of statements on the matter:
(1) Simpson 1905:
If a bubo appears it is usually ushered in by intense pain in the groin,
arm-pit, or neck which is increased by movement or pressure. The
pain at first is so severe that the attention of the patient is mainly
directed to it, all other symptoms being considered insignificant
compared to the suffering experienced in the gland affected. The
pain is followed by a swelling which constitutes the bubo.
Pain, tenderness and swelling are the general characteristics of the

bubo. The pain may be dull and aching or sharp and stabbing […]
and is independent of the size of the bubo. The smaller the size of
the bubo the more painful is it likely to be […]. Sometimes the ten-
derness is so acute that pressure over the bubo will cause wincing
and moaning from pain even when the patient is in a comatose
condition.132
Simpson describes buboes as generally intensely painful to a
degree that dominates completely the patient’s attention. Obviously,
this is a clinical manifestation which could be observed by ordi-
nary medieval persons. In fact, the pain is so intense that even
light pressure on the bubo will make patients in coma and there-
fore deeply unconscious wince and moan. The pain is character-
ized by being intense, sharp and stabbing and is triggered by
movement or pressure, which, in my opinion, justifies the use of
132
Simpson 1905: 263, 274.
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the word “sharp” and, because it almost inevitably will by triggered

repeatedly, use of the plural form “pangs” of pain is also justified.
(2) Chun 1936:
The glandular mass [of a bubo: my insertion] is very painful and
tender to the touch.
For this reason, in order to avoid pain caused by movement of
the limbs “If the bubo is in the groin, the leg on the affected side
is drawn up, somewhat abducted and twisted outwards; if it is in
the axilla, the affected arm is abducted from the trunk; during
examination it is often supported by the sound arm.”133
According to Chun, plague buboes are “very painful.” His
description of how patients keep arms or legs out from the trunk
of the body in order to avoid pain by movement justifies my trans-
lation in plural, “pangs” of pain, since it means that patients will
experience strong pain every time a limb associated with a bubo is
moved, as will inevitably occasionally occur. The characteristic
position of limbs associated with buboes would easily be noted
also by medieval contemporaries and induce questions as to the
reason.
(3) De Langen and Lichtenstein 1936:
The buboes are usually visible on the second or third day and are
as a rule very painful. If the patient is lying down, we can often see
from a distance whether there is a bubo or not, and where, because
of the typical but unusual position (according to the place of the
bubo) of the arm, head or leg, which is so held as to give the least
pain. […] it is usually most painful as long as it is small and hard and
the expressive movements of the patient during examination betray
his fear that the bubo will be touched […].
The pain of the bubo is greatest during the first days when it is still
small.134
Thus, these two Dutch scholars with their background in the
plague epidemics in Indonesia entirely agree with Simpson and
Chun who draw on research in India and China respectively. Again
the point is made that repeated intense pain of buboes is caused by
movement of associated limb or by touch, which justifies my use
of the plural form “pangs” (of pain).
133
Chun 1936: 316.
134
De Langen and Lichtenstein 1936: 192–3.
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(4) Hirst 1953:

The size of the bubo varies from that of an almond to an orange, and,
until it begins to discharge, may give agonizing pain.135
Thus Hirst, with his enormous experience with cases of bubonic
plague, gives a description of buboes that justifies the description
“pangs of pain” in the plural form, since Hirst clearly has not in
mind the single sharp sting as that of a wasp or gadfly but continu-
ous agonizing pain. De Langen and Lichtenstein and Hirst, who
do not mention pain associated with pneumonic plague, presum-
ably because they considered this clinical feature insignificant,
both emphasize that buboes are continuously very painful or ago-
nizingly painful which they consider a significant clinical point.
(5) Pollitzer 1954:
As is unanimously stated in the literature and has been borne out by
the fairly ample field observations made by the present writer, mani-
festations on the part of the primarily-affected lymph-nodes appear,
as a rule, quite early in the disease, simultaneously with or even
before, the onset of fever […]. Even when seen within the first hours
of illness, as a rule the patients already complain of discomfort or
even of some pain at the site of the future buboes.
The subjective sensations produced in the patients by the presence of
plague buboes may vary considerably, some complaining of constant
dull or even stabbing pains, others feeling little or no local discom-
fort as long as they do not move and keep in a position which lessens
pressure on the affected parts of the body. Patients with a groin bubo
keep for this purpose the corresponding thigh flexed, those with
axillary buboes lie on their back and hold the affected arm away
from the trunk, and those with cervical buboes hold their head still
and inclined to the affected side. Generally speaking, pain is more
marked in the case of smaller buboes than in that of larger ones […]
during the acute stage of the disease the buboes are invariably sensi-
tive to touch, often to such a marked degree that even comatose
patients react when the affected lymph-nodes are touched. This
marked tenderness to touch, which as a rule, appears in the earliest
stage of illness […] forms one of the most outstanding clinical fea-
tures of bubonic plague.136
Pollitzer uses the plural form “stabbing pains,” which puts in per-
spective Karlsson’s offensive accusation. Also Pollitzer describes
135
Hirst 1953: 29.
136
Pollitzer 19954: 421–2.
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buboes as intensely painful, and says that as a result patients keep

limbs associated with buboes out from the trunk of the body in
order to avoid as much as possible pain from movement, and he
also makes the same comment as Simpson to the effect that the
pain is so intense that patients in coma will react when their
lymph-nodes are touched. Again my use of the plural for “pangs
[of pain]” is justified.
(6) Cantey 1974:
Thirteen [Vietnamese] patients were hospitalized with bubonic
plague […] The [lymph] nodes were exquisitely tender to palpation
[…].137
This refers to studies of Vietnamese patients during the Vietnam
War, when the last large-scale epidemics of plague (with as many
as 10,000 deaths a year138) gave American physicians the last
opportunity up to now of studying great numbers of patients.
Butler also has his personal experience from this context.
(7) Butler 1983:
Patients are typically affected by sudden onset of fever, chills, weak-
ness, and headache. Usually, at the same time, after hours, or on the
next day, patients notice the bubo, which is signaled by intense pain
in one anatomic region of lymph nodes, usually the groin, axilla, or
neck. A swelling evolves in this area that is so tender that the patients
typically avoid any motion that would provoke tenderness of the
affected lymph nodes. For example, if the bubo is in a femoral area,
the patients will characteristically flex, abduct, and externally rotate
the hip to relieve pressure on the area and will walk with a limp.
When the bubo is in an axilla, the patients will abduct the shoulder
or hold the arm in a splint. When a bubo is cervical in location,
patients will tilt heir heads to the opposite side. This extreme tender-
ness of the buboes naturally causes patients to resist physicians’
attempts to palpate and aspirate their buboes […]. Palpation will
typically elicit extreme tenderness.139
(8) Butler 1993:
At about the same time [the onset of disease], patients notice the
bubo, which is accompanied by intense pain in the affected lym-
phatic region […]. Palpation typically elicits extreme tenderness.140
137
Cantey 1974: 281.
138
Butler 1993: 887.
139
Butler 1983: 73, 75.
140
Butler 1993: 884, 885.
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This complete collection of evidence taken from all leading standard

works on bubonic plague demonstrate that relevant statements on the
extraordinary painfulness and tenderness of buboes can be readily
found in the scholarly literature on plague. This material has been pub-
lished over a period of eighty years, covering the whole period of scien-
tific studies of plague, and given by authors who have great personal
experience with cases of bubonic plague and great knowledge of the
scholarly plague literature available at the time, has great evidential
force in the matter under discussion. It is highly significant that they
exhibit very similar clinical descriptions of the intense pain associated
with buboes: it is great, agonizing, sharp, stabbing, will occur repeat-
edly with the movement of the associated limb or neck, and is so intense
that even comatose patients wince and moan at the touch of the bubo.
This intense pain is considered to form “one of the most outstanding
clinical features of bubonic plague,” which can be taken to mean a
defining clinical feature of bubonic plague. Only bubonic plague is
characterized by the usual clinical manifestation of buboes which are
also intensely or excruciatingly painful, and characterized by sharp
“stabbing pains.”
In my thesis I also refer to more recent primary studies on bubonic
plague, citing the scholars’ descriptions of buboes as “painful and
exquisitely tender” or characterized by “extreme tenderness.”141 This
presentation of the subject is therefore complete and updated.
Thus, all the prominent authors of the standard works on plague
who also have great personal experience with plague patients empha-
size that plague buboes are characterized by intense, piercing, stabbing
and agonizing pain and that this feature is readily observable and can
readily be clinically characterized as repeated sharp pangs of pain. This
justifies my translation of the element in the Icelandic annals’ clinical
description of the Black Death in Bergen referring to intense pain,
“hordum stinga” as “sharp pangs of pain.” It corroborates also my
understanding of it as referring to the characteristic sharp, stabbing,
agonizing pain of plague buboes and, consequently, that this is a strong
indication that the Black Death in Bergen in 1349 was bubonic
plague.
141
See, for instance, Reed, Palmer, Williams et al. 1970: 479; Welty, Grabman,
Kompare et al. 1985: 641–3; Owens 1990: 155.
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If the Icelandic scholars Steffensen or Karlsson, who reject this

understanding of the Lawman’s Annal’s clinical description of the Black
Death in Bergen (see Appendix 2) had, according to conventional
standards of methodology and scholarly work, consulted any of the
standard works on plague, they would readily have ascertained the
central facts of this topic. Instead, their will to ignore all the medical
standard works on plague constituted the basis of offensive accusa-
tions against my view which is squarely based on the scholarly studies
and standard works of plague.
The authors of the standard works on plague consider the intense
pain of plague buboes to be a predominant clinical feature of bubonic
plague, so conspicuously characteristic that it in itself provides a strong
indication of bubonic plague to observers. It should be easily observa-
ble also to persons without scholarly training and should be expected
to be mentioned by medieval chroniclers when they choose to mention
the Black Death and give some clinical detail, including the inform-
ants of the Icelandic annals. In fact, there is a surprising number of
contemporary descriptions of the extraordinary painfulness of plague
buboes.
It must again be underlined that historical accounts must be seen in
historical and source-critical perspectives. They are normally given by
chroniclers without real scientific education and with rather confused
ideas about disease, generally prone to accept notions of other-worldly
intervention or misleading miasmatic notions and to express their
views with great rhetorical exaggeration. As in the case of the Icelandic
annals, ecclesiastics would often avoid specification of anatomical sites
of buboes with sexual connotations like the groin.142 There are quite
frequent contradictions, misunderstandings and other indications in
the texts of contemporaries, including those who are most often cited,
which show that they have quite likely not observed persons suffering
from or having died from plague. Certainly, there is no indication that
any of them have performed anything like a medical examination of
plague victims. The usual impression is that they render more or less
generalized second-hand or third-hand descriptions or accounts,
rumours or hearsay. This explains why blood spitting is mentioned
probably as often as buboes and that buboes also can be indicated only
indirectly by reference to the intense or excruciating pain associated
142
See for instance Benedictow 2004: 192–4.
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with them (see below). This is the case, for instance, with the Icelandic
annals’ descriptions.
The Franciscan friar Michael of Piazza’s (Michele da Piazza) account
of the Black Death’s arrival and spread in Sicily is one of the most fre-
quently cited, but features calling for source-criticism are generally
overlooked. The central clinical features of the disease as it appeared in
Catania, according to Friar Michael are that
there developed gland boils on the sexual organs, the thighs, the arms, or
on the neck. At first they were of the size of a hazel nut […]. Soon the
boils grew to the size of a walnut, then to that of a hen’s egg or a goose’s
egg, and they were exceedingly painful, and irritated the body, causing
the sufferer to vomit blood […]. The sickness lasted three days, and on
the fourth, at the latest, the patient succumbed.143
As can be readily seen, Friar Michael or rather his informants empha-
size the sharp penetrating pain, the formation of “boils” or “gland boils”
(= buboes) in the ordinary places for plague buboes, the ordinary size
of plague buboes in various phases of development, the “vomiting” of
blood, and the ordinary duration of the course of bubonic plague dis-
ease, that is three to five days.144 These pieces of clinical information,
together with the additional terrified statements of extremely high
mortality, constitute a very strong case for identifying the disease that
spread in Messina and Sicily with bubonic plague.
Sticker cites Gabriel de Mussis’s account of the clinical features of the
Black Death in Piacenza in northern Italy. In accordance with modern
standard works on bubonic plague, de Mussis starts by stating that
completely sound persons suddenly were hit by piercing pains. Next,
they were overwhelmed by great frost that made them shiver with fever
and they felt stinging spikes, as if they were pierced by arrowheads. Some
were cruelly hit under the clavicle [a phrase that probably means “in the
armpits:” my insertion], others where the belly and thigh meet [a euphe-
mism for the groin or nearby femoral area]. Here grew a smaller or larger
lump and, then, soon fulminant fever with head pains […]. Many died
on the first day of illness or on the second, most on the third or fifth day.
The spitting of blood was always deadly […]. Those who had hardened
glands died unless they did not turn soft […].145
143
Cited after Nohl 1961: 7–8.
144
In secondary septicaemic cases, it will take a couple of days before the condition
with bloody expectoration develops; a duration of this phase of three days indicates an
ordinary duration of the whole course of this type of illness of five days.
145
Sticker 1908. 52–3. My translation from German.
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De Mussis’s use of the plural forms “piercing pains, “stinging spikes,”

“pierced by arrowheads” is interesting. De Mussis provides much the
same clinical information as Michael of Piazza regarding the sudden
onset of disease, the piercing pains associated with buboes in the arm-
pits and the groin, fulminant fever, the severe headache, that secondary
pneumonic plague accompanied by blood spitting which was always
deadly, which conforms with modern observations, and information
on the duration of illness that fits the modern standard works on
bubonic plague perfectly.
In his excellent monograph on the Great Plague in London in 1665,
W.G. Bell provides a succinct summary of the clinical features men-
tioned by contemporaries, inter alia: “the rising of plague buboes was
attended by such severe pain, and a feeling as of intolerable burning as
the time for suppuration approached that the sufferers often became
raving mad.” Other usual features were that people became comatose,146
which accords with the descriptions given in modern standard works
on plague cited above.147
This analysis can be completed by citing the impressive proto-
scientific presentation of the plague epidemic in the Swedish city of
Norrköping in 1710–1 given by the local physician M.G. Block who for
his time was well educated and certainly had a clear and observant
mind. Over three pages, he gives a detailed clinical description of
bubonic plague, and towards the end of his book he provides numer-
ous detailed case histories. This comprehensive proto-scientific clinical
information conforms closely to the sections on clinical features given
in modern textbooks on bubonic plague, and it is much more detailed
than that given by late medieval chroniclers or physicians but also pro-
vides information which is similar to that given by late medieval
informants. He mentions the headache, shivering and strong fever, and
a number of other physical manifestations of the disease, but under-
scores that some features are more important than others, among
them:
That it pricks like needles everywhere in the glands and particularly
under the shoulders and in the groin. Swellings in those places, swellings
that eventually, though quite slowly mature into buboes […].148
146
Bell 1951: 127.
147
Bell 1951: 125.
148
Block 1711: 21. My translation from Swedish.
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The plural form should also be noted. Thus, also in connection with the
last wave of epidemics in Scandinavia (only Sweden and Denmark) the
same clinical information is met with again, this time as systematically
and acutely observed by a dedicated proto-scientific physician.
(1) It has been documented that modern studies of plague emphasize

that primary pneumonic plague is normally associated with little
pain and is not characterized by pleurisy or pleuritic pain. This
proves that Steffensen’s understanding of the term “hordum stinga”
as reflecting pleuritic pain associated with primary pneumonic
plague is erroneous and arbitrary. It also proves that his addition
of the word “pleuritic” in his translation of this term, “great pleu-
ritic pain,” is unjustified and misleading.
(2) It has been demonstrated that, according to the corpus of scholarly
studies of plague, bubonic plague is consistently associated with
intensely painful buboes, and that movements of an associated
limb or the neck or touch will cause sharp pangs of pain. This jus-
tifies and vindicates my translation of “hordum stinga” with “great
pangs of pain” and the use of plural form. Plural form is used also
by authors of standard works on plague. This means that it is justi-
fied to associate the Annal’s clinical description of plague cases as
characterized by sharp pangs of pain with the characteristic sharp
pangs of pain of plague buboes and take this as a strong indication
that the Black Death in Bergen was bubonic plague. Karlsson’s
accusations are unfounded.
(3) In addition it has been shown that contemporary chronicle(r)s
emphasize the intense or excruciating painfulness of buboes,
which are characterized by piercing, sharp, stabbing pains, which
justifies my translation of the intense stabbing painfulness associ-
ated with plague cases in Bergen in 1349 in the plural form and its
association with buboes.
(4) It has been shown that the Icelandic annals’ clinical description of
plague cases as associated with “vomiting” of blood conforms to
contemporary and modern medical descriptions of bubonic plague
cases with secondary pneumonia.149
149
See also above: 7–8; below: 491–3.
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(5) No evidence supports the notion that the epidemics in Iceland

1402–4 or 1494–5 spread in the primary pneumonic modality. On
several independent grounds it can be ascertained that these epi-
demics were not caused by plague in any form. There never was a
plague epidemic in Iceland.
The clear outcome of this discussion constitutes an important element
in the process of identifying the epidemic disease that ravaged Bergen
and Norway in 1349. Next, the other clinical elements of diagnostic
value provided by the Icelandic annals must be considered in the light
of modern knowledge of bubonic plague in order to ascertain whether
or not they conform to the clinical manifestations of this epidemic dis-
ease. Clinical descriptive elements of diagnostic value are provided in
the independent contemporary Icelandic fragment of the Annal of
Skálholt.150
The disease was such that men lived for three days with sharp pangs of
pain, then they began to vomit blood and next they expired.151
As can be readily be seen, this clinical description is so closely related
to that given in the Lawman’s Annal that it could come from the same
informant but deviates on one point of importance:
(1) Both annals testify that the sharp (pangs of) pain set in from the
beginning of the outbreak of the disease in humans. As copiously
documented above, this is characteristic of the pain of plague
buboes that starts before or at the beginning of the formation of
buboes. Thus, this feature also supports the case that the onset of
intense sharp or piercing pain reflects the onset of bubonic plague
disease and heralds the development of one or more buboes.
The point can be illustrated with a Norwegian case history associ-
ated with a plague epidemic in the region of Hardanger in 1600.
A young girl who was soon to be married returned one evening
from the cowshed; suddenly she let down her buckets and said:
“Now the plague stung me,” and the next day she was dead.152
150
Islandske Annaler 1888: XVIII–XX; Benediktsson 1970: 390–1: “it is quite inde-
pendent, even though some similarities with other annal redactions occur. It is an
important primary source for the period it covers” [namely 1328–72].
151
Islandske Annaler 1888: 224. Cf. above: 536, fn. 116. My translation from Icelandic
Norse.
152
Benedictow 2002: 238. My translation from Norwegian.
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(2) The duration of the course of illness accords fully with modern
medical descriptions of the development of bubonic plague in vic-
tims who also develop secondary pneumonic plague, which is nor-
mal, occurring in about a quarter of all plague cases. The bubonic
phase lasts three days before the development of secondary pneu-
monia manifests itself with the onset of bloody expectoration, and
then the patient (almost) invariably dies.
(3) Jón Steffensen’s rejection of Shrewsbury’s assertion that “primary
pneumonic plague cannot develop independent epidemics to
any degree” is not supported by documentation from the scholarly
literature on primary pneumonic plague, and must therefore be
considered arbitrary and untenable. Shrewsbury’s view stands
vindicated.
The evidence supports unconditionally and without exception a con-
clusion to the effect that the Black Death in Bergen and Norway more
generally was bubonic plague.
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CHAPTER FOURTEEN
TWIGG’S ALTERNATIVE THEORY
Introduction
Twigg is the central scholar in the brief modern history of alternative

theories of the microbiological identity of historical plague epidemics.
In his monograph of 1984, he was the first scholar to reject any role for
the plague pathogen of Yersinia pestis, whether disseminated by rats
and fleas or by droplets, and who introduces a microbiological alterna-
tive. In order to clear the way for their own alternatives, the subsequent
advocates of alternative theories to a very large extent base their rejec-
tions of any role for Yersinia pestis on Twigg’s arguments. Thus, Twigg’s
arguments for complete rejection of the Yersinia pestis theory of his-
torical plague epidemics must be central in the critical discussion of
the alternative theories in this monograph. Several of his main argu-
ments have been thoroughly discussed above and shown to be unten-
able, namely the arguments relating to the presence and role of rats, the
comparative implications of the mortality rates in the Indian plague
epidemics of the late nineteenth and early twentieth centuries, and his
confusing discussion of metastatic spread of bubonic plague, which at
least implies the denial of the importance of this phenomenon in the
epidemiology of bubonic plague. The time has come to consider his
microbiological theory and his historical line of arguments, the main
arguments which have so far not been the subject of intensive
discussion.
Twigg is the first advocate of an alternative theory of historical plague
epidemics who has chosen not to fulfil one of the central requirements
for scholarly work, namely that of systematically providing footnotes
for all facts and for all data or ideas from the works of other scholars in
the text. This contrasts unfavourably with the three monographs he has
used most for his account of the Black Death, namely F.A. Gasquet’s of
1908, P. Ziegler’s of 1969, and Shrewsbury’s of 1971, which contain 375,
532, 466, footnotes respectively; Shrewsbury’s monograph contains in
all 3290 footnotes for the whole plague history of the British Isles until
1666. All three scholars conscientiously fulfil the scholarly requirement
of systematic and complete testability, the difference in the number of
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554 chapter fourteen
footnotes between these three works reflecting differences in size and

scope and the significant number of relevant studies which had
appeared in the sixty years that divide them, and also Ziegler’s longish
introduction on the Black Death in Europe until the landing in England.
In all, Twigg’s monograph contains just twenty-one footnotes, but he
mainly provides indications of author and work in the running text,
and for each chapter a list of bibliographical references of works pur-
portedly used in writing it, without indication of the relevant pages. In
addition, at the end of the monograph comes a brief curious list called
“Major Works on Plague and Disease,” and an even briefer and more
peculiar list called “Secondary Works Not Mentioned in Text,” which
reflect the fact that he has refrained from providing more than episodic
footnotes or references. Certainly, this is at variance with a basic neces-
sary condition or requirement for producing scholarly work, namely to
assure ready testability. It is not practicable to read the whole length of
a number of the large monographs and papers mentioned in the text or
in the bibliographical list associated with a chapter in order to check or
test the numerous points in his text which occasion disbelief or sur-
prise. When Twigg refers to, for instance, “Wu Lien-Teh et al. (1936),”
this is a standard work of 530 pages; “Sticker (1908)” is over 500 pages;
“Hirst (1953)” comprises 467 pages; “Pollitzer (1954)” contains almost
700 pages, and so on. I have repeatedly given up trying to identify ref-
erences that I consider desirable to check. Twigg mentions, for instance,
that Simpson (1905) states that the “Great Plague of London took six
months to travel from St Giles’ to Stepney,” but since neither St Giles
nor Stepney is mentioned in the Index, even under London, I had to
give up identifying the reference, but luckily eventually found it by
chance while looking for something else.
It is useful to compare Twigg’s assertions with the texts of his refer-
ences for critical examination. Although I have the great advantage of
having over many years endeavoured to read all relevant medical, his-
torical and demographic studies on plague, I must throw in the towel
and admit that Twigg’s monograph is not really testable for me, at least
not within the boundaries of reasonably hard work. Unfortunately, the
same practice has been picked up by Scott and Duncan, his close schol-
arly friends and associates and producers of another alternative theory
of the nature of historical plague which is based on his arguments for
rejecting the bubonic-plague theory (see below).1
1
Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii.
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twigg’s alternative theory 555
The Alternative Theory of Anthrax
Twigg’s theory is that the plague epidemics of the past were caused
by anthrax.2 His alternative theory is a known disease with known
properties that lends itself to scientific discussion and for this pre-
cise reason can be easily rejected, and to my knowledge has been
generally rejected. Twigg’s anthrax theory contains three central
assumptions:
(1) that anthrax can cause sufficient levels of mortality to have explan-
atory potential for the demographic effects of the Black Death;
(2) that the Black Death’s pattern of spread can be correlated with the
spread of epizootics which can be shown with reasonable proba-
bility to be caused by anthrax;
(3) that the clinical descriptions of human plague cases are similar to
human anthrax and not bubonic plague.
Twigg comments on the decisive question of human mortality twice,
both times basing his argument on arbitrary assertions and assump-
tions,3 for instance (my enumeration):
It [anthrax] is, though, [1] probably equally fatal to man [as to cattle and
sheep] and this, coupled with its [2] symptoms and its [3] high mortality
rates, means that [4] it must be a prime contender for the alternative
position [as the cause of plague/Black Death]. Furthermore it needs no
vectors, [5] the spores being the agent of infection and [6] easily carried
in the air or on skins, furs and wool and it is for this reason that anthrax
has been known as “wool sorters disease.”4
As can readily be seen, this crucial passage is completely unsupported
by footnotes or references to demographic and medical evidence or
scholarly literature. It is, of course, true that anthrax is spread by spores,
as stated in point 5; however, it is also true that anthrax is mainly spread
to human beings in the form of anthrax bacteria, especially in the case
of people who have ingested contaminated meat, and it is also true that
this is by far the most common way human beings contract anthrax
(see below). Twigg is attempting here to strengthen his case by making
an implicit case for the importance of cross-infection which is errone-
ous and may be one of the reasons for the absence of supporting
2
Twigg 1983: 211–22.
3
Twigg 1984: 214, 217.
4
Twigg 1984: 217.
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footnotes or references. As stated by Brachman: “Human-to-human or

insect transmission has not been proven.”5
As a basis for discussion of this alternative theory, a brief summary
will be given of recent medical discussions of anthrax in relation to
human beings.6 Anthrax is “primarily a disease of sheep, cattle, horses,
and many other animals; humans are affected only rarely.”7 There are
three forms of anthrax: (1) gastrointestinal tract anthrax, (2) pulmo-
nary or inhalational anthrax, and (3) cutaneous anthrax. Gastroin-
testinal tract anthrax is the only form of anthrax that can take on an
epidemic character, as the other two forms occur only individually or
endemically, that is episodically or incidentally and dispersedly.
Gastrointestinal tract anthrax “usually follows the consumption of
raw or undercooked contaminated meat.”8 Importantly, this epidemic
form of anthrax is quite rare. The main reason for this is that human
beings do not graze: “In animals the portal of entry is the mouth and
intestinal tract by the ingestion of spores on vegetation.” “While ani-
mals often acquire anthrax through ingestion of spores and spread of
organisms from the intestinal tract, this is exceedingly rare in humans.
Thus, abdominal pain, vomiting, and bloody diarrhoea are rare clinical
signs.”9 In other words, whilst animals ingest anthrax spores, human
beings usually ingest anthrax bacteria with meat. For obvious meth-
odological reasons, it is not permitted to infer that mortality rates
among human beings and farm animals from ingestion of anthrax
contagion are the same; it must be formed as a hypothesis that can be
tested and confirmed by corroborative evidence, if possible, which
Twigg does not do.
However, according to Manson’s Tropical Diseases, gastrointestinal
tract anthrax commonly occurs in epidemics when cattle which
have died from anthrax in heavily infected areas are eaten by large
numbers of people. Such epidemics are apparently associated with
parts of Africa. This is explained by the mass consumption of “raw or
5
Brachman 1990: 880.
6
This discussion of anthrax is based on the following works: Jawetz, Melnick,
Adelberg 1982: 207–8; Manson’s Tropical Diseases 1982: 393; Brachman 1980: 83–93;
Sternbach 2003: 463–7; WHO, Media centre, Fact sheet no. 264, October 2001: 1–2.
www.who.int/inf-fs/en; Centers of Disease Control, www.cdc.gov./ncidod, FAQ’s –
Medical Facts About Anthrax 1–2.
7
Jawetz, Melnick, Adelberg 1982: 207.
8
www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1–2.
9
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undercooked contaminated meat,” especially among pastoral nomads

who suddenly are confronted with mass death of their cattle and wish
to use as much as possible of these animals as food before the meat
spoils. Importantly, this book provides data on lethality rates (= case
fatality rates). According to this standard medical work, “The mortality
rate is low and the great majority recover in a few days.”10 This conclu-
sion of low mortality among human beings from gastrointestinal tract
anthrax, the only form of anthrax that can take on an epidemic form, is
incompatible with Twigg’s assertion of population mortality or level of
lethality for past plague epidemics. It can, therefore, serve as evidence
of why he does not support his assertion on this point by evidence
readily obtainable in the scholarly literature.
Both cutaneous and pulmonary anthrax are strongly associated with
individual occupational exposure to contaminated hides or wool, while
the pulmonary form is often called “woolsorter’s disease,” as also men-
tioned by Twigg (see above). However, pulmonary anthrax, which is
caused by inhalation of contagion into the lungs, occurs only rarely,11
which contrasts sharply with Twigg’s undocumented assertion above of
easy dissemination by cross-infection and considerable numbers of
cases. Pulmonary anthrax is characterized by high mortality, however,
high mortality among a tiny incidence of cases among woolsorters
entails negligible population mortality.
The cutaneous form of anthrax, caused by the entry of contagion
through a cut or an abrasion in the skin (cutis), accounts for 95 per cent
or more of human cases globally. When Twigg argues that (the English)
Galfrid le Baker’s mention of a highly mortal form of plague “charac-
terized by small black pustules on the skin” refers to cutaneous anthrax,
he implies arbitrarily that it was usual or normal at the time that per-
sons had numerous abrasions and cuts which were contaminated
by anthrax contagion. Why does he not consider the possibility that
this description refers to bubonic-plague pustules, a feature also men-
tioned by the often cited Irish chronicler John Clyn? This is a clinical
feature that will be discussed comprehensively below.12 Twigg again
ignores the question of mortality, however, this is not unknown:
the lethality (case fatality) rate of untreated cases of cutaneous anthrax
10
Manson’s Tropical Diseases 1982: 393.
11
12
On plague pustules, see above: 364, 368–78.
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is about 20 per cent.13 In contrast, the lethality rate of bubonic plague is

80 per cent.14
Importantly: “There are no documented cases of person to person
transmission”15 of anthrax. Anthrax has only one genuinely epidemic
form, namely gastrointestinal tract anthrax.
Thus there are several independent sufficient conditions for reject-
ing the anthrax theory on epidemiological and medical grounds alone.
To my knowledge, historical sources do not provide believable descrip-
tions of any epidemic of gastrointestinal tract anthrax among human
beings, which is the only form that possibly could take on an epidemic
character. This corresponds to the concluding statement on mecha-
nisms of spread in the standard work on microbiology by Jawetz,
Melnick and Adelberg: “Contact with infected animals or with their
hides, hair, and bristles is the source of infection in humans.” Thus, in
an historical perspective, sources of incidence of the disease would
only include tanners’ risk of contracting this disease from work with
hides and possibly the risk to people from wearing clothing made from
contaminated hides, which will occasion episodic cases of cutaneous
antrax, and the sporadic individual incidence of “woolsorters’ disease”
in export centres of wool like London, or in the proto-industrial cen-
tres of wool cloth production like Florence, Ghent, and so on. Taking
into account the lethality rate of 20 per cent associated with untreated
cases of cutaneous anthrax, one seems justified in losing interest in
mortality rates in possible historical cases of anthrax among human
beings in the present context. The enormous mortality caused by the
Black Death and the dramatic population decline it caused are incom-
patible with the incidence and mortality of human anthrax.
One of the most conspicuous features of Twigg’s monograph is his
efforts to play down the level of mortality caused by the Black Death
(see below) and to play up the level of mortality causable by anthrax.
He does not discuss in a serious way the relative rarity of this disease
among human beings and the fact that the vast majority of anthrax
cases have the cutaneous form with a relatively moderate lethality level.
He makes no attempt to adduce an evidential platform that would allow
13
www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1.
14
I believe all useful data on lethality rates in historical bubonic plague epidemics
still can be found in Benedictow 1993/1996: 146–9.
15
WHO, Media centre, Fact sheet no. 264, October 2001: 1. www.who.int/inf-fs/
en,fact.
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him to argue that the rare type of epidemic gastrointestinal anthrax

ever caused large human population mortality rates at a regional or
national level in medieval Europe and continued to ravage Europe for
300 years.
Instead, Twigg makes the following three misleading assertions
which will be commented on in the order 2, 3, 1:
[1] the introduction of antibiotics has reduced the death rate from
cutaneous anthrax to a very low level but [2] visceral anthrax is little
affected by antibiotic treatment and [3] the death rate may be as high as
90 per cent.16
(2) Twigg’s assertion that the mortality rate of “visceral anthrax,” a curi-
ously expanded term that presumably corresponds closely to the con-
cept of gastrointestinal tract anthrax, “may be as high as 90 per cent” is
not supported by reference(s) to scholarly work(s) in the text or an
accompanying footnote, it must be rejected as arbitrary. His assertion
on this important point is incompatible with the level of normal
lethality given in Manson’s Tropical Diseases (cited above), namely that
the “mortality rate is low and the great majority recover in a few days.”
(3) According to standard works on microbiology, antibiotics are
effective against gastrointestinal tract anthrax,17 thus Twigg’s undocu-
mented assertion to the contrary is disappointing.
(1) When Twigg states that antibiotics have today reduced the lethali-
ty (case fatality) rate of cutaneous anthrax to a very low level without
informing his readers about the normal mortality rate of untreated and
unmedicated cases, he leaves his readers with the impression of a very
high normal lethality rate in cases of cutaneous anthrax in the past.
However, although a lethality rate of about 20 per cent in untreated cases
of cutaneous anthrax is moderately high, it compares unimpressively
with bubonic plague’s normal lethality rate of around 80 per cent.18
Certainly much can be said about contemporary chroniclers’ clinical
descriptions of the Black Death, but they never mention as symptoms
of the disease the “abdominal pain, vomiting, and bloody diarrhoea”
that characterize gastrointestinal tract anthrax.
Thus, Twigg’s anthrax theory has no significant historical founda-
tion. It is medically and epidemiologically untenable and cannot
16
Twigg 1984: 214.
17
18
Benedictow 1993/1996: 146–9.
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explain the mortality rates caused by the Black Death—something that

Shrewsbury’s theory also fails to do.
The Historical Basis: The Use of Obsolete and Peripheral Studies
A curious feature of Twigg’s monograph is his predilection for obsolete

works based on miasmatic and astrological theories of epidemic dis-
ease. This is particularly the case in the final and crucial Chapter 11
where he summarizes his evidence and argues the case for his anthrax
theory: “Clinical symptoms in the Black Death and in some other dis-
eases. The case for anthrax” (pages 200–22). In this chapter, J.F.K.
Hecker’s (1795–1850) monograph on The Epidemics of the Middle Ages
which was first translated into English in 1837 and reprinted in 1844
and posthumously in 1859, is referred to eleven times (and repeatedly
elsewhere).19 Hecker is also referred to indirectly through Twigg’s use
of Gasquet’s references to Hecker’s work, for example on the clinical
features of the Black Death.20 Hecker is even cited on an important
point of the Black Death’s epidemiology in England, although Creighton
has made it clear that Hecker’s superficial and deficient knowledge on
the Black Death in England is taken from J. Barnes’s monograph the
History of Edward III of 1688.21 Creighton refers disparagingly also to
Hecker’s “a priori habit of mind” for making assertions of fact without
support from sources.22 It would be surprising if Twigg has not noticed
these relevant comments, since the main work of Creighton, the last
champion in England of the miasmatic theory of epidemic causation,
predictably is frequently cited in support of his argument, for example
three times in Chapter 11.
The skilful ecclesiastic amateur historian F.A. Gasquet (Abbot
President of the English Benedictines) and his pioneering work on the
Black Death in England is referred to ten times in Chapter 11. This
work was originally prepared in the 1880s23 and first published in 1893;
the edition of 1908 used here by me and by Twigg is a reprint “with one
19
Twigg 1984: 204–7, 211. See also pages 46–7, 60–1.
20
Twigg 1984: 202–3. See Gasquet 1908: 8–9.
21
Creighton 1891: 144, fn. 1. Here Creighton refers to the English translation of
1837 of Hecker’s work on the Black Death of 1832, but Hecker had not improved his
knowledge of the Black Death in England between 1832 and 1837.
22
Creighton 1891: 144, fn. 1, 200.
23
Gasquet 1908: xxi.
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or two minor corrections, and a few additions.” The text of Gasquet’s

monograph represents pre-scientific miasmatic notions of the cause of
epidemic disease, and all medical and historical works he refers to rep-
resent this miasmatic view and pre-scientific epidemiology and medi-
cine more generally.
In addition R. Mead’s view on the clinical symptoms of plague pub-
lished in 1720 is taken seriously by Twigg;24 although Mead was born in
1673, he had never seen a case of plague in his life. This does not end
the list of miasmatic and obsolete works Twigg refers to in chapter 11,
which include W. Wood’s monograph of 1842/1865, H. Harrod’s paper
of 1867, and so on.
Within this framework which mainly is of interest and relevance for
the history of medicine, a number of contemporary chroniclers are
cited and referred to on the clinical features of the Black Death without
any attempt at explaining their social, cultural or medical framework.
Source-criticism is not mentioned or applied. Without the source-
critical training of medieval historians, Twigg inevitably becomes a
victim of what Hatcher calls “the overwrought imaginings and hope-
lessly inaccurate quantification of the chroniclers.”25 There will be occa-
sion below to address this point more specifically. Twigg, who apparently
neither likes source-criticism nor medieval demography, inevitably
subjects himself to this process of scholarly victimization at the hands
of medieval chroniclers whose assorted utterances of “overwrought
imaginings and hopelessly inaccurate quantification” are, thus, passed
on and given a new lease of life long after most of them should have
been laid gracefully to rest.
In his discussion of the last plague epidemic in the village of Eyam
in Derbyshire in 1665–6, Twigg relies on W. Wood’s monograph first
published in 1842 and also for one point of importance on the ninth
reprint of 1744 of Mead’s monograph.26 L. Bradley’s fine modern family-
reconstitution-based demographic study of 1977 on the epidemic at
Eyam27 is mentioned only indirectly in a comment to the effect that
24
Twigg 1984: 214–5. Another of Twigg’s pervasive inaccuracies crops up here: the
title of the work cited in the references on page 245 under Mead’s name was not written
by him but rather by Joseph Browne (whose book was also published 1720). Browne,
like Mead, had never seen a plague case in his life, so the comments are irrelevant in
both cases.
25
Hatcher 1977: 21.
26
Twigg 1984: 192–5.
27
Bradley 1977a: 63–94.
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Bradley disagrees with Wood’s analysis, without indicating why, which

might have revealed very good reasons. However, it shows that Twigg
knows Bradley’s fine demographic study, but like Cohn and Scott and
Duncan, does not take its findings into account. Shrewsbury’s useful
1971 demographic discussion of the same material28 is passed by in
silence. Bradley and Shrewsbury agree on the basis of modern medical,
epidemiological and demographic analysis that the epidemic at Eyam
was indeed bubonic plague.29
Twigg’s monograph abounds in such examples. His prolific use of
obsolete pre-scientific studies is obviously contrary to central tenets of
scholarly work and unavoidably raises the question: why does Twigg to
such an extent build his case on long obsolete studies, scholarly antiques
based on miasmatic epidemiological theory with characteristic astro-
logical and telluric aspects? The reason can hardly be any other than
because he needs them, because in the end Twigg has to resort to mias-
matic theory himself, albeit in a slightly modernized version, in the
futile hope that it can save the last vestiges of credibility of his theory.
In his final chapter, it becomes obvious that a theory to the effect that
the European populations should have been eating the Black Death
both on the Continent and in England or that herds of sheep and cattle
should have been transported by galleys from Constantinople to
Mediterranean ports and been driven across the Continent whilst peo-
ple eagerly devoured the flesh of obviously sick, moribund or dead ani-
mals was simply untenable and impossible to take seriously.
The Telluric-Miasmatic Theory of Anthrax
Eventually, it becomes clear to Twigg that there had to be another

very dynamic mechanism of the spread of anthrax. At this point,
central aspects of the miasmatic theory of epidemiology seemingly
offered him a solution. He takes as his point of departure experimen-
tal studies on the possible airborne passage of the foot-and-mouth
virus under some specific meteorological conditions relating to or
inspired by an outbreak of foot-and-mouth disease in livestock in
1967–8. This mechanism of spread is not mentioned in later standard
works on medical microbiology, for instance, by Jawetz, Melnick and
28
29
Bradley 1977a and 1977b.
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Adelberg.30 Airborne contagion connected with specific meteorologi-

cal conditions accords completely with classical Greek miasmatic the-
ory of the causation of epidemic disease and miasmatic epidemiology’s
central tenets on the dissemination of epidemic disease.
Against this background, Twigg argues that the
extraordinarily rapid dissemination of the Black Death suggests pulmo-
nary anthrax moving in a similar way […] this form of the disease could
very likely have been the illness which has hitherto been identified with
pneumonic plague.31
These few words contain a number of fallacies of methodology and
neglect of facts. Firstly, Twigg uses a hypothetical mechanism of aerial
spread of foot-and-mouth disease to suggest by analogy that this could
also be the case with pulmonary anthrax, which he arbitrarily com-
pares with pneumonic plague, and goes on to build on these analogies
as if they were materially established by empirical evidence. According
to modern scientific methodology, analogies can only be used for con-
struction of working hypotheses, all use of analogies for inference to
fact or reality is fallacious. It is true that classical Greek scholars and
physicians used analogies for evidentiary purposes in this way, in
accordance with their incompletely developed scientific methodology,
but that was over two thousand years ago. According to the tenets of
modern scientific methodology, Twigg must first adduce good evi-
dence showing that pulmonary anthrax can spread by air in epidemic
form according to the pattern of the viral foot-and-mouth-disease and
the bacterial primary pneumonic-plague disease. If he were able to do
this, he would also be obliged to document that pulmonary anthrax
can spread with extraordinary rapidity, faster than any other epidemic
disease which is dependent on interhuman transmission, before he
could single it out as a possible candidate for the epidemic disease in
question. However, Twigg does not attempt to satisfy these premises or
basic conditions, and his inference from rapidity of spread to pulmo-
nary plague is, therefore, a circular type of argument based on a purely
hypothetical analogy. Indeed, earlier in his monograph, in accordance
with the modern scientific literature on anthrax, Twigg restricted pul-
monary anthrax to the episodic and largely individual occurrence
among woolsorters, which has no epidemic form. There is no spread
30
Jawetz, Melnick and Adelberg 1982: 395–6.
31
Twigg 1984: 220–1.
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rate characteristic of the Black Death that can “suggest” that it was (pri-
mary) pneumonic plague; this conclusion is literally taken out of thin
air. For the same methodological reason, an analogy cannot be used to
“suggest” a factual condition, since use of the term “suggest” indicates
a level of tenability, albeit low. Conspicuously, Twigg transforms the
level of tenability associated with the concept of “suggest” into the level
of tenability of “very likely” without the mediation of evidence.
Scholarly work is associated with the principle of fallibility, which dic-
tates that on principle no scholarly statement can be absolutely true.
There is always, as a matter of principle, at least a tiny element of doubt
or uncertainty associated with scholarly or scientific statements. The
level of tenability of “very likely” is therefore about as certain as a schol-
arly statement can be and is correspondingly demanding with respect
to its evidential basis, presupposing a solid empirical material. In this
case, Twigg has not adduced any evidence, so not only is the asserted
level of tenability of “very likely” untenable, it is also methodologically
invalid and can be characterized as fallacious. Twigg goes on to use
term “speculate” to describe his reasoning, which in scientific meth-
odological parlance means not based on facts, only on logical infer-
ence. Twigg apparently does not know that analogies, like definitions
and concepts, cannot be used for evidential purposes or for inference
to fact or reality, and consequently cannot be associated with tenability,
but can only be discussed in methodological terms of usefulness as
intellectual tools for analysis. He treats levels of tenability along the
whole register from the very lowest level of speculation, via suggestion
up to almost the highest level of very likely as if they are interchangea-
ble and independent of evidence. Also this part of Twigg’s work is
methodologically confused and comprehensively at variance with the
basic tenets of (social) science.
To my knowledge, Twigg is the only modern scholar who has
been inspired by miasmatic epidemiological theory to a degree that
he also cites telluric aspects of this theory, that is, the idea that mias-
matic contagion is let out from the ground after it has been disturbed
by volcanic activities, earthquakes or astrological constellations, to be
spread by the wind and cause epidemics when it reaches human
settlements:32
32
See Hirst’s excellent presentation of these aspects of miasmatic theory in Hirst
1953: 22–72.
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It is tempting to speculate yet further and to suggest that the sequence of

earthquakes and floods in the East before the Black Death might have
disturbed anthrax in the soil and the spores were then carried by air cur-
rents to the Mediterranean and Europe.33
Telluric-miasmatic explanations for outbreaks of serious epidemic dis-
ease are a clear feature of Hecker’s epidemiological thinking in his
works of the 1830’s,34 which Twigg refers to eighteen times,35 and of
Gasquet’s monograph, which he refers to twenty-three times.36 Seen
against the background of Twigg’s prolific use of these works and other
miasmatic works (see above) in support of his anthrax theory, it can be
legitimately assumed that this is his source of inspiration. By accepting
long-discarded explanations of a serious epidemic outbreak, in this
case the principle of telluric explanation of the origin of airborne
miasma for the Black Death, Twigg has crossed a crucial line between
scientific and unscientific work.
He goes on to state that:
Anthrax is widely known in African mammals, however, and air currents
bearing spores of anthrax could easily reach northern Europe, as shown
by the deposition of Saharan dust in England in recent years.37
Again Twigg uses an analogy, in this case based on the relatively rare
instances of air transport of Saharan sand to England, which does
occur, to assert that this easily could be the case for anthrax spores, an
assertion for which he offers no evidence. How can he know that air-
borne anthrax spores from Africa “could easily reach northern Europe”
when he is unable to provide any evidence for the factual occurrence of
such transport at all? In ordinary scholarly or scientific discourse, the
phrase “could easily reach northern Europe” should imply substantial
empirical evidence for this phenomenon, quite a lot actually, in order
to be able to differentiate between the rare occurrence, the sporadic
occurrence and the quite regular occurrence that alone can prove that
this could easily be the case. Instead, the fact is that he has no evidence
to show in support of his assertion: it is based on the implication, the
methodological fallacy, that an analogy can provide or constitute
empirical evidence allowing inference to fact or reality.
33
Twigg 1984: 221.
34
Hirst 1953: 41.
35
Twigg 1984: 46–7, 60–1, 204–7, 211.
36
Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207.
37
Twigg 1984: 221.
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The analogy is false for several reasons:

(1) the assertion that sand and anthrax spores have much the same
properties in relation to airborne transport requires evidentiary
support, without which it is an arbitrary assertion.
(2) the assertion that Saharan animals could be the source of anthrax
spores that could be transported by wind to northern Europe in
the same way as Saharan sand requires evidentiary support. When
it is maintained without evidence that this can, in fact, occur, also
this assertion takes on the character of an arbitrary argument.
(3) anthrax epizootics among cattle are not uncommon in parts of
Africa (see above), and it is well known that Sahara is full of sand,
but cattle are not common in the sand oceans of the Sahara, and
large, numerous herds of contaminated cattle are required to cre-
ate significant amounts of spores. It is the parts of Africa south of
the Sahara that are inhabited by more or less nomadic pastoral
people with large herds moving through large areas which are at
the heart of the matter, and it is the question of whether or not air
currents could transport anthrax spores from these areas which is
the real problem Twigg should have addressed with energy and
dedication. The conclusion he would have reached can be stated:
that there is no historical evidence that air currents with spores
from these areas have reached the northerly parts of Europe.
Twigg resorts to unscientific miasmatic-telluric theory in order to
defend his theory. This can only be taken to reflect the obvious unten-
ability of his theory and the length to which he is willing to go in order
to construct a basis for it.
The Pace of Spread of Plague
There is another reason for Twigg’s attraction to miasmatic theory. This

is the distant thunder of the works of modern scientific plague resear-
chers with excellent medical education from Cambridge and Oxford in
England as well as leading universities in France and the U.S.A. who
made such tremendous progress in the scientific study of bubonic
plague in India, China, Madagascar, Vietnam, and elsewhere in the
twentieth century. Many of them put great emphasis on the history of
plague and comparison between the old clinical and epidemiological
descriptions and accounts of plague and their modern observations of
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thousands of plague patients and plague’s epidemiology. On this basis

and without exception they reached the conclusion that the disease
they studied and the historical plague epidemics were the same. If
Twigg had wished in earnest to learn from modern scientific discus-
sions of this topic, he could have studied the works of Simpson of 1905,
Sticker of 1908 and 1910, Wu Lien-Teh of 1926, Wu Lien-Teh, J.W.H.
Chun, R. Pollitzer, C.Y. Wu of 1936, Hirst of 1953, Pollitzer of 1954, and
papers by other leading plague researchers like Greenwood and Liston
of the IPRC, just to name the most important in this context.
Twigg mentions most of them in his text, but not on central points
of epidemiology or clinical features, only on points that do not bear
seriously on his theory. As shown above, his assertions on the mecha-
nisms and patterns of spread of bubonic plague are untenable and are
based on highly selective references and peculiar interpretations.
Simpson’s monograph, the first but necessarily “immature” modern
scientific work to emerge from the studies of British physicians and
epidemiologists in India, is, for instance, referred to twice. Twigg cor-
rectly points out Simpson’s view that the Black Death, in relation to
earlier plague epidemics, “was distinguished by its rapid spread and
destructiveness,” “Never before had it shown such diffusive qualities.”38
Twigg takes this in support of (1) his view that the Black Death could
not have been bubonic plague and (2) compares it with a purported
slow pace of spread in India and cites again Simpson who points out
that (3) the “Great Plague of London [of 1665] took six months to travel
from St Giles’ to Stepney.”39 What Twigg describes here is, of course,
contiguous spread of plague by contact between rat colonies, and the
example from London 1665 is similar to the observation of IPRC that
“the infection in the rats took six weeks to travel 300 feet” in a section
of Sion village outside Mumbai.40 This means, of course, that the plague
in London 1665 and in India of the early 1900s had a very important
feature in common, namely that they could spread very slowly in a
contiguous way. However, given this comparison I do not understand
why a structural similarity of pace of spread of bubonic plague in India
38
Simpson 1905: 23.
39
Twigg 1984: 135. He does not identify where in Simpson’s work he has found this
instance; see, however, Simpson 1905: 70. Similarly, plague took over five weeks to
move from Westminster to the city parish of St Olave, Hart Street. Cox 1910: 153.
40
IPRC 1907h: 827, cf, Map IV; Lamb 1908: 19.
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and the Great Plague of London does not constitute evidence that the
Great Plague in London was the same disease as in India, namely
bubonic plague. Twigg overlooks the fact that if his point was correct,
there would not have been any Great Plague in London; only a few
small patches of the great city would have been ravaged.
Since Twigg has used Simpson’s monograph, another important
question remains unanswered: why Twigg ignores Simpson’s informa-
tion on the great importance of metastatic spread by leaps,41 for instance,
that “in Canton, many persons, especially the well-to-do, removed to
the country, thus forming fresh foci for its dissemination; and in the
same way the outbreak in Hongkong no doubt arose from persons hav-
ing migrated from Canton to Hongkong.”42 In China as well “the infec-
tion on land has followed chiefly the routes of busiest intercourse.”43
Simpson also provides much information on spread by leaps in India,
for instance, in connection with the mass exodus out of Mumbai when
the plague epidemic suddenly blazed up: “Fugitives from Bombay and
the Bombay Presidency were not long in carrying infection to the other
provinces of India.”44
Twigg also passes by in silence the conspicuous phenomenon of
metastatic leaps in the Great Plague of London, as can bee seen from
Bell’s fine study of it, for instance: the spread of the disease by leaps in
the city and in the outparishes and liberties, establishing numerous
new centres of spread in the rat colonies more or less according to a
geometrical progression of incidence. Bell has no difficulty in showing
that the epidemiological and clinical features of this epidemic in
London correspond very closely to those of bubonic plague.45 Twigg’s
obligation to ignore the typical metastatic patterns of spread of bubonic
plague in clothing or luggage or goods that lent the Black Death and
subsequent plague epidemics dynamic powers of spread and was also
such a conspicuous feature of bubonic plague in India, reflects the fun-
damental weakness of his theory.
It is important to recognize that the diffusive powers of the Black
Death were so strong in Europe in the middle of the fourteenth century
because it arrived in a territorially interconnected and integrated
41
Above: 153.
42
Simpson 1905: 62.
43
Simpson 1905: 65.
44
Simpson 1905: 71.
45
See Bell 1951.
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civilization which offered epidemic disease in general entirely new

powers of spread. My brief introduction to this aspect of medieval soci-
ety in a journal of popular history runs like this:
The extent of the contagious power of the Black Death has been almost
mystifying. The central explanation lies within characteristic features of
medieval society in a dynamic phase of modernization heralding the
transformation from a medieval to Early Modern European society. Early
industrial, market-economic and capitalistic developments had advanced
more than is often assumed, especially in northern Italy and Flanders.
New, larger types of ships carried great quantities of goods over extensive
trade networks that linked Venice and Genoa with Constantinople and
the Crimea, Alexandria and Tunis, London and Bruges. In London and
Bruges the Italian trading system was linked to the busy shipping lines of
the German Hanseatic League in the Nordic countries and the Baltic
area, with large broad-bellied ships called cogs. This system for long-dis-
tance trade was supplemented by a web of lively short and medium-
distance trade that bound together populations all over the Old World.
The strong increase in population in Europe in the High Middle Ages
(1050–1300) meant that the prevailing agricultural technology was inad-
equate for further expansion. To accommodate the growth, forests were
cleared and mountain villages settled wherever it was possible for people
to eke out a living. People had to opt for a more one-sided husbandry,
particularly in animals, to create a surplus that could be traded for staples
such as salt and iron, grain or flour. These settlements operated within a
busy trading network running from coasts to mountain villages. And
with tradesmen and goods, contagious diseases reached even the most
remote and isolated hamlets.
In this early phase of modernization, Europe was also on the way to
“the golden age of bacteria” when there was a great increase in epidemic
diseases caused by strong increase in population density and in trade and
transport while knowledge of the nature of epidemics, and therefore
countermeasures to them, was still minimal.46
The point is that epidemiology is a subdiscipline of sociology in that it
focuses on the study of the effects of social interaction, and that the
powers of spread of epidemic diseases vary greatly with different types
of social formations and must be seen within a societal framework of
analysis. The powers of spread of the Black Death in the form of bubonic
plague were much stronger than before because it reached a European
society that offered new mechanisms and much stronger opportunities
for dynamic spread, as was the case also for other microbiological
46
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pathogenic agents.47 While Simpson can be excused for not placing his
correct observation in this historical societal perspective, since the
development of medieval economic history was only in its infancy at
the time, there is no such excuse for Twigg.
Twigg again produces a fallacy of methodology by not comparing
like with like, but comparing things that are not in pari materia to infer
from dissimilarity of (epidemiological) manifestations to dissimilarity
of (microbiological) causation. He compares plague’s pattern of spread
in the form of the Black Death in a helpless medieval Europe around
1350 with plague developments around 1900 in the Indian subconti-
nent governed by British colonial authorities “armed” with European
historical experience, modern organizational abilities and modern
medical science, albeit in an early stage of development. As shown also
above, Twigg ignores, among other things, the fact that the British
colonial administration in haste built the largest anti-epidemic organi-
sation the world has ever seen on the basis of a long and largely suc-
cessful tradition of epidemic countermeasures that had successfully
defeated bubonic plague in Europe as early as in the seventeenth cen-
tury and also on the basis of the new bacteriological understanding of
disease and increasingly on a real understanding of the mechanisms of
dissemination of plague.48 Given that European authorities succeeded
in stamping out plague at the middle of the seventeenth century, it is a
strange notion that they, with a gigantic well-organized anti-epidemic
effort based on superior medical and epidemiological knowledge at
their disposal, should not have succeeded in keeping spread and mor-
tality of bubonic plague to a minimum around 1900 and in the early
twentieth century.
The second time Twigg refers to Simpson’s work concerns a minor
point regarding which animals may contract plague.49 As can now be
readily seen, Twigg avoids discussing Simpson’s quite large historical
section where historical plague is compared with bubonic plague in
India and identity is concluded.
Sticker’s work on historical plague and modern scientific counter-
measures is treated in the same manner: these two volumes are referred
to only once, for a peripheral speculative assertion of the mortality rate
47
Cf. Benedictow 2004: 387–9.
48
49
Twigg 1984: 212.
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in the plague epidemic in Cairo 1574.50 Chun, who has written very
usefully on the presentation of the clinical features of bubonic plague,
is also mentioned once, in relation to the average duration of the course
of illness in cases of primary pneumonic plague.51 Twigg refers to
Pollitzer’s monograph in connection with questions relating to the his-
torical origin of the Black Death and the understanding of the head-
stones in the Nestorian graveyard at Issyk-Kul.52 Hirst is mentioned in
connection with a discussion of the history of the black rat in England,53
but his broad historical discussion of epidemiological and clinical fea-
tures characteristic of bubonic plague, which represents a fatal threat to
Twigg’s theory, remains unused.
These are representative examples of how restrictively and selectively
Twigg discusses the modern standard works on plague in contrast to
his predilection for obsolete miasmatic works and his problematic rela-
tionship with methodology.
Anthrax and the Name Black Death
Twigg maintains that in order to determine the microbiological nature

of the Black Death a “good starting point is the name Black Death.”54
The intention is to link the term Black Death with anthrax, a Greek
word that means coal and conveys connotations of black, because this
would signify that the use of the word black had a concrete clinical
descriptive purpose associated with anthrax.55 This is unacceptable for
several reasons. Firstly, Gasquet, to whom he first turns,56 makes it
entirely clear that the name Black Death is not contemporary with this
epidemic or subsequent plague epidemics but appears sometime after
the last outbreak of plague in Britain.57 Secondly, the characteristic
black associated with the name anthrax refers to the anthrax pustules
of cutaneous anthrax which usually develop a black colouring.58 It has
50
Twigg 1984: 46–7. See Sticker 1908: 106. Sticker is the only of these scholars who
contracted plague in India and, fortunately, survived.
51
Twigg 1984: 20.
52
Twigg 1984: 39. 45. Cf. Benedictow 12004: 48–9.
53
Twigg 1984: 77–8, 81–2, 85.
54
Twigg 1084: 202–13.
55
Twigg 1984: 213.
56
Twigg 1984: 202–3.
57
Gasquet 1908: 7–8.
58
See Manson’s Tropical Diseases 1982: 393 with picture.
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nothing to do with the only epidemic form of anthrax, namely gas-

trointestinal tract anthrax, on which Twigg’s theory in reality relies or
with the only form with high lethality rates, namely the rare pulmonary
or inhalational anthrax, although Twigg refrains from mentioning it.
Cutaneous anthrax is, as mentioned earlier, ordinarily an occupational
disease of tanners and other craftsmen or labourers working with hides
and has a lethality rate of about 20 per cent (in unmedicated cases).
This form of anthrax disease, which is the only one that is associated
with black pustules, can at most cause population mortality of some
tiny fraction of 1 per cent. It does not have explanatory potential for the
mortality rates caused by the Black Death of 1346–53.
Thirdly, by focusing on Gasquet’s obsolete account, Twigg can neglect
S. D’Irsay’s paper of 1926 on “The Origin of the Expression: Atra Mors”
in which he convincingly shows that the term “Black Death” is a mis-
translation of the term “atra mors” where atra can mean both “terrible”
and “black,” thus, the “terrible death” by mistranslation was changed
into the even more graphic term the “Black Death.” This explanation
appears otherwise to be generally accepted and to have been so for
quite a long time. D’Irsay argues also convincingly that this mistransla-
tion originated in Scandinavia, where it was first registered in Sweden
in 1555 and about fifty years later in Denmark. It may seem that this
was a mistranslation that was quite likely to occur, especially for per-
sons without a good Latin education, and it may have occurred repeat-
edly and independently before the sinister and frightening connotations
caught the imagination. This happened much later: according to Hirst
and Shrewsbury, the term the “Black Death” is used in history-oriented
literature59 in England for the first time in 1823, and was, according to
Shrewsbury, for the first time introduced in English medical literature
in 1837 with the translation of Hecker’s monograph The Black Death in
the Fifteenth Century.60 Clearly, the term the “Black Death” was intro-
duced into English by persons and adopted by a population who had
never seen a case of plague or its clinical manifestations. In normal
scholarly discourse, this would be taken as decisive proof that plague
does not have a clinical feature characterized by the colour black and
that the origin of the adjective “black” must have a non-clinical origin.
Twigg knows well and refers repeatedly to Ziegler’s monograph where
59
Hirst 1953: 32.
60
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this mistranslation of atra mors is underlined as “the most likely expla-

nation,” its Scandinavian origin is mentioned, and where all alternative
explanations of the term the “Black Death” are rejected because they
are later than the plague period.61 Twigg refers to D’Irsay’s paper in
the bibliographical list at the end of this Chapter 11,62 but ignores it in
the text. Twigg’s attempt to link the (misnomer) “Black Death” with the
black colour of (cutaneous) anthrax pustules is unsuccessful and
misguided.63
Surprisingly, in support of his view on this point Twigg cites the
French veterinarian E. Leclainche’s work on veterinary medicine of
1936: “In the terrible epidemic of smallpox of 1345–50 (la mort noire,
der Schwarze Tod), the horses, the sheep and the goats died in thou-
sands.”64 Thus, highly unusually, Leclainche asserts that the Black Death
was an epidemic of smallpox that also caused high mortality among
domestic animals. However, according to modern standard works on
microbiology, “variola [= smallpox] infects only humans and mon-
keys,”65 consequently, the concomitant epizootic must have been
another disease. One could have expected that this rather far-fetched
and microbiologically untenable view which also runs contrary to
Twigg’s anthrax-theory, would have induced him to take a rather scep-
tical attitude toward the competence and quality of Leclainche’s work.
Instead, he states enthusiastically: “Variole is smallpox (Latin variola)
and not only did this great outbreak kill domestic animals but it was
referred to as the black death.”66 He has a motive for doing so: suddenly,
many pages after he has discussed the origin and meaning of the term
the “Black Death” and despite much effort had not succeeded in adduc-
ing evidence that the name was contemporary, he triumphantly quotes
Leclainche’s assertion that the epidemic at the time was called the Black
Death, “la mort noire, der Schwarze Tod.” However, he cannot provide
his readers Leclainche’s source for this sensational find and potentially
important contribution to the history of the Black Death, because there
is none. This is also the reason neither French historians nor German
historians have picked up Leclainche’s assertion. In modern French
61
Ziegler 1970: 18.
62
Twigg 1984: 245.
63
Twigg 1984: 204–7.
64
Twigg 1984: 211. My translation from French.
65
66
Twigg’s italics.
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scholarly work on the Black Death, the epidemic is unequivocally iden-

tified as bubonic plague. In the words of Dubois in the most recent
summary of French research on the Black Death: “almost everywhere
in France, the plague has assumed the bubonic form with secondary
manifestations” (the small reservation relates to primary pneumonic
plague).67 Leclainche was a veterinarian without training in the craft of
the historian and the historical aspects of his work are fatally flawed by
his lack of historical knowledge of medieval society and of training in
historical source-criticism and the application of historical methodol-
ogy more generally.
Anthrax’s Historical Association with Other Epizootics among Domestic

Animals and Plague
The same fundamental problems can also be readily seen in Twigg’s use
of Leclainche’s supposed information that “in 801 there was plague in
Charlemagne’s empire which took men and animals alike and in 840
there was plague in men and horses.” Anyone who has taken a serious
interest in the history of plague will know that there were no plague
epidemics at the time of Charlemagne. The last possible outbreak of
plague in the Justinianic plague pandemic was in 766 in Rome or per-
haps in Naples and Sicily in 750.68 The last epidemic within the area of
present-day France may have occurred in 694, and the last quite certain
French epidemic of plague in this pandemic took place in Southern
France in 655. All epidemics of this pandemic with their geographical
extension are presented in a paper by Biraben and Le Goff of 1969; they
are presented systematically over twenty-two pages which include a
table with geographical information and individualized maps in
Biraben’s monograph of 1975 which Twigg has entered in his bibliogra-
phy.69 Twigg could easily have determined that Leclainche’s assertions
were unhistorical and left his work aside. Leclainche could have
used Sticker’s valuable presentation of the Justinianic pandemic in his
first volume (1908).70 So could Twigg, who must be assumed to know
67
Biraben 1975: 7–18; Dubois 1988: 313–6. My translation from French.
68
Little 2007: 14; Sallares 2007: 288; McCormick 2007: 292.
69
Biraben and Le Goff 1969: 1484–510; Biraben 1975: 26–48. They have missed the
spread to England by some of the epidemics. See for instance Maddicot 2007:
171–214.
70
Sticker 1908: 26–35.
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Sticker 1908 since he refers to it once, albeit on a peripheral point of

mortality in the plague epidemic in Cairo of 1574–6 (above).
Serious or severe epidemic diseases among human beings were usual
in the Middle Ages. As Twigg correctly states: it “is very likely that the
people of the Middle Ages suffered from a wide variety of diseases.”71
However, contagious diseases among cattle and sheep and other domes-
tic animals were also a general feature of life and these animals suffered
from a variety of diseases, anthrax and foot-and-mouth disease, which
are commented on by Twigg, but also sheep scab, sheep pox (variola
ovina), brucellosis and trichinosis. Leading English agricultural histo-
rians agree that epizootics frequently took a serious toll of English live-
stock in medieval England: “Major epidemics of disease caused serious
losses to the sheep population in England in the late thirteenth and
early fourteenth centuries. Some flocks were reduced by as much as
two-thirds.”72 This means that it was quite usual that epidemics among
human beings and epizootics among domestic animals took place more
or less concomitantly and that there was no pathogenic or dissemina-
tive connection between them. Contemporaneousness of events does
not constitute proof that they are causally related, it justifies only the
establishment of a working hypothesis to the effect that this could have
been the case, with the function to induce the scholar to look for cor-
roborative evidence. Consequently, it is a fallacy of methodology to
conclude without further specific investigation that livestock and
human population were hit by the same disease, as Twigg usually infers.
Specific corroborative evidence must be adduced. And anthrax is not
the only disease that can affect both farm animals and local popula-
tions in quite close epizootic and epidemic developments; this is also
the case with brucellosis and trichinosis.73 Also for this reason it would
be a fallacy of methodology to conclude that concomitant epizootic
and epidemic developments must reflect anthrax—specific evidence
would need to be adduced. If specific evidence cannot be produced,
Twigg must admit that he has raised a working hypothesis that he is not
able to prove and thus has no case.
Twigg enthusiastically writes repeatedly about the numerous epiz-
ootics among domestic animals reported in the chronicles and other
71
Twigg 1984: 210.
72
Trow-Smith 1957: 153–7, 240–1; Dyer 1988: 29; Grant 1988: 154, 185; Astill and
Grant 1988: 216–7.
73
See, for instance, Manson’s Tropical Diseases 1982: 348–55, 191–4.
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sources from the Early Middle Ages into the Late Middle Ages.74 The
readers must be excused for assuming that Twigg considers this to be
evidence of anthrax, since the accounts on this point cannot serve any
substantial purpose for his project if they reflected a considerable
number of other epizootic diseases. However, eventually a major prob-
lem confronts Twigg: if anthrax had been around for many centuries
before the Black Death, it becomes impossible to explain the excep-
tional mortality caused by the Black Death. So, he must introduce a
new disease into Europe, namely anthrax in the form of the Black
Death. This flies in the face of what is known about the history of
anthrax, which is usually assumed to be mentioned in the Bible and in
sources from Antiquity,75 and English agricultural historians are cer-
tain that it was present in pre-plague England.76 It also flies in the face
of what is known about the level of mortality rates caused by the Black
Death (see below). Actually, Twigg’s line of argument turns out to be
circular: “Although recorded on many occasions before 1348, murrains
had never been accompanied by such an unprecedented human epi-
demic and this leads me to think that the Great Pestilence was caused
by an organism not only common to man and animals, but because of
its severity, perhaps new to both of them.”77 Thus, anthrax must be a
new disease to fulfil Twigg’s preconceived idea that the Black Death
could be anthrax.
Twigg does not make a serious attempt to demonstrate the tenability
of his second central assumption, namely that the Black Death’s pattern
of spread could, even by the most creative exercise of imagination, have
resulted from the fact that from Spain to Norway, from England to
Russia, European populations were consuming “raw or undercooked”
meat contaminated by anthrax and according to a temporal and spatial
pattern co-ordinated with and compatible with the spread of plague. At
the time, livestock was not a usual cargo, certainly not over considera-
ble distances, and because the epidemic outbreaks in seaports were
normally not preceded by epizootics among cattle and sheep, the cru-
cial role played by ship transportation of the Black Death at long or
intermediate distances is incompatible with the spread of anthrax. Nor
was meat such a major part of diet (see below).
74
Twigg 1984: 200–1, 211, 217.
75
Sternbach 2003: 1–3; Brachman 1990: 877.
76
Grant 1988: 185; Smith 1988: 208.
77
Twigg 1984: 217.
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Twigg’s assumptions take on an increasingly hypothetical and

speculative character: “The route by which plague is reputed to have
reached Europe could be the very same one that anthrax used.” “If
anthrax had come from the East it could have been swiftly spread across
Europe from Marseilles and other ports.”78 Thus, it is a fantastic sce-
nario Twigg outlines for his readers of big herds of cattle being trans-
ported by galleys first from Kaffa to Constantinople, from Constantinople
to Mediterranean ports, especially Marseilles, from whence they were
driven across Europe, disseminating spores and contagion and produc-
ing instant mass mortality everywhere. Everywhere people gladly
devoured contaminated meat from slaughtered sick animals or animals
having died from “murrain” without ever or anywhere coming to sus-
pect that it could be dangerous, although they saw people dying every-
where in droves, people that only had in common the fact that they had
eaten meat from animals killed by “murrain.” Inexplicably, poor people
who usually could not afford meat but had to do with porridge and
coarse bread had even higher mortality than the affluent and rich.79
In fact, Twigg is unable to show that concomitant epizootics and epi-
demics were usual even in England. For this reason, B.M.S. Campbell
points out in his review of Twigg’s monograph that Twigg’s theory is
undermined by the absence of detectable abnormal mortality among
demesne livestock during the Black Death.80 Campbell is not impressed
by Twigg’s attempts at documenting the contrary by basing his account
on Hecker’s pre-scientific work of 1837 which for plague is based on
Barnes’s monograph on the History of Edward III of 1688 (see above):
“Hecker says that the plague in England was soon accompanied by a
fatal murrain among the cattle, which, left without herdsmen, fell in
their thousands.”81 Why does Twigg base his theory on a long obsolete
work, and why does he not provide Hecker’s source, since it is of such
vital importance to the viability of his theory?
Instead, Twigg goes on to cite a small part of a chronicle-based sen-
tence by Rees about the Black Death in London in 1348 to the effect
“that animals as well as men were affected.” However, Twigg refrains
from citing the following part where Rees applies source-criticism and
78
Twigg 217–8.
79
Benedictow 2004: 262–6, 368, 375–7.
80
Campbell 1985: 314. Cf. Smith 1988: 208.
81
Twigg 1984: 211.
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adds cautiously: “but accurate evidence is not easily obtained,”82 which,

in my view, makes the statement practically valueless. Medieval chron-
iclers must be used with great caution even when their accounts or
information are not obviously incredible or unreliable. Their informa-
tion must be testable by similarity of independent accounts or other
forms of source material. This point can be further demonstrated by
citing the first part of Rees’s chronicle-based statement left out by
Twigg: “scarcely one-tenth survived [in London],”83 which should be
impossible even for bubonic plague with a lethality rate of 80 per cent
of those infected. Are the views of a chronicler who makes such an
evidently hopelessly exaggerated assertion really credible? Is it true that
Rees’s account on this point can serve to support a case for a concomi-
tant epizootic and epidemic in London? How can it be made compati-
ble with Ziegler’s correct observation that the Black Death broke out in
London earlier than in the surrounding districts, actually by a margin
of several months?84 This can only serve to illustrate the great caution
with which medieval chroniclers should be treated. Icelandic chroni-
clers assert that only fourteen people survived in London.85
Twigg’s attempt to take refuge in the international trade of hides,
furs and wool on the basis of E.M. Veale’s fine, but quite narrowly
England-oriented monograph, is unconvincing.86 Nothing is said in
this study about skins or furs as vehicles of the spread of zoonoses to
human populations at the time, nor about anthrax, nor about any other
animal disease,87 which shows that Twigg is forced to proceed by spec-
ulation. Assuming speculatively that anthrax was actually spread by
this trade, this scenario would only result in the sporadic incidence of
cutaneous anthrax with a lethality rate of about 20 per cent and rare
cases of pulmonary anthrax, two forms of contagious disease that,
taken together, can cause population mortality rates of fractions of 1
per cent (see above). It cannot be accepted as a serious proposition that
82
Rees 1923: 29.
83
Ibid.
84
Ziegler 1970: 135; Benedictow 2004: 134–7.
85
Islandske Annaler 1888: 275–6.
86
Twigg 1984: 217–8. Nothing negative is meant by my characterization of Veale’s
monograph as narrowly England-oriented (its title is The English Fur Trade in the Later
Middle Ages), only that its focus or perspective poorly serves Twigg’s sweeping Europe-
wide line of argument. The same goes for its temporal perspective which, as the title
shows, is strongly oriented towards the post-Black Death period.
87
Veal 1966.
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these forms of anthrax could have spread in large waves over the conti-
nent and across England, causing havoc everywhere. This is why it has
not been possible to adduce evidence to this effect.
Since Twigg is not able to provide evidence demonstrating the con-
comitant spread of mortal epizootic disease among manorial herds
during the Black Death, he is lead to emphasize his speculative
approach. A few pages later he resorts to another pre-scientific work,
this time by H. Harrod of 1867, which also speaks clearly for itself: “On
the Manor of Heacham, Norfolk, there was murrain from 1346 to 1411
without pause and it attacked horses, cattle, sheep, pigs, chickens,
ducks, geese, swans, pea-hens and even hives of bees.” It is, of course,
impossible that the same zoonose should be the cause of an epizootic
among all these animals. At the basis of this statement lies the mias-
matic theory which is mono-causal and also can explain why birds and
bees are severely hit, since miasma is spread by contaminated air.
Finally, Twigg refers to E.L. Sabine’s paper on “Butchering in Medieval
London” in which it is stated that the “periods of 1314–20 and 1346–89
were times of murrain among domestic animals,” in the second period
also among poultry and wild birds, and specifically among sparrows in
1366.88 This should make it clear that “murrain” is a word used to des-
ignate any or at least a large number of diseases among animals and
that murrains in this more general meaning of zoonoses were an
ordinary part of medieval life, before the Black Death and after the
Black Death. Murrain is the contemporary concept of epizootic, equiv-
alent to the contemporary concept of pestilence for epidemic; in the
case of pestilence bleeding of human victims was usual, and in the case
of murrain bleeding of livestock was usual.89 Importantly, Harrod and
Sabine do not maintain that there was concomitant spread in time and
space of murrains among domestic animals and mortality among peo-
ple in the Black Death. Twigg has not produced evidence to the effect
that anthrax spread concomitantly with the Black Death in England, as
Campbell correctly points out.
The scholarly literature on the Black Death and subsequent plague
epidemics typically consists of studies of outbreaks that are not pre-
ceded by any epizootic among cattle and sheep. One important reason
that epizootics among livestock did not usually develop on a grand
88
Twigg 1984: 215.
89
Trow-Smith 1957: 153–7, 240–1; Astill and Grant 1988: 216.
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scale comparable with the Black Death is that medieval people were
not so helpless as Twigg must assume. They had learned from long
experience and made strong efforts to contain the spread of murrain.
“For example, animals that died of murrain were burnt, and their heads
placed on stakes to tell travellers to avoid the area.”90 Thus, medieval
people employed some of the main methods used today to eradicate
epidemics of anthrax, foot-and-mouth-disease and scrapy. For the
same important reason, medieval people did normally not eat domes-
tic animals which had died from outbreaks of murrain, i.e., from dan-
gerous epizootic diseases.
The Black Death’s Origin and Spread and the Anthrax Theory
Twigg puts much emphasis on an account of the Black Death’s spread,

especially the early phase, and he has an important reason or objective
for doing so: “It is essential to examine the biological logistics of the
Black Death in order to attempt to determine whether this particular
epidemic could have been bubonic plague.” In his third chapter, titled
“The Black Death – Origins and Spread to Europe” he says that his goal
is “to examine the origin of the Black Death and the way it reached
Europe, in the light of modern knowledge of plague biology.”91 Twigg
wishes to use the history of the Black Death’s origin and spread to
show that it is incompatible with bubonic plague but compatible with
anthrax. This is a legitimate and potentially useful way to address the
question of the microbiological identity of the Black Death and to con-
sider possible alternatives. However, Twigg’s quite poor knowledge of
medieval history and source-criticism and limited reading of the avail-
able modern accounts of the history of the Black Death combine to
result in various assertions and discussions which are out of line with
reason and reality. Because so much of his account is factually wrong,
for practical reasons only a small representative sample of data and
arguments with relevance for his objective can be discussed.
Several contemporary chroniclers assert that the Black Death started
in the lands of the Golden Horde in south-eastern Russia, in a region
containing a large plague reservoir where people still contract bubonic
plague today. They also assert that it was spread by galleys from the
90
Astill and Grant 1988: 216–7.
91
Twigg 1984: 43–4.
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Italian trading station at Kaffa in the Crimea to Constantinople and

seaports on the Mediterranean littoral. This outline of the origin of the
Black Death can be safely confirmed by the early history of outbreaks.92
It is correctly recognized as a serious threat to several of the alternative
theories, because it establishes a continuous line from an area of a
known plague reservoir to the introduction of plague in Constantinople
and in important commercial hubs of the Mediterranean littoral. The
threat to Twigg’s theory is especially great, since the chroniclers have
nothing to say about epizootics among livestock spreading concomi-
tantly with the Black Death in the regions where it broke out in the
spring of 1346 and until it reached the camp of the army besieging
Kaffa.93 Twigg and Scott and Duncan endeavour on erroneous grounds
to claim that the Black Death could as well have come to Mediterranean
Europe from Alexandria or Syria, and Scott and Duncan have pro-
duced a map showing as established fact that the Black Death spread
from Alexandria to Messina in Sicily.94 For Scott and Duncan it is cru-
cially important to link the origin of the Black Death to Africa, since
the haemorrhagic diseases of Ebola and Marburg are closely associated
with Western Africa; the fact that these diseases have no known history
in north-eastern Africa or the Middle East is ignored. They also present
a completely outdated and misleading map of the spread of the Black
Death that does not show the origin in south-eastern Russia and the
spread out of Kaffa (see below).
A central aspect of this topic is obviously the issue of the spread of
plague over long distances. To his credit, Twigg is the only advocate of
an alternative plague theory who attempts to do this explicitly in rela-
tion to the Black Death’s first phase of spread: most of the other
advocates of alternative theories ignore the problem or accept unques-
tioningly Twigg’s discussion of the problem as Scott and Duncan do.95
Twigg rejects the possibility of long-distance transportation of
bubonic plague by ship from Kaffa by agency of the nexus of rats and
fleas on untenable grounds.96 However, a hundred pages later Twigg
asserts that when bubonic plague was raging in India a hundred years
ago, it was repeatedly transported from there by steamship all the long
92
93
94
95
96
Twigg 1984: 47–55; Benedictow 2004: 17–21, 51–73. See also above chapter 4.
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and time-consuming way to England. In this connection he states cor-

rectly that “Ships represent the greatest danger of introducing plague,
mainly by means of rats and fleas in the cargo,” and goes on to mention
a number of occasions when this occurred.97 In this passage, Twigg
reveals that he is fully aware of the fact that bubonic plague spreads
easily by ship over long distances, i.e., by metastatic leaps (per saltum),
although he systematically refrains from taking it into account in his
epidemiological analyses of the Black Death.
The reality of metastatic leaps reflects the fact that rat fleas can sur-
vive away from their rat hosts for quite a number of weeks in humid
and moderately warm climate typical of much transportation by ship,
much longer than Twigg asserts, again without a substantiating foot-
note: “although in ideal conditions X.98 cheopis may live for a month
without its host it is doubtful if at the end of that time it could transmit
plague.”99 This is strongly at variance with Hirst’s statement that in
favourable circumstances, “at temperatures below 15° C. the chief vec-
tor of bubonic plague, X. cheopis, can certainly survive in a very heavily
infected state for at least fifty days,” and this is not the limit: “it is highly
improbable, however, that the maximum longevity of unfed, infected
rodent fleas is known.”100 It can be usefully added that this rat flea sur-
vives unfed in a very heavily infected state for 23 days at 27 °C. In
Madagascar, researchers discovered that this rat flea could survive for
months on grain debris,101 which demonstrates the significance for the
spread of plague of the transportation of corn and farina, which were
the most common goods in medieval transportation.
The length of time dangerous rat fleas can survive a voyage is further
extended by the period of the epizootic among the ship’s rats that even-
tually leads to the release of infected fleas from dead rats in a situation
where many of these fleas do not find new rat hosts. In this perspective,
the number of rat colonies on board large ships such as galleys
(and cogs) and also the relative localization of their territories in the
ship take on significant interest,102 since the strong reduction of a rat
colony to this point takes ten to fourteen days (see above). This is at the
97
Twigg 1984: 47–54, 147.
98
X. = Xenopsylla.
99
Twigg 1984: 85.
100
Hirst 1953: 324, 330–1.
101
Hirst 1953: 330–1.
102
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heart of the matter when Twigg correctly writes that the “galleys could
therefore presumably support many rats,”103 because the presence of
two or more rat colonies that were successively attacked by plague
would readily add four or more weeks to the time preceding the point
when rat fleas would be on their own. The point is the following: rats
defend their territories and the food resources within them and they
respect the boundaries of adjacent rat territories in order to avoid being
attacked, which means that another rat territory will not be invaded
until its rat colony is severely reduced and unable to defend it. When
the rats of an unaffected rat colony invaded the territory of such a
defenceless rat colony, they would pick up their fleas, and thus the
process would be repeated and the time horizon of the epizootic would
be further extended and potential epidemic developments would be
correspondingly postponed. Thus, there is a clear potential for a sub-
stantially expanded time horizon before plague epidemics break out on
galleys. For the same reason the long-term survival of infected rat fleas
will tend to be much longer than Twigg assumes.
If Twigg’s objective was to give a tenable, updated account of the
early phase of the Black Death’s spread on the basis of best possible
facts, it is difficult to understand the scholarly grounds for his prolific
use of Hecker’s pre-scientific work on medieval epidemics of 1837
(posthumous reprint of 1859) and of Gasquet’s account written around
1890,104 and for his neglect of M.W. Dols’s fine monograph on the Black
Death in the Middle East of 1977, or Biraben’s monograph on plague of
1975 or his paper of 1979,105 and several other excellent works that were
available at the time he was writing his monograph. The vast majority
of works on the Black Death were written not only after Hecker’s work
but also after Gasquet’s, and this is the case for all works written after
modern medicine, epidemiology and bacteriology were established.
Inevitably, Twigg’s temporal outline of the Black Death’s spread from
the Crimea to the Mediterranean coasts is wrong, as is his outline of its
further spread over Europe, even for his native England. Inexplicably,
he provides a map of the Black Death’s spread across Europe that he
informs his readers is taken from a small paper on the Black Death by
103
Twigg 1984: 51.
104
Twigg 1984: 45–7, 60–1. On these few pages, Hecker and Gasquet are referred to
five and seven times respectively (and many more times elsewhere). Cf. Above: 565,
fns. 35, 36.
105
Biraben 1975–1: 48–92; Biraben 1979: 30–40.
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W.L. Langer in Scientific American of 1964. However, Langer has not

drawn it. It is also published in Ziegler’s monograph106 which he has
used extensively, referring to him by name twenty times in his text.107
This map is taken from a general paper on famines and epidemics in
the fourteenth century by É. Carpentier published in 1962, two years
before Langer’s paper.108 In this paper, she makes a pioneering attempt
at sketching an outline of the spread of the Black Death at an early stage
of plague research based on quite a small sample of studies, which was
due to her limited access to studies in other languages. The result was
seriously flawed, and it does not show the spread from the Crimea,
which should have been important to Twigg given his point of depar-
ture, but starts in Southern Europe. It is so inaccurate or erroneous for
the spread of the Black Death in the British Isles that it is difficult to
understand how a British scholar was not struck by it. How profoundly
flawed the map is can be easily ascertained by comparison with the
map I provide in my monograph on the Black Death109 and is reprinted
on page 2 above which is based on a detailed description of its spread
over almost 200 pages taking into account the national research from
all countries that were ravaged by it.110 Scott and Duncan also chose to
republish Carpentier’s map, but since they too have chosen to ignore
the standard requirement for scholarly monographs to provide foot-
notes, nothing is said of the map’s origin or background, and they let
their readers believe that it could be of their own making.111
Ten years before Twigg published his monograph, Biraben had pub-
lished a much improved, although still deficient, map of the Black
Death’s spread across Europe.112 Twigg mentions this work in the two
lines preceding Carpentier’s map, but on a point regarding the Black
Death’s arrival in Bordeaux. Biraben’s very different and much improved
map shows the Black Death’s origin in the Crimea. In 1979, Biraben
published a much improved map on the spread of the Black Death in
the Middle East which should have been of particular interest to Twigg
at the time he wrote his monograph, but it remains unmentioned.113
106
Ziegler 1970: 106–7.
107
Twigg 1984: 48–2, 49, 54, 55–3, 62, 78, 79–2, 82, 85, 90, 175, 189–4, 220.
108
Carpentier 1962: 1062–92.
109
Benedictow 2004: 1–2. See also the map in Benedictow 2005: 44.
110
111
112
Biraben 1975: 88–9.
113
Biraben 1979: 30–40, map on p. 34.
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Also Dols renders a much better map than Carpentier’s in his fine
monograph on the Black Death in the Middle East of 1977.114
What makes Carpentier’s map so attractive? Is it that it shows the
spread of the Black Death at six-monthly intervals in long curved lines
without reflecting the important part that ship transportation played in
the process of dissemination and thus “conceals” the role of metastatic
leaps. The numerous indications of metastatic leaps by ship are exactly
the conspicuous aspect of the map I have drawn, fully supported by
evidence in my text.
Carpentier’s map does not show the Black Death’s spread out of
south-eastern Russia from Kaffa on the Crimea by ship. Twigg can
therefore indicate a theory of the Black Death’s geographical origin and
route of spread to Europe very different from the established view that
it broke out in southern Russia and was spread from Kaffa by Italian
galleys. Instead, he cites Hecker’s pre-scientific work of 1837115 where it
is stated that “before the plague reached Europe it had killed daily, in
Cairo, between 10,000 and 15,000 people.”116 This is wrong. In Egypt,
the Black Death first reached Alexandria in the early autumn of 1347
by a major metastatic leap from Constantinople, and this was the deci-
sive epidemic event in this part of the world, which established the
great epicentre of spread in the Middle East and North Africa. The
Black Death’s spread out of this great and bustling city did not start
until the late autumn, and by normal spread rates it did not reach Cairo
until, as it seems, the summer of 1348,117 since the epidemic raged at its
worst there in October–December.118 This also means that the Black
Death had reached southern England and north-western France shortly
before or at about the same time it reached Cairo, and had already rav-
aged a large part of Europe. Mortality rates by plague cannot be dis-
cussed on the basis of the type of information provided by Hecker.
Dols’s careful specialist discussion of mortality rates is valuable. All this
is uncritically taken over by Scott and Duncan.
Twigg’s assertion that the Black Death could have been shipped to
Europe from Syria at the same time it was shipped from Kaffa is
114
Dols 1977: 36–7.
115
Although Twigg has used the posthumous edition of 1859, 1837 is the real histo-
riographic age of the work.
116
Twigg 1984: 46.
117
118
Dols 1977: 182.
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unfounded and untenable. Scott and Duncan accept this view, since it
somewhat shortens the distance to West Africa which is the only known
region where Ebola disease and Marburg disease occur. Thus, the
Crimea is an impossible origin for their alternative contagion for ship-
ment to Constantinople and the Mediterranean littoral. The fact is that
the Black Death spread from Alexandria to Syria, was raging in Gaza in
April and May of 1348 and in Damascus in July, a year after the out-
break in Constantinople, and at the time when the Black Death had
ravaged large parts of Southern Europe and had even begun spreading
in England out of Melcombe Regis (Weymouth) and was closing in on
Paris from Rouen. Twigg’s extensive use of Hecker’s pre-scientific work
of 1837 for his account of the early spread of the Black Death is intrigu-
ing.119 At the time he was writing his monograph, Twigg should have
used Dols’s excellent study of 1977, also Biraben’s monograph of 1975
and his paper of 1979120 which have much valuable information to offer
on this topic. However, Dols and Biraben are able to write their mono-
graphs on the assumption that the Black Death was bubonic plague
without landing in any obvious epidemiological difficulties. Metastatic
leaps of bubonic plague by ship play a central role, in the words of Dols,
for instance: “Al-Maqrizi informs us that the Black Death reached
Egypt in the early autumn of 748/1347—about the same time that it
arrived in Sicily. It may have been spread simultaneously to Asia Minor
and the Levant by merchant ships.” “The fact that the Black Death
arrived in Egypt at approximately the same time that it reached Sicily
would strongly suggest its transmission by the brisk Christian mari-
time trade from the Black Sea and Constantinople.”121
Twigg’s efforts to prove that the Black Death cannot have been
bubonic plague are undermined by other serious weaknesses of facts
and assumptions. Twigg states that the “Genoese would, at the earliest,
have left Kaffa during October and at the latest by December,” and
assumes arbitrarily that the Genoese galleys which he claims arrived in
their home city in January had been sailing directly from Kaffa.122 This
is wrong: in Constantinople the outbreak was recognized in early July,
which in the case of bubonic plague means that the contamination was
introduced in early May. Actually, chroniclers mention that Genoese
119
Twigg 1984: 46–7.
120
Biraben 1979.
121
Dols 1977: 57–60.
122
Twigg 1984: 51, 54.
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galleys fled from Kaffa in the spring of 1347 and contaminated the
metropolis, which as can easily be seen fits the facts.123 It can be shown
that Twigg knows these accounts.124 The temporal progression of these
accounts also fits with the central facts of the further spread: the out-
breaks in Alexandria in early autumn 1347, in Messina on Sicily at the
end of September and in Marseille by 1 November,125 not in February,
as Twigg asserts.126 These facts are related in considerable detail in
Dols’s monograph.127 In this way, Twigg clears the ground for an argu-
ment to the effect that “Flea breeding must have been very low at that
time both on ship and ashore.”128 On the contrary, many of these events
took place at the height of the flea-breeding season.
Twigg is very reluctant to take into account the fact that Constanti-
nople was contaminated in the Black Death’s first phase of spread by
galleys that had fled from Kaffa, making only an off-hand comment
that Gasquet (1908) thinks that plague was “probably carried” from
Kaffa to Constantinople.129 Twigg attempts to avoid or downplay the
point that Constantinople could function as an intermediary base for
further dissemination into the Mediterranean littoral by other ships
contaminated in the harbours of the metropolis, and that they could
even have been contaminated before the outbreak by exchange of
goods, in a similar way to what was reported to have occurred in the
harbour of Melcombe Regis (Weymouth) in England.130
Twigg needs to adduce evidence to the effect that long voyages are
incompatible with plague biology and argues his case on the assump-
tion that all ships from Kaffa sailed directly to their Mediterranean des-
tinations, mainly Venice and Genoa, which makes the continuous
voyage at sea (i.e., without stops for trade or to acquire supplies) as long
as possible. It enables him also to ignore the notion that many of the
ships which spread plague along the Mediterranean coasts in the
autumn of 1347 could have been contaminated in Constantinople.131
Crucially, Twigg does not mention that the Genoese and Venetians
123
Benedictow 2004: 60–5, 69–73; Dols 1977: 53.
124
Twigg 1984: 46.
125
Benedictow 2004: 53, 63–4, 69–73, 96–101.
126
Twigg 1984: 55.
127
Dols 1977: 53–61.
128
Twigg 1984: 54.
129
Twigg 2984: 47.
130
131
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along the shipping lanes had quite number of other minor trading sta-
tions and ports that they used for rest and provisioning. In the words of
N.J.G. Pounds, there was “a ring of trading stations along its [the Black
Sea’s] coastline,” for instance, Mauro Castro on the estuary of the Dnestr
and Trebizond,132 and after having left Constantinople, for instance,
Chios, Nauplion, Coron, Modon and Monemvasia, Corfú (Kerkyra) on
the shores of Greece, and on the last stretch homewards up the Adriatic
the Venetians used the ports of Ragusa (Dubrovnik), Spalato (Split)
and Zara (Zadar), whilst the Genoese especially used the ports of
Messina and Naples for their last stretch homewards.133 This also means
that they had the opportunity to halt the voyage for shorter or longer
periods of time and to hire additional sailors. Even an elementary
introduction to the commercial history of the Middle Ages like R.S.
Lopez’s fine little monograph The Commercial Revolution of the Middle
Ages, 950–1300 mentions that “the Genoese established a cluster of
colonial outposts all around the Black Sea.”134 Thus, Twigg’s presump-
tion that returning Venetian and Genoese galleys would have to sail
directly to their patriae is without basis in elementary facts of medieval
trade history. In this way, Twigg has construed an artificial argument
against bubonic plague being shipped out of a region where there is a
permanent plague reservoir in order to clear the ground for his own
theory, although no concomitant epidemic of anthrax is mentioned in
the lands of the Golden Horde by the chroniclers (see above).135
For his presentation of the routes of the Italian galleys homewards
from their easternmost trading station at Kaffa Twigg refers to E.H.
Byrne’s small monograph on Genoese shipping in the High Middle
Ages. However, this work is oriented towards their western trade routes,
towards Barcelona, Málaga, Tunisia and Ceuta, and towards the Levant.
It focuses on topics relating to shipping and business and relates rather
peripherally to actual sailing and the system of sea lanes and ports used
along the routes. Nonetheless, Byrne gives some pieces of information
on ports of call along the sailing routes.136 As can be seen, much more
useful information on this topic can be found in modern standard
132
The ancient Greek colony of Tyras, later called Akkerman, from 1946 with the
Slavic name of Belgorod(-Dnestrovskiy), in Romanian Cetatea Alba.
133
Pounds 1974: 360–7.
134
Lopez 1976: 109.
135
Bratianu 1929; Pounds 1974: 360–8.
136
Byrne 1930/1970: 36–7, 44, 52.
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works on medieval economy like Pound’s still very useful monograph

of 1974 which has also a rich standard apparatus of footnotes as well as
fine bibliographical entries at the end of each chapter—as scholarly
books should.137
Medieval chroniclers’ rhetorical exaggerations and loose relation-
ship with facts are some of their most obvious features. What medieval
chroniclers assert and what they do not mention are a rich source of
great surprises to modern scholars.138 For this reason, assertions of the
pace of spread that cannot be tested against independent sources, and
in cases of data relating to cities, against local population records, can-
not be accepted. Twigg considers it appropriate, on the contrary, to cite
the chronicler Gabriele de Mussis, but he cites him indirectly, accord-
ing to Creighton’s summary,139 who was, as pointed out above, the last
champion of miasmatic theory in England. Twigg cites Creighton to
the effect that,
there were no cases of plague on board ships, although the very atmos-
phere or smell of the new arrival seemed sufficient to taint the whole air
of Genoa and to carry death to every part of the city within a couple of
days.140
Firstly, as already pointed out by Gasquet, it is not true, as Creighton
repeatedly asserts, that Gabriele de Mussis had himself been in Kaffa
and left with a Genoese galley for his home town and that his account
therefore is based on personal observation. In fact, de Mussis stayed in
his home town of Piacenza and pieced together his account on the basis
of what he heard from sailors or merchants and other sources of hear-
say. His account can readily be shown to be based on misinformation
and misconceptions and miasmatic notions.141 It is also not true that
there were no cases of plague on board: “It so happened that when the
ships left Caffa—some bound for Genoa, some for Venice, and some to
other parts of the Christian world—a few of the sailors were already
infected.”142 Obviously, Creighton shapes his summary of de Mussis’s
account in a way that serves his campaign for miasmatic theory against
the rise of the new science of bacteriology or microbiology and puts
137
Twigg 1984: 52, 54.
138
See above: 78–82, 219–24.
139
Creighton 1894: 144–9.
140
Twigg 1984: 52, cf. 54. Twigg’s italics; Creighton 1891: 148–9.
141
142
Cited after Gasquet 1908: 19–20.
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special emphasis on the theory that the ships carried merchandise con-
taminated with miasma. And in fact de Mussis’s account is formed
according to contemporary miasmatic notions of epidemic disease.143
Creighton’s presentation of this material is therefore doubly imbued by
miasmatic notions. Twigg neglects the basic approach of the historian’s
craft, namely to identify the original source and start source-critical
work from there, or he would have noted Gasquet’s correct rendering
of de Mussis account, a work he knows well and refers to by the author’s
name twenty-three times in his running text.144 Miasmatic notions can
imply extreme contagiousness by touch and extreme spread rates since
spread is not dependent on contact but is effected by wind. On this
basis, Twigg can conclude that the disease introduced from Kaffa to
Genoa could not have been bubonic plague. However, would any epi-
demic disease known to modern medical science spread across Genoa
in a couple of days, even intensely infectious diseases like smallpox or
influenza, since they are dependent on interpersonal contact for trans-
mission? Is it not only miasmatically contaminated air that can spread
an epidemic disease in this way, because people will inhale it as it blows
down their streets and in through their windows? Is it really a medi-
cally and epidemiologically qualitative difference between de Mussis’s,
Creighton’s and Twigg’s accounts? Are they not all based on miasmatic
assumptions?
Scott and Duncan take great interest in much the same events,
namely the Genoese galleys’ arrival in Messina on Sicily, and subse-
quently in their home town. They take over wholesale Twigg’s argu-
ments which can seemingly serve to undermine the bubonic-plague
theory and as such clear the ground for their own alternative theory.
De Mussis’s account is in fact yet another definite proof that the dis-
ease was not anthrax. It cannot be accepted that the galleys arrived in
Genoa from Kaffa with herds of cattle or sheep on board which were
seriously sick from or had recently died from anthrax and that the pop-
ulation of Genoa eagerly consumed the flesh of these animals all across
the city with extraordinary epidemic speed, actually in two days.145
143
144
Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207.
145
I have assumed that Twigg did not believe that the galleys arrived from Kaffa full
of contaminated wool that was immediately spread all over the city and that the great
majority of Genoa’s inhabitants were woolsorters who en mass contracted anthrax by
inhalation, and even this flight of fancy would be insufficient for explanation, since we
also must assume that the woolsorters did not early detect that work with wool at the
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According to elementary scientific principles, Twigg should be obliged

to demonstrate in concrete detail how this could have been possible
and on this basis form a realistic and tenable explanatory model; the
fact that he has declined to do so means that his assertion is unfounded
and can be taken as evidence that such modelling is impossible. Even if
every inhabitant of Genoa were infected, the lethality rate would only
have been about 20 per cent, only a fraction of Italian mortality rates in
the Black Death estimated on the basis of population records and other
types of demographic sources, for instance one-third of the mortality
rate in Florence.146 Also Scott’s and Duncan’s alternative theory of a
filoviridal disease is excluded, since these diseases spread only by direct
physical contact and transmission of living contaminated cells, which
makes for an exceedingly slow spread and tiny outbreaks (see below).
The outbreak in Genoa appears to have been recognized at the end
of 1347, not in January, as Twigg states.147 Assuming that it was bubonic
plague, the contamination would have been introduced into the city
about seven weeks earlier and would have had much time to prepare
the ground for an outbreak in January after having developed for at
least a couple of months, provided that the temperature was moder-
ately chilly for the season. However, there is no source material availa-
ble which can provide an empirical basis for a spatio-temporal outline
of the Black Death’s spread across the city. The inherent dangers of
accepting the “overwrought imaginings” and “hopelessly inaccurate
quantifications” of medieval chroniclers can be further illustrated.
Twigg’s monograph exhibits no trace of the scepticism of medieval
sources and the great importance of source-criticism that is uppermost
in the minds of all medievalists worth their salt. Twigg claims, for
instance, that 56,000 persons died from the Black Death in Marseilles.148
This figure is taken from Ziegler’s monograph, and since Ziegler,
according to the ordinary standards of scholarly work, provides a
supporting footnote it can be ascertained that it comes from a pre-
scientific149 study of 1869,150 which allows identification of the original
source as a contemporary chronicle. However, Ziegler took this figure
time was extremely dangerous. Of course, significant epidemic outbreaks of pulmo-

nary anthrax have so far not been discovered.
146
147
Benedictow 2004: 71; Twigg 1984: 55.
148
Twigg 1984: 55.
149
Anglada 1869.
150
Ziegler 1969: 64, 293, 312.
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and its footnote from Gasquet’s monograph who more accurately

informs his readers that the figure is 57,000, represents the death toll
for a month and, therefore, constituted only a small part of the total
mortality which according to the implied information must in the end
have numbered hundreds of thousands of victims.151 Thus, this is a case
of serial uncritical and careless copying of information in which only
the first author has read the original study and none has read the origi-
nal source or applied source-criticism. This type of serial dependence
characterizes Twigg’s historical account as a whole (far more than
Gasquet’s and Ziegler’s monographs).
The demographic history of Provence has been written, although
Twigg has not taken account of this. According to E. Baratier, the expert
on Provence’s medieval and early modern demography, the city of
Marseilles contained only about 15,000 inhabitants in 1315, and pre-
sumably also on the eve of the Black Death,152 a piece of information
that at the time Twigg wrote his theory had been available for almost a
generation, and was also available to Ziegler. Thus, Twigg is prepared to
accept and to convey to his readers the suggestion that five times as
many people died in the Black Death in Marseilles in one month of the
epidemic as actually lived there. According to Baratier’s study, 52–3 per
cent of the householders in Provence died in the Black Death, both in
the urban centres and in the countryside,153 which corresponds to a
population mortality rate of about 60 per cent.154 This means that Twigg
by ignoring Baratier’s work avoids citing this order of population mor-
tality for a large region and explaining how it can be compatible with
the mortality rates of anthrax. He has also failed to find empirical data
showing or at least suggesting the concomitant raging of an anthrax
epidemic among cattle and sheep and to demonstrate that there is close
contemporaneity between the spread of the Black Death among human
beings and the spread of an anthrax epizootic.
Twigg’s account of the Black Death’s spread out of Marseilles, a mile-
stone in its history, and its extension into a much broader picture of its
spread across large parts of Europe is also wrong.155 The crucial point is
151
Gasquet 1908: 39.
152
Baratier 1961: 66–7.
153
Normal demographic adjustments with respect to the population growth in the
time between the end of the epidemic and the writing of the registers indicates rather
a mortality among the householders of 54–55 per cent.
154
155
Twigg 1984: 55–62; Benedictow 2004: 126–45.
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his untenable assumption that bubonic plague spreads only by contact

between contiguous rat colonies: “If it is assumed that rat populations
were contiguous throughout the region—and they would need have
been—the rate of spread across France is as follows […].” It is this false
premise, the denial that bubonic plague spreads over distances by met-
astatic leaps by rat fleas in clothing, luggage or merchandise, which
permits Twigg to construct obviously untenable spread rates from
Marseilles to Carcassone or from Carcassone to Bordeaux or from
Marseilles to Avignon or from Avignon to Lyon, or from Marseilles to
Paris, thus producing phoney proof that the Black Death cannot have
been bubonic plague. All his indications of the Black Death’s time of
arrival at these locations are systematically erroneous and his spread
rates correspondingly misleading. According to Twigg’s account, the
Black Death spreading northwards from Lyon should have broken out
in Burgundy in July and August and inexplicably have reached Paris in
time to break out there in June. However, the Black Death did not break
out in Paris in June, but towards the end of the third week of August.156
This highlights the important fact that the Black Death did not spread
from Marseilles to Paris, but from Rouen to Paris,157 because it arrived
in Rouen with a ship from Bordeaux by an instance of a metastatic leap,
and produced an outbreak which began 24 June.158
Twigg’s rejection of the notion that bubonic plague spreads by leaps
and acceptance of obsolete miasmatic and erroneous information on
the spatio-temporal progression of the Black Death across Europe
combine to make his discussion of the events in his own country quite
absurd. He seems to accept that the Black Death broke out first in the
southern seaport of Melcombe Regis (Weymouth), shortly before 24
June, referring indirectly to the Grey Friars Chronicle which provides
this information, but then all reason evaporates. “There can only be
speculation about where it came from,” he asserts, although it is une-
quivocally stated in the Chronicle with some concrete detail that it came
with a ship from Gascony.159 This is normally and reasonably taken to
mean that the Black Death was brought to England by a ship from
156
Benedictow 2004: 107–8; Dubois 1988: 316.
157
Benedictow 2004: 97–9, 101–8. Cf. Dubois 1988: 314–6.
158
Twigg states that the source for his (misleading) presentation of the Black Death’s
spread out of Paris is Gasquet’s monograph of 1908, however his text is very close, al-
most a verbatim, rendering of Ziegler’s account which is largely but not entirely based
on Gasquet’s account. Twigg 1984: 56–7; Ziegler 1969: 64–5. Cf. Gasquet 1908: 39–53.
159
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Bordeaux where the Black Death had been raging for several months.160
Rouen was infected by a ship from Bordeaux which caused an outbreak
there almost simultaneously with the outbreak in Melcombe Regis
(Weymouth). However, Twigg speculates that the contagion could have
been shipped from Calais to Melcombe Regis, although the Black Death
broke out in Calais in December, half a year later than in Melcombe
Regis.161 He also speculates that the Black Death could have arrived in
Melcombe Regis from northern French ports or the Channel Islands.
The earliest outbreak in a northern French port is the outbreak in
Rouen which does not precede but is about simultaneous with the out-
break in Melcombe Regis, which could suggest that these two seaports
were contaminated by ships sailing from Bordeaux in the same convoy,
as merchant ships often did at the time.162 The suggestion of an origin
in the Channel Islands is not based on a dateable source and cannot be
used for determining the Black Death’s time of arrival.163 Twigg assumes
also that the Black Death could have been on board ships sailing directly
from the Mediterranean. This implies that at a time of unique disaster
and immense difficulties for organizing great trade expeditions, galleys
should have left Genoa or Venice unusually early for a voyage of roughly
4500 km for the Genoese with a duration of roughly three to four
months and substantially longer for the Venetians. If the disease they
brought with them had been anthrax, the voyage would have taken
place with contaminated herds of live cattle or sheep on board which
immediately on arrival alongside the quay of the harbour of Melcombe
Regis would have to be driven through England. I cannot imagine how
this disease could function on board among animals and men for such
a long journey, but the burden of proof is on Twigg. Twigg goes on to
cite other chroniclers with later datings of the original outbreak in
England and other ports of arrival, although none of these alternatives
are compatible with the known pattern of early spread in England
which is based on the sources.164
160
Benedictow 2004: 101–4,
161
Biraben 1975: 74; Dubois 1988: 316; Benedictow 2004: 108.
162
According to the information provided by the chroniclers, plague broke out in
Melcombe Regis shortly before 24 June, in Rouen about 24 June, a small difference in
time which probably reflects the fact that Rouen was a considerably larger urban cen-
tre, a city of some 30,000 inhabitants; quite likely these two urban centres were con-
taminated at the same time.
163
Ziegler 1970: 125.
164
Benedictow 2004: 126–34, 137–40.
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Twigg’s account of the spread of the Black Death in England is unten-

able, as shown also above in the chapter on seasonality.165 The main
reason is that Twigg bases his account of the Black Death’s spread across
England on the false assumption that spread over land was dependent
on rat-to-rat contact, according to the scholarly myth he pioneered that
bubonic plague spreads only between contiguous rat colonies. This
enables him to assert correctly that this mechanism of spread could not
produce the observed pace of spread, “not even one and a half miles
per day.” Actually the average pace of spread on the ground of the Black
Death in England was substantially slower, about 1–1.5 km a day, which
still is much faster than the spread rate between conterminous rat colo-
nies.166 Twigg denies that human beings perform the central role in the
spread of plague by transporting infected rat fleas in clothing, luggage
or goods, by ship or by land, bringing about metastatic spread. His con-
clusion is therefore based on the denial of fact. This argument is taken
over by Scott and Duncan: they accept unconditionally his account of
the spread of the Black Death in England.
Twigg’s Demographic Argument
It is important for Twigg to argue for the lowest possible level of mor-
tality in the Black Death in the hope that it will not be obviously incom-
patible with his highly exaggerated and speculative assertions of
mortality causable by anthrax (see above). In his view, the “mortality in
the years 1348–9 has frequently been exaggerated and treated as though
no other epidemic periods could be compared to it.”167 For this view he
provides no reference. At the time Twigg was writing his monograph,
there was a broad consensus on the level of mortality caused by the
Black Death, namely Hatcher’s estimate of 1977 in a small but outstand-
ing book on the interaction of economic, demographic and plague-
related developments in late medieval England. Highly conscious of
the fact that the vast majority of the population was constituted by peas-
ants in the broadest sense of the term Hatcher based his estimate mainly
on manorial and other types of local mortality data. However, due to
a certain paucity of data he also underlines the significance of the
165
Twigg 1984: 57–68; Benedictow 2004: 126–45.
166
Twigg 1984: 58; Benedictow 2004: 142, cf. 229–31.
167
Twigg 1984: 72.
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mortality rates for the beneficed clergy who had much the same
territorial distribution but highly different characteristics as a social
category. He concludes that this material bears “testimony, with a lack
of precision but a compelling force, to a death rate of at least 30–5 per
cent,” and that the “most judicious estimate of the national death-rate
in 1348–9 in the present state of knowledge: 30–45 per cent.”168 In
Hatcher’s view, the minimum mortality level was thus about a third of
the population, the average apparently nearly 40 per cent. One should
note that Hatcher in the gentlemanly tradition of Oxbridge academics
seeks a cautious balance of the facts with respect to the mortality esti-
mate, which makes J. Titow, the highly regarded English agricultural
historian, remark in his review of the book that “it is difficult to see on
the evidence here assembled, how it could have possibly been any
lower.”169 Obviously, this level of mortality was much too high to be
compatible with Twigg’s theory.
Presumably, this is the reason Twigg turns instead to Russell’s pio-
neering monograph British Medieval Population of 1948 for his mortal-
ity data. This means that he must pass in silence by the comprehensive
and sharp criticism of this work and also much fine new research that
had been published in the following thirty-six years. Russell engages in
little source-criticism and he makes a number of assumptions with
respect to central demographic structures and developments that have
been quite generally rejected in the discussion following the mono-
graph’s publication. In 1969, T.H. Hollingsworth generously concluded
that “Russell’s chief virtue, in fact, is that he gives others something to
refute. All his figures may be altered eventually, but the debt to him will
remain.”170 Or as Hatcher also elegantly formulates his view: “One of
the major sources of nonconformist beliefs is the work of J.C. Russell.”171
For quite a number of solid scholarly reasons, the mortality figures
have been subjected to particularly damaging criticism, for instance by
M. Postan, G. Ohlin, and Hatcher.172
In this context, the very special nature of Russell’s material on
mortality in the Black Death must be strongly emphasized. It relates to
the mortality among tenants-in-chief, the supreme and extremely
168
Hatcher 1977: 21–6.
169
Titow 1978: 466.
170
Hollingsworth 1969: 58.
171
Hatcher 1977: 13.
172
Postan 1966: 561–2; Ohlin 1966: 78–80; Hatcher 1977: 23–4.
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exclusive class of feudal nobles who held land directly from the king,
the barons of the realm; he based his research on a category of docu-
ments called inquisitions post mortem which effectuated the transfer of
such feudal land following the death of the possessor (in the epidemic).173
The social unrepresentativeness for inference to general mortality and
distribution of mortality according to age, gender and social class more
generally is overwhelming. It contrasts sharply with Hatcher’s endeav-
ours, in accordance with the basic tenets of sociology and demography,
to base his general mortality estimate as much as possible on data rep-
resentative of the social classes constituting the vast majority of the
population.
Technically, Russell used a population of tenants-in-chief of 505 per-
sons of whom 138 or just over 27 per cent died, but this figure is beset
by severe problems.174 The mortality of 138 tenants-in-chief is much
too small to constitute a base for reliable statistical inferences and too
unrepresentative both with respect to social class and with respect to
age to be of any use for generalizations with respect to general mortal-
ity or mortality according to age or gender.175 Conspicuously, 23 per
cent of the population of tenants-in-chief died in the following plague
epidemic of 1361–2, despite general agreement that this was a much
smaller epidemic: Hatcher is obviously right in his conclusion that this
reflects the fact that the samples are too small to provide useful
statistics.176
With respect to the younger age categories, this material is so tiny
that estimates of mortality based on it or including it must be rejected
as useless. It comprises no infants who, in the case of males according
to Model West life table, level 4 (life expectancy at birth of 25 years), are
liable to a normal mortality rate of 32 per cent,177 but according to these
statistics astonishingly suffered no case of mortality in the year of the
Black Death. Ages 1–5 are represented by three children of whom one
died making for a mortality rate of 33 per cent for these five age catego-
ries, which is, of course, a valueless exercise in statistics. Only one of
thirteen children of ages 6–10 died, producing an incredibly low
mortality rate of 7 per cent in the Black Death, whilst, according to the
173
Russell 1948: 214–8.
174
Russell 1948: 216.
175
See, for instance, Hatcher 1977: 24. Cf. above: 421–2; Benedictow 2004: 342.
176
Hatcher 1977: 23–4.
177
Coale and Demeny 1983: 43. See, also, Benedictow 2004: 249, 350.
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life table, normal mortality in these ages would be 19.5 per cent.178
According to Russell’s material, children of these ages had the luck to
have only a small fraction of their normal mortality in the year of the
Black Death. This is the reason I have previously rejected using the
material gathered by Russell for mortality estimates.179 Hatcher points
out that, according to evidence from the chronicles, the Black Death
“struck mainly at people in the prime of life” but underlines carefully
the great uncertainty associated with this type of evidence.180 However,
a few years later Z. Razi’s study of the manor of Halesowen appeared,
which Twigg could have put to good use. Here Razi concludes that “the
child mortality in the Black Death was very heavy,” that, in fact, “child
mortality in the plague must have been catastrophic.”181 Quite a number
of pages away from his table, Russell points out that the “chroniclers
have to tell of very heavy mortality of children.”182 However, using a
wording echoing Russell’s own endeavours to minimize the impression
of seriously flawed material183 and ignoring the severe criticism of it,
Twigg notes with considerable understatement that this material con-
stitutes “an unfortunately small sample,”184 (unfortunately) without
specifying the methodological and source-critical implications of the
characteristic “unfortunately.” This permits Twigg to proceed to use
Russell’s material as if the sample is not “unfortunately small,” as if it is
not too small and mortally flawed for almost any demographic use.
Undaunted, Twigg goes on to use Russell’s estimates both of general
mortality and age-distribution of mortality in the Black Death. He
starts with age-distribution which, according to demographic science,
is particularly demanding with respect to the quality of material. His
point of departure is the valid argument that diseases vary in the mor-
tality rates they inflict on specific age classes and “if this information is
available and is accurate it can be of some assistance in helping to nar-
row the field in the identification of past epidemics.”185 Surprisingly,
178
See Benedictow 2004: 350.
179
Benedictow 2004: 342, 350.
180
Hatcher 1977: 24.
181
Razi 1980: 104.
182
Rusell 1948: 231.
183
Russell 1948: 262. “The information from the table (10.13) suffers from being a
relatively small sample.”
184
Twigg 1984: 63.
185
Twigg 1984: 63.
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Twigg pretends that such information is “available” and “accurate” in

the form of Russell’s figures, which is at variance with all comments by
other scholars. Russell concluded that the plague fell more heavily on
older men than on the young.186 G. Ohlin, the demographer, challenged
this conclusion, and demonstrated that Russell’s source-critical and
statistical approaches were flawed and that age, according to this source
material, made no difference to this particular risk of death in this
social class,187 a piece of important information that was available to
Twigg but is ignored or overlooked. This means that Twigg’s age-
specific premise is untenable.
However, this is only a disappointing beginning. Twigg goes on to
argue that the Black Death and bubonic plague in India around 1900
were different diseases. He asserts that this can be demonstrated by
comparing Russell’s table showing the age-distribution of the mortality
in the countryside among the English baronial class in the Black Death
in 1348–9 and a table produced by the IPRC in 1907 showing mortality
in bubonic plague in Mumbai City among a caste-structured popula-
tion consisting mainly of poor and destitute social classes.188 On this
basis, he concludes that it is “clear without any elaboration that there is
considerable difference between these two disease mortality patterns”189
and that this constitutes evidence that the Black Death could not have
been bubonic plague, but must have been some other disease. Ignoring
for the moment the devastating criticism of Russell’s material, this rep-
resents neglect of basic sociology and social science as integral parts of
demography and epidemiology. It would have been sensational at least
or rather inexplicable if these two tables had showed similar distribu-
tion of age-related mortality. The only acceptable usage of such a com-
parison is to demonstrate the differentiation of mortality pattern caused
by great disparity in social, economic, political and cultural circum-
stances. It is exactly the absence of “elaboration” according to social
science that permits Twigg to make this inference. On the same page,
the IPRC gives mortality figures distributed according to religion
showing strong differentiation of mortality according to this criterion
186
Russell 1948: 216–7.
187
Ohlin 1966: 78–80.
188
Since Twigg does not provide a footnote to this comprehensive material pub-
lished by the Commission this year (which may suggest a secondary source of informa-
tion), I will give it: IPRC 1907g: 763.
189
Twigg 1984: 63–4.
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alone.190 This use of Russell’s data is uncritically taken over and pre-
sented by Scott and Duncan as proof that the Black Death could not
have been bubonic plague because in comparison to the epidemic real-
ities in India “the overall mortality of bubonic plague is much lower”
and “killed predominantly those in the 6–40 year age group.”191 If Scott
and Duncan had taken interest in English medieval demography which
is at the heart of the matter here, they would have known that in a
population with an average life expectancy at birth of around 25 years
the “6–40 year age group” constituted the predominant proportion of
the population.192
Next, Twigg turns to the question of general population mortality.
Russell dares to claim that the mortality of the nobility is representative
of general population mortality. This assertion must be dismissed out
of hand, which has been emphatically done by several scholars.193
Inference to general population mortality on the basis of this material
is an obvious fallacy of the methodology of social science. The assertion
flies in the face of one of the central findings of demography, namely
that mortality across European society in time and space tends to be
strongly skewed according to age, gender and social class. The general
predilection of the Grim Reaper for infants, young children, poor and
destitute people, and his relative lenience with the upper classes, are
documented beyond all reasonable doubt or dispute. Russell argues,
also erroneously, on the basis of the skewed age-structure of his data
that real mortality must have been lower than the 27 per cent shown by
his material (138 deaths among 505 tenants-in-chief).194 Using in addi-
tion the Poll-Tax registers of 1377 for retrospective analysis, in a way
that has also been severely criticized,195 he concludes with a mortality
rate for tenants-in-chief of 20 per cent, which is directly transformed
into an estimate of general population mortality. This estimate is enthu-
siastically accepted by Twigg as the point of departure for his own
discussion of the level of mortality, disregarding Hatcher’s serious
190
IPRC 1907g: 763–4.
191
192
See, for instance, Benedictow 2004: 249.
193
See. e.g., Titow 1969: 68; Hatcher 1977: 22–4; Razi 1980: 100; Benedictow 2004:
342.
194
Russell 1948: 216, 230.
195
Postan 1966: 561–2; Hatcher 1977: 13–4; Titow 1969: 67–8, 84–5; Benedictow
2004: 259–60.
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warning: “there are strong reasons for believing that Russell’s estimates
of English population in 1348 and 1377 are gross understatements.”196
Russell’s estimate can be dismantled in various ways, not only on the
basis of the small size of the material and of its lack of social diversity
and representativeness. Twigg must be the only scholar in the last sixty
years who accepted Russell’s contention that average household size in
medieval England was 3.5 persons, and not 4.5, which alone makes for
a difference of almost 30 per cent in population size. On this basis,
Russell estimates England’s population on the eve of the Black Death at
3,757,000 inhabitants. This estimate differs sharply from Hatcher’s esti-
mate in his widely admired account of 1977, a generation later, of
“4.5–6 million, with the balance of possibilities pointing to the higher
reaches of this range.” Already the following year, in a study therefore
also available to Twigg, the minimum side of this estimate was revised
upwards by E. Miller and Hatcher to 5–6 million people, an estimate
with which R.M. Smith agreed a decade later.197 This development
regarding pre-plague population estimates casts sharp light on the
weakness inherent in Russell’s pre-plague population estimate. This is
also the case with later estimates of late medieval English population
size. In 1988, Hallam revised the population estimate further upwards
to about six million inhabitants on the eve of the Black Death, with
which again Smith agreed a few years later,198 and this is the present
status of research on which there is broad agreement among British
scholars in the field of medieval demography; Hatcher and Bailey also
appear close to accepting this figure in 2001.199 On the ground of popu-
lation estimates alone, mortality in the Black Death must have been
very much higher than Russell claimed. According to Russell, the
English population was around 2.25 million immediately following the
Black Death,200 an estimate which is quite close to prevailing scholarly
opinion. This means that, at the time Twigg wrote his monograph,
combining the prevailing scholarly opinion on pre-plague population
size and Russell’s post-plague population estimate, the mortality caused
by the Black Death had reduced the population from 5–6 million to
196
Hatcher 1977: 13.
197
Hatcher 1977: 68; Hatcher and Miller 1978: 29; Smith 1988: 191. Cf. Miller and
Hatcher 1995: 393; Hatcher and Bailey 2001: 31.
198
Hallam 1988: 536–7; Smith 1991: 48–9.
199
Hatcher and Bailey 2001: 31.
200
Russell 1948: 263.
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2.25 million, or by 46–62.5 per cent. Shortly afterwards, the population

estimate of about six million on the eve of the Black Death was
confirmed and accepted, meaning that the figure of 62.5 per cent was
confirmed according to the premises laid down here. This is exactly the
figure at which I arrived on the basis of my analysis of seventy-nine
manorial studies,201 most of which were available to Twigg at the time
he wrote his monograph. Why did Twigg not collect the data on mano-
rial mortality rates as I did, providing a broad picture of mortality
among the peasant classes who constituted the vast majority of the
English population? As my data unequivocally show, the mortality rate
among the customary tenants who represent the upper classes of peas-
ant society must have been in the order of 55 per cent. Supermortality
among the rural proletariat, the all-but-landless classes and among
children and women means that the real population mortality rate
must have been significantly higher.202
In addition, at the time Russell and Twigg wrote their monographs
the mortality rates of the beneficed parish clergy was known to be at
least or close to 40 per cent, which Russell in reality gives up on explain-
ing.203 Twigg makes considerable efforts to undermine the mortality
studies based on institutions of the beneficed clergy during the Black
Death. He starts by asserting erroneously: “It is generally accepted that
the vacation of a benefice automatically implies the death of the incum-
bent and some writers have assumed that all vacations during 1348–9
were due to death from plague.”204 This has, as mentioned, certainly not
been true since Seebohm’s work of 1865 and possibly until Gasquet’s
monograph appeared in 1893 where it is made clear that vacancies
were due not only to death but also to “exchange, or resignation”
and that such cases must be deducted.205 Twigg’s statement is fol-
lowed by a reference to Thompson’s work of 1947 on the organization
of the English clergy in the Late Middle Ages. However, the point that
vacancies were due also to resignations, exchanges of livings, plurali-
ties206 and absenteeism is strongly emphasized by Thompson in his
201
202
203
Russell 1948: 221–2, 230.
204
Twigg 1984: 59.
205
Gasquet 1908: 86.
206
The concept of plurality refers to the quite frequent occurrence that the incum-
bent also held (an)other benefice(s) and was represented in the parish by his vicar.
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pioneering studies of 1911 and 1914 of the registers of institutions of

the dioceses of Lincoln and York.207 This has since been generally taken
into account by scholars; Hatcher for example states that “one has to be
especially careful to eliminate all vacancies excepting those arising
from death.”208 However, if Twigg had mentioned Thompson’s two
excellent studies, it would be difficult for him to avoid mentioning that
after having taken these problems of resignations of vacancies into
account and deducted them from the material, Thompson still found
mortality rates of 40.2 and 44.2 per cent respectively, without taking
into account institutions in vacancies caused by the Black Death per-
formed in the following couple of years, which would have added sub-
stantially to the mortality rates (see above). Lunn’s study of the diocese
of Coventry and Lichfield’s bishop’s register where also all resignations
are noted have produced a mortality rate of 40.1 per cent, likewise
without taking into account Black Death-related institutions in vacan-
cies which were filled in the following couple of years. Pickard found a
mortality rate among parish priests in the diocese of Exeter of 51.5 per
cent in the period of the Black Death, but when surplus institutions
after deduction of normal mortality in the following years are taken
into account, the real mortality rate appears to have been about ten
percentage points higher. Resignations have been found in the diocese
of Ely’s bishop’s register and the two studies performed on them have
reached mortality rates of 57 and 60 per cent respectively, which should
make mortality at around at least the same level certain whatever
the possible inaccuracy of the registration of resignations and other
causes of vacancies.209 In sharp contrast to Twigg’s account, Hatcher
concluded in 1977 that “great weight must be attached to a revised
average death-rate of around 35–40 per cent for beneficed clergy.”210
None of these mortality figures for the beneficed clergy in various
dioceses is below 40 per cent and the average must be something
like 45 per cent. Thorough source-critical and epidemiological discus-
sion of the mortality among the beneficed clergy in my monograph
on the Black Death led me to conclude that the available data summa-
rized in Table 31211 should be considered “minima or more likely
207
Thompson 1911: 303–4, 315–6; Thompson 1914: 97–102.
208
Hatcher 1977: 25.
209
210
Hatcher 1977: 25.
211
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underestimations,”212 with the implied suggestion that the real mortal-

ity rate was on the order of 50 per cent. After having gone thoroughly
over the studies and evidence cited above a second time, above I con-
clude that the mortality rate probably was even higher when Black-
Death-related vacancies which were filled in the following years are
consistently taken into account. The discrepancy between these esti-
mates and Hatcher’s is not the important point here, which is what
Twigg should have known and taken into serious consideration at the
time he was writing his monograph, and the fact that the available esti-
mates of mortality among the parish clergy would have had damaging
consequences for his theory. How could it be that the mortality of ten-
ants-in-chief in the Black Death should be under half of the average
mortality among the regular clergy of a dozen monastic houses built of
stone like the castles of the lay lords, namely 45 per cent?213
Twigg mentions Hatcher’s population mortality estimate of 1977 of
30–45 per cent, especially his central estimate of 35–40 per cent but
neglects to take it into account.214 The way this is justified should be
considered: Twigg asserts that “Hatcher considered that the estimate
produced by the E.A. Kosminsky (1955) of a national death rate of
30–45 per cent is the most reasonable one.” This is not correct, the
estimate is entirely Hatcher’s own based on an independent, cogent
and thorough discussion of sources, studies, data and problems.215
Kosminsky, the Soviet historian of the Academy of Sciences in Moscow,
does not make any population estimate for any time in the High Middle
Ages or in the Late Middle Ages. On the contrary, Kosminsky rejects
the notion that there was a long-term late medieval sharp population
reduction. He acknowledges that there was a “decrease in population in
the 14th and 15th centuries,” however, he maintains that it was not
“directly related to the Black Death of 1348–9 and the epidemics of the
1360s” since “the decline in population began earlier than the Black
Death, and that it continued longer than could be accounted for by the
results of the plague.” Instead, Kosminsky launches his own doctrinaire
Marxist explanation of a population decline based on the evolution of
feudal rent, class struggle, a crisis of feudalism, the development of
212
213
Hatcher 1977: 22.
214
Twigg 1984: 72; Hatcher 1977: 25.
215
Hatcher 1977: 21–5.
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“the labour service system,” and “especially burdensome forms of

exploitation,” “a further intensification of serfdom,” “the most intense
feudal exploitation of the English peasantry” and, finally, the conclu-
sion: “The growth of feudal exploitation began to exhaust peasant agri-
culture and at the same time to whittle down the productive forces of
feudal society, destroying the conditions for reproduction of the labour
force.”216 Thus, according to Kosminsky, the real reason for the late
medieval population decline, in the modest form which he accepts, was
caused by the intense exploitation of the peasantry within the frame-
work of feudal society and its detrimental effects on reproduction
among the peasant classes. Does Twigg cite this misleading assertion
about the source of Hatcher’s mortality estimate because he needs to
discredit Hatcher’s estimate, since it is incompatible with his anthrax
theory? Why does he associate Hatcher’s estimate with Kosminsky’s
dogmatic Marxist analysis which Hatcher, in fact, dismisses out of
hand?217
Only four years after Twigg’s monograph was published, Smith
increased the estimate of mortality in the Black Death to around 50 per
cent on the basis of much the same data that were available to Twigg.218
It was just a question of taking a serious and unprejudiced interest in
the subject. Without going into the matter in further detail, we can be
certain that the available data at the time Twigg wrote his monograph
had made it clear that the level of mortality, the generalized mortality
rate in the Black Death, was very much higher than Russell had
claimed.
This explains Twigg’s curious emergency landing in Russell’s unten-
able and obsolete mortality figures: all other current and reliable data
and discussions of the subject at the time he was writing his mono-
graph showed such high mortality rates in the Black Death that they
would directly invalidate his anthrax theory. Only this can explain
Twigg’s statement that
Earlier estimates of a death rate of one- to two-thirds of the population
through plague (Seebohm, 1865; Gasquet 1908) have been reviewed and
modern work shows that the population had begun to decline before
216
Kosminsky 1955: 14, 22, 32. He repeats this analysis a few years later, see
Kosminsky 1957.
217
Hatcher 1977: 12–3.
218
Smith 1988: 208–9. Cf. Benedictow 2004: 342–77.
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1348 and that the plague losses in 1348–50 were perhaps nearer 20 per
cent of the population (Russell, 1948).219
In order to save his theory, Twigg must compare Russell’s figures, which
at the time he wrote his book were more than a generation old, and
throughout this period had been generally rejected, with studies
published in 1865 and 1908, passing by all relevant later scholarly
works, and all scholarly work on the topic between 1948 and 1984.
Instead, it should have been clear to Twigg for quite a number of years
that Seebohm’s and Gasquet’s estimates were still respectable, even had
gained in respectability, especially if it is taken into account that they
both tended to give priority to a mortality rate of around 50 per cent,
the magnitude of the population loss in the Black Death which Smith
arrived at in 1988.220 The pre-plague population estimate of five million
used by Gasquet is also much closer to modern population estimates
than Russell’s and the post-plague estimate of something like 2.5 mil-
lion corresponds quite closely to modern estimates.
However, Russell’s untenable and generally rejected estimate was
still too high for Twigg and could still serve as grounds for falsification
of his theory or at least for rendering it highly improbable. Taking into
account the normal lethality rate of anthrax, a population mortality
rate of 20 per cent would imply quite unrealistically that every person
in England of whatever social class, gender or age, had eaten anthrax-
contaminated meat. This is the reason Twigg needs arguments for fur-
ther reductions of the estimate of the specific mortality caused by the
Black Death. He argues that one must also take into account “the pres-
ence of a variety of infectious and other diseases, the twenty per cent
reduction of the population must include these and cannot be attrib-
uted to plague alone.”221 Twigg wisely does not attempt to indicate how
many percentage points he would like to deduct on the basis of this
argument but leaves it to the reader to make a substantial further
deduction on the impression of a plethora of serious infectious diseases
and other diseases that affected population mortality. According to
demographic science, Twigg’s argument here really concerns normal
mortality in the period which should be deducted in order to produce
an estimate of the net mortality effect of plague in the period of the
219
Twigg 1984: 70–1.
220
Hollingsworth 1969: 264; Gasquet 1908: 225–7, 237–8.
221
Twigg 1984: 72.
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Black Death. However, Russell has already deducted normal mortality!

Assuming (erroneously) that the Black Death lasted for three years,
1348–50222 he states: “The reduction of the initial loss to 20 per cent
proceeds from better calculation of plague losses, which could take
into account age specific mortality […], discounting of ordinary
mortality of the three years and avoidance of other statistical difficul-
ties.”223 Thus, in order to produce as low a mortality rate as possible,
Twigg deducts twice the normal mortality in the period of the Black
Death. The mortality rate of 20 per cent and the information on deduc-
tions stand on the same page and in direct connection as qualifying
explanations of the concluding mortality rate.
Correcting for age-related bias in his original material, Russell
reduced his original estimate of mortality among tenants-in chief from
27.3 per cent to 23.6, which shows that Russell made a deduction for
ordinary mortality in the three plague years of 3.6 per cent.224 Russell
reduced this mortality estimate further, as mentioned, to 20 per cent by
using the Poll-Tax registers of 1377 for retrospective analysis. This
means that Twigg would like to arrive at a net plague mortality figure
of 16.4 per cent. However, fearing that this is not a sufficiently low mor-
tality rate to be suitable for making a convincing case for anthrax,
Twigg presents the following speculative argument: “It is not beyond
the bounds of possibility that more than one new and exceptionally
virulent disease organism invaded Europe during this period.”225 One
may legitimately wonder what Twigg thinks he can gain for the defence
222
In England, the Black Death broke out shortly before 24 June 1348 and lasted
into the late autumn of 1349 that is, somewhat less than a year and a half.
223
Russell 1948: 367.
224
Russell 1948: 216. Distributed on three years, Russell’s deduction for normal
mortality implies a notion of normal yearly mortality at the time of c. 1.2 per cent, a
figure I find difficult to understand, although it presumably relates to the untenably low
normal mortality rates, also according to Russell’s own reactions, emerging from his
material on tenants-in-chief. Russell 1948: 210–1. A normal annual mortality rate of
3.6 per cent is quite usual for the early modern period, especially the eighteenth cen-
tury, in Western and Northern Europe. In an epoch-making paper for medieval demo-
graphic research, Hatcher has shown beyond any doubt that late-medieval normal or
average mortality rates were much higher than corresponding early-modern mortality
rates. Hatcher 2003. His views correspond closely to my own views, Benedictow 1996b:
29–91, 189–91. Benedictow 1996c: 156–74; Benedictow 2003: 238–44; Benedictow
2004: 250–6. Russell’s deduction for normal yearly mortality and Twigg’s should have
been significantly higher.
225
Twigg 1984: 72.
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of his theory by forwarding this arbitrary idea without any empirical or

evidentiary support.
Concluding Remarks
In a paper published in 1996, Scott and Duncan supported or were at

least attracted to Twigg’s anthrax theory with respect to their discussion
of an epidemic in Penrith and the surrounding region in the 1590s
which contemporaries called plague. In their discussion of this theory,
the difficulties remain unresolved in incompatible statements on the
characteristic or defining features of anthrax. They start by asserting
that anthrax “can be spread easily from person to person”226 and make
on this basis a number of quite strange speculative efforts in order to
produce an epidemiological theory to this effect. However, on the
next page they point out that “human infection is almost invariably
from animal sources.”227 Clearly, Scott and Duncan eventually recon-
sidered their support for Twigg’s anthrax theory and invented their
own theory.
All the other advocates of alternative theories reject Twigg’s theory
(as they all reject each other’s theories). Karlsson rejects it on the
ground that “no mortality of any kind of animals is ever mentioned in
the [Icelandic] annals.”228 This is not correct: serious epizootics causing
great mortality among the cattle and the sheep respectively in the island
are mentioned in the annals, in fact they were so serious that they
caused widespread starvation and also considerable mortality among
the human population since “many farmsteads were deserted.” As it is
said that this occurred when “no ship arrived from Norway,” the source
of the infections must have been internal in the island.229
Twigg has presented an alternative theory of the microbiological
nature of historical plague with such significant epidemiological and
historical flaws that it has been generally rejected as an obviously
untenable theory. Nonetheless, Karlsson, Scott and Duncan, and Cohn
credit him with the great epidemiological erudition and insight to have
shown in a definite way that the Black Death could not have been
226
227
228
Karlsson 1996: 281.
229
See, for instance, Islandske Annaler 1888: 324, 383.
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rat-borne bubonic plague. The reason is that Twigg’s rejection of his-

torical plagues as being bubonic plague functions as a justification for
the construction of their alternative theories.230
230
Cohn asserts that I, like some other named scholars, “cite Twigg in their bibliog-
raphies but in their texts give his arguments no hearing at all.” Cohn 2002: 53. This is
not true, as all other of his comments on my thesis. At the time I wrote my thesis,
Twigg’s theory had not received any favourable comments from other scholars, which
constituted a case for not focusing on it in a thesis aimed at clarifying the microbiologi-
cal identity of medieval plague in the Nordic countries. In this situation, it appeared
appropriate to focus on what disease medieval plague could have been and not on
what was agreed that it could not have been. However, I have not passed Twigg’s theory
by in silence as Cohn asserts. I point out that the “suggestion of anthrax has not
attracted any support for obvious reasons” and assume in good faith that it is a good
argument that, “according to the standard works on microbiology, ‘the mortality rate is
low and the great majority recover in a few days’ .”230 At the time, I could not foresee the
necessity or potential usefulness of detailing my views on Twigg’s monograph. Nunc
factum est.
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CHAPTER FIFTEEN
THE ALTERNATIVE THEORY OF SCOTT AND DUNCAN
Introduction
Scott and Duncan are an historian (historical demographer) and biolo-

gist respectively. They present their alternative theory in two works
with the character of monographs published in 2001 and 2004. The first
monograph must be considered the principal work; the second is
mainly an abridged and popularized version of the first. However, it
also contains new developments and changes of opinion on important
points which remain empirically unsubstantiated and unexplained.
These works have an academically unsatisfactory form. In the first
monograph they do not provide the usual apparatus of footnotes, but
like Twigg, refer to works in parentheses in the running text without
indication of pages, which makes the task of checking the correctness
of the references extremely difficult and time-consuming. It is also a
form that is poorly suited to multiple references and for enlarging or
deepening comments. It is not possible within a reasonable time frame
to read whole monographs or papers in order to hunt down purported
passages of support or objects of criticism. It might be argued that
scholars who know the relevant studies intimately after decades of dili-
gent work in this field of research will have great advantages, but this
should not be the case. According to the standards of scholarly work,
every point or assertion should be easily testable by students as well as
by scholars, by every reader irrespective of background. This problem
is aggravated because many assertions or pieces of purported informa-
tion are not accompanied by any reference. The first book contains a
bibliography, but many of the works entered in it are not referred to in
the text and quite a number have no direct bearing on their alternative
theory. In their second monograph, Scott and Duncan have dispensed
completely with references and bibliography. It is implied that one
should start by reading their first monograph on this topic, but this
makes the idea of writing a popularized version for amateur historians
and enthusiastic readers of history a bit pointless, and so this mono-
graph also has an unsatisfactory form as popularization. This contrasts
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the alternative theory of scott and duncan 611
sharply with the pervasive effort made by Ziegler to make his popular
history of the Black Death in England readily testable (although he was
not an historian by profession).
In the prefaces to their monographs, Scott and Duncan refer to
Twigg as a “stalwart friend,” “salute” his “pioneering work and acknowl-
edge gratefully his generous help in the early stages of this project.”1
They also state that he “was the first to recognize that the Black Death
was not an outbreak of bubonic plague,” presenting this conclusion as
a point not open to doubt, as would be the ordinary scholarly attitude
for good methodological reasons. Inevitably, this attitude means that
they accept unquestioningly his arguments against the bubonic plague
theory and base this part of their case on his monograph instead of
reading the primary research studies and the standard works on plague
and acquiring independent knowledge (see below). These arguments
are meticulously discussed above both in Part 2, “Basic Conditions for
Bubonic Plague in Medieval Europe” and in relation to Twigg’s work
and theory in the preceding chapter, and have been shown to be gener-
ally untenable or invalid. Here the focus will therefore be on Scott and
Duncan’s theory. However, one should note that, according to their
information, the alternative theory of filoviridal disease was suggested
by Twigg.2 Since this category of disease is as different from anthrax as
well-nigh possible, this implies that Twigg not only has rejected his
own theory of anthrax but also openly admits that this idea must have
been as far intellectually astray in the academic “woods so wild” as
well-nigh possible. It is not clear why his rejection of the bubonic-
plague theory should be any more trustworthy than his sudden radi-
cally different suggestion of an alternative theory.
Disparaging Views of Historians and Physicians: Motive and

Objective
Like other scholars who wish to introduce a revolutionary new theory

in a field of research that has been developed by large numbers of dedi-
cated scholars over several generations, Scott and Duncan have a lot of
rejecting to do. They make a number of sweeping negative assertions
about the work of unnamed plague scholars in general. All or at least
1
Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii.
2
Scott and Duncan 2004: viii.
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612 chapter fifteen
the great majority of scholars who have been engaged in primary plague
research and who have written the outstanding standard text books on
plague and their historical perspectives are inevitably implicated. All
these assertions are untrue, for instance:
Nobody compared the two diseases [historical and modern plague: my
insertion] objectively and for the whole of the twentieth century this
view, based solely on the appearance of one symptom [buboes: my inser-
tion], was written on tablets of stone and universally accepted without
question. […] No scientist should base conclusions or develop a hypoth-
esis on the basis of a single observation or experiment. No doctor would
make a diagnosis on the basis of a single symptom: instead he would
examine his patient carefully […].3
The need to present such untenable accusations is revealing. All the
authors of the standard works on plague, Simpson, Sticker, Wu Lien-
Teh, Hirst, Pollitzer and Butler, present a wide range of clinical mani-
festations of plague and also acknowledge that this was the case with
historical plague epidemics. See, for instance, Hirst’s discussion of this
subject in his monograph. Even Hirst’s citation of the contemporary
Irish Friar John Clyn’s description of plague cases in the Black Death
contains five important clinical features (my numbering): “[…] many
died of [1] boils and abscesses, and [2] pustules on their shins and [3]
under their armpits; [4] others frantic with pain in their head, and [5]
others spitting blood […].” When medieval chroniclers comment on
the Black Death’s physical manifestations they quite often give several
clinical features. When Hirst concludes his discussion of this topic, he
does not refer to one clinical feature, but states: “There can be no doubt,
however, judging from the detailed descriptions that have come down
to us, of the clinical identity of the plagues of ancient and modern
times.” Hirst also mentions other distinguishing features, comparing
the plague pandemics of the Early Middle Ages, the Late Middle Ages
and Early Modern Ages, and the modern pandemic that started in
1894: “All three pandemics spread along the main lines of communica-
tion in a similar way at a similar rate; it seems improbable, therefore,
that their epidemiology can really be very different.”4 To my knowl-
edge, no scholar has focused on buboes alone, although, as shown
above, the normal occurrence of buboes in diseased persons consti-
tutes a defining feature of bubonic plague and, despite Scott and
3
4
Hirst 1953: 13, 121–2.
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Duncan’s disparaging remarks, would suffice as a clinical criterion

allowing certain identification of bubonic plague. This is confirmed by
their own source on bubonic plague, a chapter in a general textbook on
infectious diseases by A.B. Christie5 (see below).
Scott and Duncan go on to make generalized assertions of intellec-
tual incompetence and dishonesty against all scholars who have sup-
ported the bubonic plague theory:
Their universal and unquestioning acceptance of the view that […]
plague was no more than a series of epidemics of bubonic plague […].
This universal and unquestioning acceptance in about 1900 of the view
that haemorrhagic plague [their own theory presented as indisputable
and uncontroversial truth] was no more than a series of epidemics of
bubonic plague was a complete reversal of the opinion that had previ-
ously been held for over 500 years [completely untrue], and the history
books had to be rewritten. Various tales about the plagues had to be
embroidered or even adapted to fit with the new story of bubonic
plague.6
Once blind acceptance of bubonic plague has been abandoned […].7
Not only are medical scholars the subject of such sweeping denigrating
assertions, historians are also collectively belittled for their massive
incompetence and/or intellectual dishonesty, in this case on the basis
of two arguments (my numbering):
Unfortunately, historians of Europe in the 20th century, almost univer-
sally, have concluded that all plagues in the Middle Ages were bubonic, in
spite of the fact that [1] the people at that time saw clearly that it spread
person-to person and [2], even in the 14th century, had already instituted
specific quarantine periods. A major objective of this book is to examine
the historical facts dispassionately, eschewing any preconceived notion
[…].8
The subject of contemporary views of epidemic disease has been dis-
cussed above on several occasions.9 In relation to this quotation, it must
be said that one of the conspicuous features of Scott and Duncan’s
monographs is their negligence of historical epidemiology, how people
in the past attempted to understand the mass occurrence of disease and
5
Christie 1980: 762.
6
7
8
9
Above: 78–82, 342–5.
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614 chapter fifteen
mortality in an area. However, small glimpses of this subject slip out,

inadvertently as it may seem, a few times in their works, implying that
they actually have some real knowledge of it. This occurs first in their
paper of 1996, before their alternative theory was developed, and again
in their first monograph when they cite this paragraph verbatim:
[…] it was believed that ‘miasma’ or noxious vapours in the atmosphere
were responsible for the disease, and that miasma could be retained in
clothes or bedding for long periods and transported, possibly by domes-
tic animals, from house to house (Slack 1985).10
In 2001, they remembered what they had known in 1996 on the basis
of Slack’s fine presentation of contemporary miasmatic views and their
behavioural consequences. Seventy-five pages later in the same mono-
graph, there is another sudden corroborative glimpse, and this time in
an original phrase:
The general populace believed that they caught the plague because the
infection was in the air of the place.11
This glimpse of historical epidemiology is prompted by their wish to
explain away contemporary notions of the short time elapsing between
the infection of a person by plague and the outbreak of the disease,
which is inherent in miasmatic theory, but runs contrary to their arbi-
trary assertion of a very long time of incubation (see below). Then,
another sixty pages later, they describe the anti-epidemic measures
taken by the rector of Eyam:
When the plague was over, Mompesson ordered that all woollen clothing
and bedding should be burnt and he set an example by burning his own
effects so that, as he said in a letter to his uncle, he had scarcely enough to
clothe himself. Presumably they believed that the infection might be con-
tained in the clothing because the symptoms of the pestilence could reap-
pear 3 weeks after a person had died.12
These words make no impression on Scott and Duncan, and on the
next page they reiterate their mantra: “It is clear from the foregoing that
at the time of the epidemic the people of Eyam believed that it was
caused by person-to-person contact.” These glimpses reveal the highly
problematic character of their repeated assertions that people of the
10
Scott, Duncan and Duncan 1996: 19; Scott and Duncan 2001: 145.
11
12
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Middle Ages or the Early Modern Period “saw clearly” that plague
spread by interhuman cross-infection. Instead, when medieval and
early modern people did not believe that epidemic disease was God’s
punishment for their sins, they would alternatively or concurrently
believe or think that it was caused by miasma.
According to miasmatic theory, miasma was composed of poison-
ous vapours from rotting matter which rose from the ground and were
spread by the wind. Miasma could stick to clothing, bedding, and other
objects used by sick people that were called fomites: people could con-
tract disease from touching such fomites. In contrast to Scott’s and
Duncan’s repeated assertions, contemporary people’s impressions of
what they actually observed contain close reflections of what modern
research on bubonic plague has clarified, namely that bubonic plague is
spread by clothing, bedding, luggage and merchandise (see above).
What is new is the modern knowledge that the normal vehicle of spread
is infected rat fleas concealed there. This explains also early notions of
the usefulness of quarantines, of isolation of diseased persons and
objects used by them, including merchandise, and prohibition of trade
with areas where epidemics were raging. As now can clearly be seen,
their assertions that historians have not observed the obvious are
unjustified and untenable.
Scott and Duncan refer to Slack’s magisterial monograph on plague
in Tudor and Stuart England. This monograph contains a broad pres-
entation of contemporary people’s opinions on the causation of epi-
demic disease, vast material on the empirical reflections of bubonic
plague, and many citations of primary studies and standard works on
plague which permit the intensive use of comparative methodology for
identification of the disease, and should have shown that Slack and
other historians are competent and intellectually honest persons who
have come to support the bubonic-plague theory for good reasons.
The Material Scholarly Basis of Scott and Duncan’s Alternative

Theory
Like Twigg, Scott and Duncan have a strong predilection for outdated
works and signally ignore works representing current research. This is
the case with their prolific and enthusiastic use of Creighton’s mono-
graph on the History of Epidemics in Britain (to the Extinction of Plague)
of 1891. Scott and Duncan praise this work, not from the perspective of
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616 chapter fifteen
the history of medicine, but uncritically as an outstanding work of

undiminished value, and in the same passage, anoint him as the “doyen
of epidemiologists”:
His approach in his classic work, which was to provide a chronicle of
death and disease in the life and people of England, was that of a profes-
sional historian and he worked with great care on his sources. We have
relied heavily on his data series in our earlier work.13
No modern medievalist would suggest that Creighton was fond of
source-criticism and his use of medieval chroniclers is characterized by
gross naivety; but it is only fair to add that Creighton was not an histo-
rian, as Scott and Duncan maintain, but a physician and anatomist, a
fact clearly stated on the front page of his monograph. Creighton has
an agenda: among British medical scholars he was the last unflinching
champion of miasmatic theory of epidemic disease and spent much of
his academic life in the defence of this theory.14 His relation to medical
science is characterized by proto-scientific attitudes and an incomplete
scientific methodology. Inevitably, his scholarly beliefs and agenda
caused to include in his work much material, discussions and views
that today would be unceremoniously rejected as unscientific and
untenable. Carmichael sums up this problem thus: “Scott and Duncan
borrow heavily from Charles Creighton’s History of Epidemics in the
British Isles (1891–4), a famous compendium made by a relatively
unknown medical practitioner who was bent on gathering evidence
against the germ theory of disease.”15
Even the IPRC, who were fully occupied with their battle against
plague, felt obliged to carry out specific experiments to disprove
Creighton’s views, since he still enjoyed some authority in some quar-
ters at the time:
The belief that the infection of plague resides in the soil has been enter-
tained and advocated by Creighton (1905) who adopted it in his History
of Epidemics in Britain (1891) and reaffirmed it in 1905 after having paid
a visit of investigation to India. He thought the infection rose to the inte-
rior of dwellings with he ground air and was commonly taken in by man
with the breath.16
13
14
See, for instance, Hirst 1953: 57, 74, 93. This point is made also by Carmichael
2003: 255.
15
16
IPRC 1907f: 711.
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The fact that rats or guinea pigs contracted plague only in the presence
of rat fleas was demonstrated definitely and indisputably in the Com-
mission’s first paper.17 Scott and Duncan refer to or cite Creighton’s
monograph a total of fifty-six times,18 not once so much as intimating
a word about its problematic nature.
This puts in perspective also Scott and Duncan’s assertion that
Creighton “probably knew something about the biology of bubonic
plague when he was writing in 1891, because this was being elucidated
at the time.”19 In fact the first breakthrough on plague biology was
Yersin’s identification of the plague bacterium in 1894, three years after
the first publication of Creighton’s monograph,20 and concomitantly
with the reprint in 1894 (with the second volume taking the history of
epidemics in England to Creighton’s own time). It would take two dec-
ades before the blocking mechanism that makes fleas infective was
discovered and this crucial biological aspect of the transmission
of bubonic plague was clarified. Scott and Duncan maintain that
Creighton should “probably” have known something about the biology
of plague before anything was known about it, and the evidence on
which the high level of tenability of “probable” is based, remains inex-
plicable. Indeed, at the time Creighton wrote his monograph(s) he
rejected the germ theory of epidemic disease, and since he continued
to do so his whole life, and did so specifically in the case of bubonic
plague, the scholarly elucidation of the biology of bubonic plague was
of no consequence to his views. The theory of miasmatic epidemiology
is the underpinning of all his work.21
With this background, Scott and Duncan’s comment on W. Furness’s
book on The History of Penrith which was published in 1894, three
years after Creighton’s monograph, becomes interesting: “it was
written at a time before the true biology of bubonic plague had been
17
IPRC 1906a: 425–82.
18
Scott and Duncan 2001: 15, 80, 86, 110–1, 149–50, 152, 159–60, 163, 165–6, 170,
173, 183, 189, 193–5, 197–9, 201, 204–6, 209, 212, 216, 218–20, 228, 243, 245, 257,
261, 362.
19
20
Yersin 1894: 664–7. Cf., for instance, Simpson 1905: 64; Sticker 1910: 5; Lien-Teh
1936a: 21–3; Hirst 1953: 106–9; Butler 1983: 15–22, Butler has, in fact, written a short
biography of Yersin on pages 10–25.
21
This can be seen also from the subsequent reprint of the first volume in 1894 to-
gether with the new second volume which takes Britain’s epidemic history “to the
present time.” See the bibliography here.
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618 chapter fifteen
elucidated.”22 They are in such urgent need of arguments that this

repeatedly overshadows their better judgement. Scott and Duncan
argue as if they do not know anything about Creighton, his scholarly
position and ambitions. The point is that they wish to argue that
Creighton’s monograph can be taken in support of their own theory of
the nature of historical plague epidemics which likewise is not based
on any role for black rats and their fleas, because it is based on mias-
matic theory. In other words, they wish to make a case for why they can
base their alternative theory on much material that is structured and
interpreted according to miasmatic epidemiological theory.23
Since Creighton knew only one type of contagion, namely miasma,
he “did not believe in the specificity of epidemic disease”: any disease
could be plague or develop into plague, which makes his monograph
very special and fraught with dangers. Thus, for Creighton “plague was
a kind of typhus of the soil, typhus being due to poison generated in
unhealthy air”; typhus could, for instance, easily develop into bubonic
plague, and bubonic plague was also “due to a poison emanating from
putrescent corpses.” “Not only could typhus be transmuted into plague,
but he wrote in 1894 of ‘the breeding of typhus from the effluvia of
dysentery. ’”24 Creighton comments on the second plague epidemic of
1361–2 by speaking of a “recrudescence, then, of the seeds of plague in
English soil […],” which shows that he considered both the Black Death
and the subsequent wave of plague was caused by miasmatic gases
emanating from the soil.25 Scott and Duncan have read and used this
passage in Creighton’s work and therefore know this well, but will not
share this information with their readers. They present his assertion
that this second plague, at least in some places, among them Florence,
was as destructive as the Black Death, disregarding or overlooking the
fact that Creighton’s references are to the contemporary Florentine
authors Petrarch and Boccaccio,26 and that neither of them have the
second plague in mind, but the first, the Black Death.27 The assertion
about mortality in the second plague in Florence is at variance with
22
23
24
Hirst 1953: 74–5.
25
Creigthon 1891: 203.
26
27
Boccaccio wrote Il Decamerone around 1350; Petrarch never lived in Florence
because his father had been exiled from the city, but mostly in Avignon, although he
visited Florence briefly in 1350 when he also befriended Boccaccio.
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Herlihy and Klapisch-Zuber’s modern standard work on late medieval

Florentine demography.28 The assertion regarding levels of mortality in
the two first plague epidemics in Florence is also incompatible with
E. Fiumi’s classic studies on late medieval Florentine demography.29
Since Herlihy and Klapisch-Zuber’s monograph was published in 1978
and Fiumi’s studies in the 1950s, they were readily available to Scott
and Duncan.
Creighton accuses bacteriologists of “disdaining any discussion of
the possibility of a tertium quid, such as Pettenkofer’s soil activation
factor or Sydenham’s mysterious atmospheric influence.”30 This puts in
perspective the very problematic nature of Scott and Duncan’s repeated
assertions that people in the sixteenth century were fully aware that
disease spread by “person-to-person contact.” Their monograph’s index
contains a wide array of words like “measles,” “malaria,” and “house-
hold contact rate,” but the most important term of the historical medi-
cine and epidemiology on which they rely, “miasma,” does not appear.
When Scott and Duncan inform their readers that they “have relied
heavily on his [Creighton’s: my insertion] data series in our earlier
work,” this shows that they base their work on unscientific and obsolete
data which inevitably imbue their work with protoscientific miasmatic
analyses and historical material with dire consequences for tenability
and validity.
This also puts in perspective the fact that there is hardly any concrete
reflection in Scott and Duncan’s monographs of acquaintance with
modern research literature on bubonic plague. This pertains not only
to the primary medical research literature but also to the fine standard
medical works on bubonic plague written by outstanding scholars with
great first-hand experience of plague in the field and in the laboratories
and unrivalled knowledge of the research literature on this disease.
This is also the case with the standard works cited in their bibliography,
namely Pollitzer 1954, Wu Lien-Teh 1926, and Wu Lien-Teh, Chun,
Pollitzer et al. 1936. Hirst’s and Sticker’s central standard works and
E.-R. Brygoo’s small monograph summarizing French medical plague
researchers’ comprehensive and important work in Madagascar are not
even mentioned in their bibliography. Only one work of the IPRC’s
huge production of pioneering plague studies is mentioned with a
28
Herlihy and Klapisch-Zuber 1978: 195–6.
29
Fiumi 1950: 89–94, 110–1, 119–58; Fiumi 1958: 480–1.
30
Hirst 1953: 93.
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620 chapter fifteen
specific reference, but in a way that makes it (almost) certain that they
have not read it (see below), and by implication anything else from this
important corpus of primary research on bubonic plague.
When standard works on plague are mentioned, for instance, “Wu,
1926” = Wu Lien-Teh’s standard work on primary pneumonic plague,
or “Wu et al., 1936” the standard work co-authored by Wu Lien-Teh,
J.W.C. Chun, R. Pollitzer and C.Y. Wu in 1936,31 their assertions as to
what they contain are erroneous, which may be taken to indicate that
they have not read them. “Wu et al., 1936” is a confused reference to
two different authors named Wu, namely Wu Lien-Teh and C.Y. Wu,
who wrote four of the chapters or sections, an indication that they have
not held the monograph in their hands. In this reference, the opinion is
attributed to the author that the high mortality of 50 per cent in the
epidemic of bubonic plague in Marseilles 1720–2 could be due to the
fact “that pneumonic plague was responsible for a high proportion of
the deaths.”32 In these chapters, nothing to this effect is stated in any of
the three instances where this epidemic in Marseilles is mentioned.33 It
is a fictitious reference serving the purpose of defending Scott and
Duncan’s assertion that mortality rates in bubonic plague are generally
small in order to hide the inadequacy of their own alternative theory
for explaining high mortality rates (see below). Other references,
for instance, to Chinese and Indian plague history, are similarly
erroneous.34
31
Scott and Duncan 2001: 7. Cf. ibid. 47.
32
33
Wu Lien-Teh 1936a: 5; Wu Lien-Teh 1936b: 226; C.Y. Wu 1936b: 511.
34
“[…] the disease [bubonic plague] has been identified (presumably correctly) and
recorded in detail from China since ad 37 (Wu, 1926, Wu et al., 1936) […],” “there are
said to have been 233 outbreaks [of bubonic plague: my insertion] in China between
ad 37 and 1718. However, nothing to this effect is stated in Wu Lien-Teh 1926. This
makes it clear that Scott and Duncan do not know this standard work and its brief
historical introduction on this mode of plague, but have taken the reference from else-
where for second-hand or third-hand use. The second monograph they refer to, Wu
Lien-Teh, Chun, Pollitzer and Wu 1936, is an outstanding standard work on plague
written by a team of prominent plague researchers. The historical introduction on
plague is not written by Wu et al., but by Wu Lien-Teh alone. In the historical introduc-
tion, Wu Lien-Teh 1936a, he makes it clear that among the epidemics mentioned in
Chinese historical sources between 224 b.c. and a.d. 1718 none is referred to by words
or terms that imply plague, only by unspecific general terms meaning pestilence or epi-
demic. This register of epidemics is taken from the Imperial encyclopaedia that was
produced under the orders of Emperor Kang-Hsi in 1726 and is cited by Wu Lien-Teh
at the end of the chapter. However, Wu Lien-Teh also took upon himself the task of
reading through the old Chinese medical literature where he found at long last (after
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Scott and Duncan inform their readers that, for their medical and
epidemiological knowledge of bubonic plague, they rely on a textbook
by A.B. Christie providing a general introduction to infectious diseases,
more precisely on “the first edition of his book Infectious Diseases:
Epidemiology and Clinical Practice, published in 1969.” They maintain
that he “has provided an admirable account of the epidemiology of
modern bubonic plague and the following pages are very much based
on his overview.”35 Their praise reflects their need to lead attention away
from the fact that they base their knowledge of bubonic plague on a
chapter in a general textbook on infectious diseases which has serious
weaknesses. Despite their numerous and consistent references to the
first edition of this textbook of 1969, this edition does not contain any
chapter on plague, neither does the second edition of 1974. A chapter
on plague is first introduced in the third edition of 1980, which could
suggest that most of their references were produced by someone else.36
This shows that Scott and Duncan did not have any ambition to
acquire good knowledge of bubonic plague through earnest, independ-
ent reading of the primary medical research literature or the standard
medical works on bubonic plague that summarize the research litera-
ture and the vast personal experience of their authors. Instead, they
“years of patient search among such books”) evidence of bubonic plague in a.d. 610,
a.d. 652 and next, not until 1642 and in 1644, when there is a reference to bubonic
plague with secondary pneumonic manifestations. Why do Scott and Duncan start in
a.d. 37, when Wu Lien-Teh starts in 224 b.c.? They cannot have read Wu Lien-Teh’s
text, as they pretend. They may possibly have been influenced by some flawed com-
ments by Twigg to the same effect, Twigg 1984: 23. These are only a few illustrations of
their pervasive negligence of the primary works on the history of bubonic plague which
characterizes their monographs and which makes them dependent on second-hand or
third-hand accounts from which they select the elements that may support their alter-
native theory. This serves a function; in this case it permits them to seemingly under-
pin an assertion to the effect that bubonic plague was a disease that was “predominantly”
rampant far away from Europe, in India and Central and Eastern Asia, but did not
come from these parts of the world to Europe until the third pandemic, 250–300 years
after historical plague epidemics ended. Scott and Duncan 2001: 7–8, 171, 389. Instead,
there are interesting reasons to assume that bubonic plague came to China from
Europe, as the first epidemics in China correspond in time to the Justinianic pandemic,
and the seventeenth-century epidemics correspond to the early modern plague epi-
demics in Europe and appear to have established at least one plague reservoir, namely
in Yunnan province. Plague in India is mentioned only in 1031 and 1615, and then
again not until the nineteenth century. Benedictow 2004: 42–3.
35
36
The reference to Christie’s textbook may have been found in Twigg’s monograph,
although Twigg uses it only for information on other contagious diseases and refers to
the edition of 1980. Twigg 1984: 209, 213, 215, 245.
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622 chapter fifteen
base their work on a chapter of twenty-four pages37 in a general text-

book on infectious diseases, written primarily for medical students or
as a manual for general practitioners by an author with a tiny research
background on plague. However, only three of these twenty-four pages
relate directly to plague among human beings which is of primary rel-
evance to their work.38 Most of the pages are used for formal bacterio-
logical and medical information and epidemiological descriptions of
the types of rodents and fleas that entertain enzootic and epizootic
plague in nature today and how they could come into contact with
peridomestic rodents and, thus, produce the potential for endemic or
epidemic plague developments. Obviously, and for easily understand-
able and acceptable reasons, Christie is mainly concerned with plague
cases or in more general terms plague-related situations which physi-
cians may encounter in plague areas today, mostly in developing coun-
tries. Also for obvious reasons, in a textbook aimed mainly at medical
students or general practitioners who need concrete practical informa-
tion on diseases that they are likely to meet in their practice, plague is
considered a peripheral disease of low priority in relation to much
more usual and therefore important contemporary diseases. This is the
reason that plague was left out of the two first editions and, when a
chapter on plague was eventually inserted into the textbook, it was
written with hardly any interest in historical plague epidemics. In con-
trast to, for instance, Hirst’s or Sticker’s standard works, information on
plague in this textbook is not selected or organized for the purpose of
facilitating comparison between modern bubonic plague and historical
plague epidemics, but for very different and respectable purposes. It
does not provide the information really required by Scott and Duncan
and leaves, therefore, much leeway for unfounded assertions on char-
acteristic features of bubonic plague.
In comparison, Pollitzer’s monograph Plague of 1954 has 698 pages
and 1478 footnotes with full bibliographical references included; Wu
Lien-Teh’s monograph A Treatise on Pneumonic Plague of 1926 has 464
pages with 1329 footnotes with full bibliographical references included.
The important standard work by Wu Lien-Teh, Chun, Pollitzer and Wu
of 1936 which Scott and Duncan refer to without having read com-
prises 547 heavily annotated pages containing 910 references to plague
37
When four pages on tularaemia are deducted.
38
Christie 1980: 760–2.
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studies. Hirst’s monograph on historical plague epidemics of 1953,

which is not even mentioned by Scott and Duncan, is constructed
entirely on historical lines and systematically compares modern stud-
ies with the various reflections and manifestations of historical plague
epidemics, has 481 footnotes based on 407 works according to Author
Index. Scott and Duncan can legitimately disagree with these excellent
scholars, but the requirements of good scholarly work and rules of aca-
demic engagement are very different from those they follow. It is disap-
pointing that they do not have the confidence in the quality of their
own work to make their premises, objections and assertions easily test-
able according to the ordinary standards of scholarly and scientific
work. This stands out in contrast to the vast amount of scholarly studies
which are meticulously presented and discussed according to ordinary
scientific requirements by all those fine scholars they denigrate with
their misleading and disparaging assertions (see above).
Christie’s chapter on plague exhibits serious weaknesses both in the
knowledge of plague and in familiarity with primary plague studies
and the standard works on this disease. He actually believes, for
instance, that the fact that rats eat the carcasses of rats which had died
from plague is an important factor in the spread of plague among rats:
“A rat might get plague from eating a rat or other rodent dead of the
plague, though rats are not always easy to infect in feeding experiments.
In Bombay only 38 per cent of wild rats could be infected when fed on
dead infected rats, though 70 per cent of Punjab rats were infected in
this way.”39 In support of this assertion he refers to the very first report
of the IPRC published in 1906 in The Journal of Hygiene, albeit only to
the first page, leaving it to the critical reader to plough through the fol-
lowing 115 pages in the hunt for the basis of his assertion, which proves
to be non-existent, as any scholar acquainted with the IPRC’s works
would instantly know. Instead, the IPRC published their first study of
this topic in their Report no. XIII the following year. Although it is
pointed out in this Report that rats caught in Mumbai or the Punjab
can be infected by feeding them “with the viscera of dead plague rats,”
that is “with grossly infected material” (Lamb), the Commission’s con-
clusions are clear: “It would appear that in nature intestinal infection
rarely or never takes place, and that in consequence rats do not become
39
Christie 1980: 756.
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624 chapter fifteen
infected by eating the carcasses of their comrades.”40 Thus, the Commis-

sion’s conclusion is the opposite of that which Christie attributes to
them. This conclusion is also reiterated in Lamb’s summary of the
Commission’s studies until May 1907.41 Later, the IPRC carried out fur-
ther experiments on rat epizootics in special godowns where many rats
were eaten but “that there is no reason for thinking that alimentary
infection played any part in the production of these epidemics.”42 The
“Advisory Committee for Plague Investigation in India,” who super-
vised the IPRC’s work, concluded very clearly:
Rats may be infected by feeding them upon the bodies of other rats dead
of plague. The distribution of the lesions in the bodies of naturally
infected rats correspond with that in rats experimentally infected by
means of fleas and not with that in rats infected by feeding. The
Committee, therefore, conclude that in nature plague is spread among rats
by the agency of rat fleas.43
This makes Christie’s assertion, which is supported by Scott and
Duncan, to the effect that human beings can contract bubonic plague
from the eating of undercooked camel flesh most unlikely, and it is not
supported by the papers referred to. It is a fact that camels can contract
and die from plague, but as to the epidemiological significance, interest
should focus on the role of fleas.
One is entitled to wonder how the fictitious reference to the IPRC’s
work came about. For his description of the main forms of plague
Christie appears to base his presentation unduly on a paper by Choksy44
of 1909 which exhibits an incomplete terminology and insight into the
basic forms of plague (see the presentation above on the basis of subse-
quent primary research and the standard works on plague). Choksy
has, for example, an incomplete or deficient understanding of the dif-
ference between primary septicaemic plague and secondary septicae-
mic plague. Probably, this is the reason that Christie appears to believe
that “if an infected flea injects pathogens into a healthy host, these go
straight into its bloodstream,”45 which is an assertion to the effect that
primary septicaemic plague is the normal form of plague infection,
40
IPRC 1907a: 381.
41
Lamb 1908: iii–iv, 34–5, 41. Several studies appeared in later issues of Journal of
Hygiene but had been used by Lamb. See also IPRC 1907c: 421–35; 1907d: 436–56.
42
IPRC 1910a: 332.
43
IPRC 1910e: 566. The author’s italics.
44
Not a member of IPRC.
45
Christie 1969: 753.
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a form which arises when a flea discharges contagion directly into a

blood vessel. In reality, it is normally a peripheral phenomenon com-
prising a few per cent of plague cases. Philip and Hirst, who have made
the best study of this form of plague, underline “the comparative rarity
of the primary septicaemic variety of plague.”46 This is important
because primary septicaemic plague is so fulminant that it rarely causes
the development of secondary pneumonia which gives rise to primary
pneumonic plague, and the average duration of the course of illness
of a statistically valid number of such cases was 14.5–15 hours,47 which
is at variance with the normally observed duration of the course of ill-
ness of bubonic plague of 3–5 days. When plague contagion is dis-
charged directly into a blood vessel, the mode of infection will not
affect the lymph nodes, which is associated with subcutaneous intro-
duction of infection through abrasions or cuts in the skin, as will nor-
mally be the case with the bites of infective fleas, and will therefore
not lead to the formation of buboes. Or to put it more succinctly, infec-
tive rat fleas will normally discharge plague contagion at a subcutane-
ous level where it will be in the catchment area of the lymphatic system
and will, accordingly, be drained through a lymph vessel to a lymph
node which consequent upon the infection will begin to swell
and develop into a bubo. Another related point is that primary septi-
caemic plague is so fulminant that there will not even be time for the
development of buboes and other typical clinical features of plague.48
Christie’s misunderstandings make the term “bubonic plague” and the
dominant mode of bubonic plague difficult to explain. However, he is
not consistent.
Christie correctly describes the first phase of the development of
secondary septicaemic plague, that is, when plague contagion “begins
its course via the regional lymphatics [after a bite of a blocked flea],” but
goes on to maintain that in these cases “the infection travels on through
the lymphatic vessels and nodes and invades the blood stream,”49 which
is another erroneous assertion of general bacteraemia and primary
septicaemia in plague cases. In fact, in almost half of plague cases the
infection is confined wholly or predominantly to the lymph nodes,
46
Philip and Hirst 1917: 534.
47
Philip and Hirst 1917: 530, 535, see also above: 7–8.
48
Philip and Hirst 1917: 530–8.
49
Christie 1980: 751–2, 762.
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626 chapter fifteen
which is their primary function.50 Christie soon forgets, it seems, his

erroneous description of secondary septicaemia altogether and reserves
the term septicaemic for primary septicaemic plague. It is cases of nor-
mal bubonic plague that develop into secondary septicaemic plague
when bacteria filter into the blood stream from the bubo after plague
toxin have broken down the surrounding lymphatic tissue. Such cases
of secondary septicaemic plague tend to develop sufficiently slowly to
allow the development of secondary pneumonia so often mentioned in
the sources in the form of “spitting of blood.” This is the clinical form
of plague that can give rise to primary pneumonic plague. According to
the plague research literature, secondary pneumonic plague develops
in 10–25 per cent of all plague cases (see above). Unfortunately, Christie
erroneously maintains that only 5 per cent of plague cases develop sec-
ondary pneumonic plague51 which is a misunderstanding probably
arising from a rapid and superficial reading of Choksy’s text where he
refers to the distribution of plague types in an epidemic in Hong Kong
in 1904.52 This is a piece of information from the very infancy of plague
research, and a good illustration of the problems arising from ignoring
most of the primary research studies and the standard works on plague.
Unfortunately, due to Scott’s and Duncan’s failure to read these works,
they rely on Christie’s brief and flawed presentation of these important
aspects of plague disease.53
Christie’s comments on primary pneumonic plague are written on
the basis of a few peripheral studies without use of the central works on
this mode of plague disease.54 For this reason, he cannot benefit from
the great quantity of knowledge available on this disease that was
obtained in connection with the only two known large or largish epi-
demics of this disease, namely the Manchurian epidemics of 1910–1
and 1920–1. He does not even know that the Manchurian epidemics
were primary pneumonic plague and not bubonic plague as demon-
strated by his assertion that “60,000 hunters caught plague from
marmots which they sought for their skins between 1910 and 1911
in Manchuria,”55 which demonstrates ignorance of the factual
50
Benedictow 1993/1996a: 242–64, where available data on septicaemia are
summarized.
51
Christie 1980: 762.
52
Choksy 1909: 352.
53
54
Christie 1980, references nos. 11, 33, 97, 112, 116.
55
Christie 1980: 760.
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circumstances and also of the main scholarly works on primary pneu-

monic plague. This is confirmed by the accompanying reference which
shows that Christie has picked up this piece of misinformation in a
general introductory work on human parasitology written by two para-
sitologists, Chandler and Read 1961, which contains about 3.5 pages on
plague where the focus is legitimately on the role of fleas as parasites.
The fact that primary pneumonic plague is spread by cross-infection
through the agency of droplets is not mentioned and the reference to
the events in Manchuria shows that the parasitologists know nothing
about this modality of plague which is not spread by insects.56
Unfortunately, Christie’s account is uncritically picked up and used
by Scott and Duncan, since they have not acquired enough independ-
ent knowledge to enable them to recognize such misinformation.57
However, Scott and Duncan do not refer to Christie on this point, but
refer instead incorrectly to “Wu et al. 1936.” Of course, Wu Lien-Teh,
who was director of the North Manchurian Plague Prevention Service,
has not written this, neither in his report on the epidemic in Manchuria
in 1910–1, “First Report of the North Manchurian Plague Prevention
Service,” The Journal of Hygiene 13 (1913–4): 237–99, nor in his report
on “The Second Pneumonic Plague Epidemic in Manchuria,” The
Journal of Hygiene 21 (1922–3): 262–88, nor in his monograph on pri-
mary pneumonic plague of 1926, nor in his three chapters in the stand-
ard work of 1936. It is simply a fictitious reference. Scott and Duncan
also refer to Chandler and Read 1961, Christie’s reference, so the origin
of their citation is obvious. Since they do not provide information on
the relevant pages in the works to which they refer, this practice can be
easily concealed and is difficult to reveal. Although the erroneous char-
acter of the untenable reference to Chandler and Read is uncovered in
this case and in other cases above and below, the unpleasant question
of the extent of this practise remains unresolved.
Christie provides also untenable (really obsolete) information on
extrinsic incubation time of Xenopsylla cheopis, i.e., the amount of time
from which a flea becomes infected until it becomes blocked and infec-
tive, also called the infection-infectivity interval. The average cannot be
“about 21 days”58 because this is incompatible with the rhythm or pace
56
Chandler and Read 1961: 653.
57
Scott and Duncan 2001: 66; Scott and Duncan 2004: 179.
58
Christie 1980: 754. Cf. Eskey 1938: 52–3; Eskey and Haas 1939: 1473.
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628 chapter fifteen
of development of plague from when contagion is introduced into a rat

colony to the transition into an outbreak among human beings, i.e. the
latency period of 19–27 days, for which it is now possible to provide a
fully satisfactory explanation. The scholarly consensus on the extrinsic
incubation time of Xenopsylla cheopis is 3–9 days (under normal cir-
cumstances), with the emphasis on the lower reaches of this range.59
These remarks on Christie’s chapter on plague will serve to underline
that Scott’s and Duncan’s uncritical and unstinting praise of it is not
warranted, although it certainly has some strengths in the form of cor-
rect information. One should also take into account the comprehensive
critical remarks on this text book and Scott and Duncan’s use of it given
above.60 However, most importantly it does not provide the informa-
tion needed to construct a comparative model between the epidemio-
logical and clinical manifestations, the defining features of bubonic
plague, and historical plague epidemics. But neither do Scott and
Duncan construct a real typology of the clinical and epidemiological
manifestations of filoviridal diseases which can serve as the basis for
the other part of the comparative model. This is the reason that Scott
and Duncan do not produce a valid and tenable comparison of bubonic
plague and Ebola or Marburg disease that can serve as a valid basis for
their conclusion or alternative theory. Conspicuously, Christie’s chap-
ter contains significant elements that are strongly at variance with their
theory, but which remain ignored and unmentioned.
The Demography of Historical Plague
It has been demonstrated above in the discussion of Twigg’s demo-

graphic arguments that they are deficient and outdated. Scott and
Duncan express their indebtedness to Twigg “for his overview of the
available [demographic] information and for drawing attention to the
shortcomings of the data.”61 This demographic overview is, as shown,
based on J.C. Russell’s obsolete and highly problematic study of mortal-
ity among the baronial class based on inquisitions post mortem and on
Shrewsbury’s discussion of mortality among the beneficed clergy on
data mostly produced by Lunn in a lost thesis.62 This means that all the
59
See Appendix 3: 682–7.
60
Above: 87–91, 338–9.
61
62
Benedictow 2004: 344–5, 353–4, 356–7, 411.
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excellent work that has been carried out on English medieval and early
modern demography after 1948 is ignored, that is, most of the available
research in these fields of study. Their ignorance of English demo-
graphic history of the period is demonstrated by their assertion that
“these are the only statistics available to us.”63 Uniquely in the European
historiography of the Black Death, there are in fact available to them
seventy-nine manorial studies of the mortality among rural popula-
tions which constituted around 85 per cent of the English population at
the time, and these studies are distributed over large parts of England’s
territory, thus, the number of studies and their distribution provide a
good level of social and demographic representativeness. They show a
general level of mortality in the Black Death of 60 per cent or slightly
higher.64 Scott and Duncan ignore also a number of mortality studies
based on another type of manorial registers, tithing lists relating to
frankpledge jurisdiction that are not quite so good sources, but good
enough to allow estimates that independently reveal the unsustainabil-
ity of their conclusion on the mortality level caused by the Black Death
(see below).65
Their ignorance of English demographic history is so pervasive that
they, like Twigg (or rather following Twigg), assert that “the population
of England did not fully recover for 150 years,”66 i.e., that it only regained
its pre-plague demographic strength around 1500. Instead, around
1500, the size of the English post-Black-Death population was at its
minimum, “and there are few signs of sustained recovery before the
second quarter of the sixteenth century.”67 However, Scott and Duncan
insist erroneously and, as is so often the case, without a supporting
footnote or reference, that
Historians have long been puzzled by the paradoxical rapid recovery of
the population of England after the undoubted heavy mortality of the
Black Death […].68
Who are these historians? So far as I know, the objective fact is that at
least since Postan’s important paper of 1950 on the late medieval demo-
graphic crisis69 historians have not been puzzled by any rapid recovery,
63
64
Benedictow 2004: 362–8, 375.
65
66
Scott and Duncan 2001: 6, 20, 98.
67
Hatcher and Bailey 2001: 31; Hatcher 2003: 93–101, 105.
68
69
Postan 1950: 328–44.
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630 chapter fifteen
because they have, on the contrary, been puzzled by the duration and
the magnitude of the decline and the late start of sustained recovery. In
fact, the English population had not regained its pre-plague strength
on the eve of the Industrial Revolution about 200 years after the begin-
ning of the recovery, almost 400 years after the Black Death.70
Around 1500, the English population was “scarcely more than 2 mil-
lion people in the country,” still very much lower than Russell’s pre-
plague estimate of 3.7 million, in fact almost a half. So, what can be the
basis of Twigg’s and Scott’s and Duncan’s assertion on this point? They
do not refer to any other study for support. English historians have
generally dismissed out of hand Russell’s estimate of 3.7 million as far
too low. Most English scholars agree now that the population num-
bered about six million inhabitants on the eve of the Black Death and
this is, then, the current scholarly consensus (see above). Thus in 1500,
the English population was around or only slightly above one-third of
its pre-plague size and it had not fully recovered its pre-plague size 400
years later. Scott and Duncan pay a high price for relying on a zoologist
for their historical demographic data, instead of taking on the ordinary
scholarly task of acquiring satisfactory knowledge of this central piece
of data for their subject.
Scott and Duncan’s special relationship to English demographic his-
tory serves a purpose, namely, to keep estimates of mortality and the
reduction of the population in the Black Death down to levels that
would not be obviously incompatible with their alternative theory, that
historical plague was caused by a filoviridal virus. Filoviridal diseases
are characterized by very inefficient methods of transmission with cor-
respondingly limited powers of dissemination and mortality, so ineffi-
cient that high population mortality rates must be excluded (see below).
Thus, in a monograph in which they discuss the possible microbiological
nature of the most devastating epidemic in history, they present an
alternative contagion which is characterized by small or tiny outbreaks
(see below) which would not be observable in medieval sources. On
the other hand, they proclaim that bubonic plague cannot cause high
mortality rates, although this is documented71 and they admit that this
was the case with the epidemic in southern France 1720–2.72
In addition to the studies on the inquisitions post mortem and on the
beneficed clergy, Scott and Duncan base their assessment of the
70
Benedictow 1993/1996: 105–8.
71
See, for instance, Hirst 1953: 103. See also above: 201–2.
72
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mortality caused by the Black Death in England on studies of

much later plague epidemics, namely on the mortality rate estimated
for the plague epidemic in Penrith in 1597–8, and on a reference
to unsubstantiated assertions of mortality in Italian cities at the
level of 40–50 per cent based on data relating to the period 1476–657.73
This must be fallacious: what occurred in Italy 135 years later at the
time of the Renaissance and the transition to the Early Modern Period,
or 250 years later in Scotland in the established phase of early modern
society cannot have evidentiary bearing on the assessment of the
mortality effects of the Black Death. Scott and Duncan should instead
have based their discussion of this topic on the available estimates of
the mortality rates for Italian cities and rural districts in the Black
Death. They show much higher mortality rates, in the range of 50–60
per cent.74
Scott and Duncan maintain that mortality in the city of York in the
Black Death was 32 per cent and that the city, thus, “was relatively
lightly affected.”75 M. Sellers states in The Victoria History of the County
of York that seventeen of the twenty-one beneficed parish priests in the
city died, representing a mortality rate of 81 per cent, which is the only
demographic data on mortality in the Black Death available for the
city.76 This piece of information is also cited by Shrewsbury.77 On this
fictitious basis, Scott and Duncan “conclude that the mortality in the
more populous parts of England during the Great Pestilence may well
have been at least 30%.”78 This assertion implies that when less popu-
lous areas are taken into consideration, which have a significantly lower
level of total mortality, one may perhaps arrive at something like 25–30
per cent. Thus, they produce a mortality estimate in the Black Death
based on a fictitious assertion as to the mortality in York and an arbi-
trary assertion that mortality rates would have to be lower in rural
England. Since not a single population mortality rate is available for an
English urban centre in the Black Death, how can they know that mor-
tality rates would be lower in rural England? This mortality estimate is
obviously methodologically as well as factually seriously flawed and
73
Scott and Duncan 2001: 103, 303–4, 312–4.
74
75
76
Sellers 1913/1974: 440. For available data on urban mortality among the English
beneficed clergy, see Benedictow 2004: 359.
77
78
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632 chapter fifteen
must be rejected. The estimates of medievalist demographers like

Hatcher or R. Smith should have been used.
Since about 85 per cent of the English population lived in the
countryside,79 the crucial point must be that the manorial studies,
seventy-nine manorial studies with a wide geographical distribution,
show an average mortality rate among the customary tenants of about
55 per cent, corresponding to a generalized population mortality rate
of at least 60 per cent.80 This estimate must be close to the mortality rate
of the English population, which is incompatible with Scott and
Duncan’s need for a low mortality level which could possibly save their
alternative theory.
The reference to the “more populous parts” appears intended to con-
vey the opinion that the level of mortality generally was higher in the
more populous parts of England than in the less densely or sparsely
populated parts of England, Northumberland and County Durham
being specifically mentioned.81 This is contrary to the well established
fact that the mortality rates among the rural populations at twenty-six
manors in County Durham and at two manors in Northumberland
show the same level as in the more populous parts of southern
England.82 The point is that this usual density-dependent structure of
increasing mortality rates with increasing density of population serves
Scott and Duncan’s alternative theory, because it is based on a type of
disease spread by cross-infection, and this is an inherent feature of all
diseases spread by this method. Instead, the absence of correlation
between population density and level of mortality (or inverse correla-
tion) implies a disease that is spread by different mechanism(s), in this
case by rat fleas. In a specific chapter above on this subject, it has been
shown that inverse correlation between population density and mor-
tality is a consistent and unique feature of bubonic plague which is also
exhibited by historical plague epidemics, and that this unique feature
reflects the fact that this disease is transmitted and disseminated by rat
fleas. This feature therefore constitutes a defining feature of bubonic
plague and a means of identification of the microbiological nature of
historical plague as bubonic plague. It was also shown that Scott and
Duncan’s discussion of this subject was untenable.83
79
Hatcher and Bailey 2001: 140, cf. 50.
80
Benedictow 2004: 362–7, 375–6.
81
82
Benedictow 2004: 344, 347–8, 364–7.
83
See above: chapter 8, especially pp. 301–11. Cf. above: 34–8.
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The Reed-Frost Theory of Epidemiology
After this presentation of some central or characteristic features of

Scott and Duncan’s monograph, it is the paramount task to construct a
comparative model that can serve as a real basis for identification of
the microbiological nature of historical plague epidemics. Scott and
Duncan base their epidemiological analysis leading to the establish-
ment of their own alternative theory on an unpublished epidemiologi-
cal model by L.J. Reed and W.H. Frost. This model was presented by
J. Maia, a Portuguese scholar at the University of Porto, in a paper of
196884 and has subsequently generally attracted little interest. An
important reason for this is probably that it is of such limited use. As
Maia strongly emphasizes on the first page: “As presented, the theory
applies only to simple situations as illustrated by an outbreak of mea-
sles in a closed group.”85 Obviously, this means that the Reed-Frost
theory is of very limited usefulness and of peripheral interest for the
study of epidemic diseases spread by cross-infection, particularly viral
diseases disseminated by droplets. It also means that it is not usable for
the analysis of diseases transmitted by other means or mechanisms, for
example by insects, and in relation to populations under circumstances
which cannot be considered to approximate a closed group. Obviously,
the Reed-Frost model is unusable and invalid for the study of bubonic
plague in medieval society on both counts.
As underlined by Maia, at the time this model had only been “uti-
lized in the teaching” of epidemiology at the Johns Hopkins University.
Consequently, knowledge of it was limited at the time and today it is
almost unknown by epidemiologists and more generally oriented
reviewers. This situation will therefore introduce an element of caution
in the way reviewers relate to their theory, since they might otherwise
tend to assume that Scott and Duncan had respectable intentions and
made this choice because it provides useful insights not provided by
established epidemiological theories. The Reed-Frost model completely
dominates Scott and Duncan’s various epidemiological discussions and
analyses, it is mentioned by name thirty-six times throughout their
monograph and many more times indirectly; this prolific use provides
84
Maia 1968: 167–200.
85
A closed demographic group is one not affected by immigration or emigration so
that, for instance, all changes of size will be due to the net outcome of births and deaths
among the persons constituting the population.
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634 chapter fifteen
the false impression of fresh new insights and great importance.86

However, in the same journal in which Maia’s paper appeared, in the
immediately following paper serious objections to the Reed-Frost
model are raised by another scholar, Helen Abbey, who was working at
the Johns Hopkins University.87 This shows that the editors of Human
Biology must have had serious objections or reservations which required
immediate comments, and which explains why the Reed-Frost model
and the theory on which it was based never was published by the
authors and is known only indirectly through Maia’s paper. Scott and
Duncan have, as it seems, chosen to ignore all this and also to keep
their readers in ignorance of it.
On page 355, at the end of Scott and Duncan’s monograph of 2001, a
terrible truth inadvertently slips out: “Furthermore, typhus epidemics
do not follow Reed and Frost dynamics because it is a disease with an
arthropod vector.” Typhus is transmitted by lice which are insects, one
of the four classes of animals which constitute the phylum of arthro-
pods. Bubonic plague is transmitted and disseminated by another type
of arthropods, namely fleas, mainly rat fleas, usually of the species
Xenopsylla cheopis associated with black rats. Consequently, the corol-
lary must also be true, namely that the Reed-Frost model is not usable
for the study of bubonic plague, because it is “a disease with an arthro-
pod vector.” Throughout their monograph Scott and Duncan never
even hint that the Reed-Frost model is, according to its own underlying
premises, unusable for the analysis of epidemics of bubonic plague, and
that it is potentially usable only for the analysis of epidemic diseases
spread by interhuman cross-infection and as such mainly restricted to
viral diseases transmitted by droplets in closed populations.
It is in this perspective that one should consider Abbey’s severe
objections:
The Reed-Frost Theory of the spread of epidemics has been tested on two
series of observations derived from disease and population conditions
which approximate the assumptions of the theory [closed population: my
insertion]. The first series is composed of epidemics of measles, chicken-
pox and German measles in boarding school populations […]. The sec-
ond series consists of epidemics of measles in families each of which is a
86
Scott and Duncan 2000: 28, 32, 45, 70, 79, 80, 85, 89, 90, 107, 121, 123, 148, 151,
159, 165, 170, 173, 190, 229, 236, 247–8, 249, 250, 263, 328, 263, 355–6, 359, 362, 364,
366, 368, 372.
87
Abbey 1968: 201–33.
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universe having four (reported) susceptible members. The model was fit-
ted to the reported cases by generation of the disease and reported
number of susceptibles at the beginning of the epidemic. The theory fails
to fit either series of observations.88
This explains why the Reed-Frost theory and the model of the spread of
epidemics based on it have never attracted significant interest even in
the case of viral diseases spread by cross-infection, not even at the uni-
versity where it was conceived. It must to a large extent be considered a
failed epidemiological theory.
Thus, at the heart of Scott and Duncan’s monograph is a sinister
secret. In a monograph designed to show that historical plague cannot
have been bubonic plague and to provide an alternative theory, they
have deliberately and in complete secrecy chosen to use an epidemio-
logical model that, according to the methodology of social and medical
science, cannot be used to test historical evidence produced by epi-
demics of bubonic plague. In principle, the Reed-Frost model is not
appropriate for probing or examining the pivotal and crucial question
at the heart of the discussion of whether or not historical plague epi-
demics could have been bubonic plague transmitted by rat fleas or
could or must have been another disease. As such the whole mono-
graph is based on a fallacy of methodology.
Inevitably, this must be obvious also to Scott and Duncan. In the first
presentation of the Reed-Frost model, they introduce, for instance, the
concept of “serial generation time” which “has been defined as the
period between the appearance of symptoms in successive cases in a
chain of infection that is spread person-to-person.” They state also that
it “seems that the causative agent of plague was most infectious, and
droplet transmission person-to-person was most efficacious under
warm conditions.”89 Here it is explicitly stated that the Reed-Frost
model by definition can only be used for analysis of epidemics spread-
ing by interhuman cross-infection, and by implication is unusable for
the study of diseases spread by insects. Unfortunately, nothing is said
about the further limitations and weaknesses of the model as being
restricted to viral diseases, and thus also for this reason unusable
for the study of bubonic plague. Only diseases disseminated by
droplets are being specifically mentioned (measles, chickenpox, and
88
Abbey 1968: 231.
89
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636 chapter fifteen
rubella/German measles). This must also be the reason that Scott and
Duncan spuriously claim that filoviridal haemorrhagic disease spread
by “droplet transmission person-to-person”90 (see below).
It is a general characteristic of medical or social-science models that
the interaction of the input of premises and the structure of correlates
constituting them will tend to reproduce their underlying suppositions
or presumptions, and also that incorrect inputs will tend to produce
obviously unreasonable or untenable outcomes. The Reed-Frost model
is constructed in a way that will tend to make all inputs of historical
evidence produce confirmation of Scott’s and Duncan’s pre-conceived
view that historical plague was a viral disease spread by cross-infection.
When such a model is applied to evidence pertaining to an epidemic of
bubonic plague, a type of disease which it is not constructed to handle,
it will tend to produce the features of a phantom disease with an
unknown set of characteristics or manifestations. This is also the case,
as will be seen below, when Scott and Duncan have to admit that their
alternative disease is completely unknown or an unknown strongly
mutated variant of filoviridal disease. Every time Scott and Duncan
conclude that the epidemiological analysis of a plague epidemic accord-
ing to the Reed-Frost model proves that it cannot have been bubonic
plague, it represents a fallacy of methodology, for instance, also on page
355: “In conclusion, all the major plague epidemics exhibited Reed and
Frost dynamics typical of an infectious disease with a long incubation
period.”
The Filoviridal Theory of Historical Plague: A Study in Academic

Fiction
Scott and Duncan’s alternative theory of historical plague is that it was

caused by filoviridal disease, some form of Ebola or Marburg haemor-
rhagic disease. These epidemic diseases occur in some parts of Western
sub-Saharan Africa and in Sudan; they are caused by two closely related
viral pathogens constituting the family of RNA viruses called the
Filoviridae.91 Outbreaks of these diseases have never been registered
90
91
Registered in the two Congolese states, and in Gabon, Sudan, and the Ivory Coast,
according to www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebola.htm 2003: 1–4;
and www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebotabl.htm 2003: 1–3
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outside sub-Saharan Africa, and it appears mostly in Western Africa, a

fact which from the outset gives Scott and Duncan’s alternative theory
quite a problematic character, since this fact indicates very strongly the
necessity of specific local condition(s).
The scholarly mode of working is to endeavour to disprove one’s own
hypothesis, which means that a scholarly discussion of a hypothesis
will be imbued with the crucial scholarly values of source-criticism,
doubt and counter-arguments about the validity or tenability of the
various points made and the level of quality of supporting material. If
earnest endeavours to disprove a hypothesis do not succeed, then
something of value and a level of tenability for the hypothesis have
been achieved. The selection of whatever arguments or evidence fit a
hypothesis or theory is a way of working that will inevitably lead to the
seeming corroboration of any hypothesis, but is obviously without
scientific or scholarly value. Nothing is more valuable in scholarly
work than doubt, source-criticism, counter-arguments and counter-
evidence.
Scott and Duncan claim that they will examine the “historical facts
dispassionately, eschewing any preconceived notion.”92 This is hard to
reconcile with the fact that they declare that historical plague epidem-
ics were “haemorrhagic plague” and not bubonic plague in the intro-
duction of their monograph,93 before any evidence has been presented
and discussed, and is, then, monotonously reiterated as an established
fact throughout the monograph. This is rather an example of the tri-
umph of pre-conceived notions and “passion.” It means that their prin-
cipal monograph does not have an academic form in the fundamental
sense that it is not structured according to its inherent nature as a
thesis, i.e., introducing a problem, a possible solution or explanatory
hypothesis and at least a strategy and likely relevant material for resolv-
ing the problem. This will structure the further process of researching
the thesis: the scholar will go on to collect, collate, and examine
the evidence in order to test the possible validity and tenability of the
hypothesis or to seek out a solution, and form a conclusion at the end
of the thesis.
Since Scott and Duncan start by proclaiming their theory to be true,
they pretend that they can legitimately conclude that any characteristic
92
93
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638 chapter fifteen
feature of historical plague epidemics must be reflections or manifesta-

tions of their phantom haemorrhagic disease. (1) When historical
sources state that plague victims in historical epidemics presented with
buboes and at exactly the same corporal locations as modern bubonic
plague, this simply proves that the normal occurrence of buboes and
their normal locations are characteristic features of haemorrhagic
plague.94 And the corollary (1B): if contemporary physicians or barber-
surgeons incised mature buboes, this proves that such simple surgery
was a suitable treatment for haemorrhagic buboes.95 (2) When the
“symptoms were violet and black spots and blotches […] or small red
spots” this is “indicative of a haemorrhagic disease,” as was “the bubo
and pustules.”96 (3) “The signs, symptoms and autopsy reports of vic-
tims of bubonic plague are entirely different from these: they do not
display God’s tokens. Nor is there widespread necrosis of the internal
organs.”97 (4) When the duration of the disease is 3–5 days, this proves
that this is the duration of the course of illness of haemorrhaghic
plague.98 (5) When the epidemics at Penrith and Eyam and other epi-
demics have a long duration of 14–5 months, this shows that haemor-
rhagic disease is characterized by this duration. (6) When these
epidemics are most dynamic in warm summer and autumn weather,
and last so long because they are suppressed by cold winter weather
and recrudesce in spring with the warmer weather, this seasonal pat-
tern proves that filo-viridal disease, which according to their assertions
are spread by droplets, thrives in warm weather, not in cold weather,
and so on.99 Obviously, this is a clear instance of the fallacy of method-
ology called circular inference. Scott and Duncan have turned this into
a systematic approach on which they base their alternative theory. The
absolute condition or principle of falsifiability for scholarly and scien-
tific assertions and subsequent merciless empirical testing are thrown
out of the court of methodology at the cost of making their assertions
invalid and untenable. This makes it essential to perform further test-
ing or checking of their assertions by comparing them to the known
clinical and epidemiological manifestations of filoviridal diseases and
94
Scott and Duncan 2001: 306, 362, 380–1, 388.
95
96
97
98
Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1.
99
Scott and Duncan 2001: 119–37, 148, 152–3, 190, 193, 364–6.
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bubonic plague in order to identify possible correspondences. The six

topics just listed and the question of incubation period, which in this
case is closely associated with the question of latency periods com-
mented on above and with their theory of dissemination, will be the
focus of the discussion.
According to Scott and Duncan, the point of departure for their
work leading to the principal monograph of 2001 and their alternative
theory to the effect that historical plague was caused by filoviridal
disease is a paper Scott, Duncan and S.R. Duncan published in 1996:
“The Plague in Penrith, Cumbria, 1597/8: Its Causes, Biology and
Consequences.”100 A useful beginning for the further discussion of their
work is the opening statement in the preface of the principal mono-
graph referring to this study of plague epidemics in north-western
England 1597–8: “A plague struck this part of England and spread
rapidly in 1597–8 and it was obvious from a basic training in zoology
that this was not an outbreak of bubonic plague.”101 This assertion refers
to the untenable notion, thoroughly discussed above, that bubonic
plague spreads only very slowly between conterminous rat colonies.
There is nothing about the spread of the epidemic at Penrith that is
incompatible with the ordinary pattern and spread rates of bubonic
plague. With this background, one should note that, in the discussion
of the nature of the disease in their paper, they consider that it exhib-
ited features compatible with bubonic plague and also anthrax, undis-
turbed by elementary zoological knowledge. In their monograph, this
is ignored, which clears the way for an entirely new and revolutionary
theory.
The crucial observations are:
(1) Twenty-two or twenty-three days elapsed from the first plague
death in Penrith, that of a stranger called Andrew Hogson, and the
next plague death (depending on the time of the day he died);102
“Wasn’t this a very long interval for a normal infection? Surely this
was remarkable.”103
(2) The duration of the epidemic, which lasted fifteen months, “a
remarkably long time for an infectious “epidemic.”
100
Scott and Duncan 1996: 1–21; 2001: 115–48; 2004: 153–63.
101
Scott and Duncan 2001: xiii.
102
Scott and Ducan and Duncan 1996: 3; Scott and Duncan 2001: 116, 128.
103
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640 chapter fifteen
(3) The development rhythm of the epidemic in three phases: (i) the
epidemic began with a single death in late September 1597 and
rose to a small autumnal peak in November–December, (ii) during
the winter (January–February) there was only one plague death,
(iii) the pestilence appeared again in spring 1598 and rose to a peak
in June–July before slowly subsiding in the autumn.
(4) The seasonality of the epidemic.
(5) The duration of the course of illness, namely 3–5 days.104
Scott and Duncan analyse these main features of the epidemic at
Penrith with the Reed-Frost model and conclude that:
The third phase clearly follows the typical Reed and Frost dynamics of an
infectious disease spread person-to-person (see section 2.5). This phase
lasted about 8 months and, in this respect, the outbreak is comparable
with the epidemics in the dioceses during the Black Death (see Fig. 4.2)
and with plagues in other rural towns, examples of which are shown in
Fig. 5.2. The duration of the main part of the epidemic in each of these
populations was always long, usually between 7 and 10 months, and this
is indicative of a long serial generation time, as shown in Fig. 2.5 This
conclusion is supported by the initial events at Penrith, where 22 days
elapsed after the death of Andrew Hogson before the next victim was
buried, giving a minimum serial generation time of 22 days.
A feature of Fig 5.1 is the slow build-up of the epidemic in early spring,
which is also indicative of a long serial generation time and a low mean
contact rate (see Fig, 2.5). Figure 5.3A shows Reed and Frost modelling
[…].
All Read and Frost models predict that over 90% of the population would
be infected, which was not the case with [bubonic] plague […] the mod-
elling is instructive and it demonstrates how the shape of the mortality
curve (see Figs. 5.1 and 5.2) is determined by the long serial generation
time and the low effective contact rate […].105
This is excellent material for a study of the fallacious use of a model: all
of the various elements produced and explained according to the
premises and predictions of the Reed-Frost model are formed by the
internal suppositions and structures of this model. This is the case, for
instance, with the purported long serial generation time which will
lead them to a fallacious and untenable assertion on incubation time
and further to their theory of historical plague as filoviridal disease.
104
105
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All of the epidemiological features mentioned are instead entirely

compatible with bubonic plague as has been shown in various chapters
above: on the pace and rhythm of development of plague epidemics,
latency periods, seasonality, duration of time from infection to death
and the sequence of initial deaths, and the duration of the course of
illness.
Another obviously very important epidemiological feature is the
duration and pattern of development of historical plague epidemics.
Scott and Duncan simply declare that the duration of the epidemic at
Penrith was “a remarkably long time for an infectious epidemic. Once
again, the villain has left his mark.”106 On this basis, they maintain that
the duration of an epidemic of fifteen months was a defining feature of
epidemics caused by filoviridal virus infection (“the villain”), which
they identify also with the duration of the epidemic at Eyam of four-
teen months. However, they conspicuously fail to provide any com-
parative information on epidemics caused by a filoviridal virus in order
to substantiate the claim that this duration is a (defining) property of
this disease. The reason is, presumably, that a single instance of an epi-
demic caused by a filoviridal virus of anywhere near this duration has
never been observed; epidemics of these diseases typically last a few
months.107 The epidemiological point is clear and concrete: filoviridal
viruses are transmitted by inefficient mechanisms requiring transmis-
sion of living cells and therefore direct physical contact between two
persons in circumstances where mutual cuts or abrasions in the skin
permit transmission of contaminated cells. This means that the chain
of transmission is tenuous and tends to be rapidly broken, making for
episodic and small or tiny outbreaks. By 2003, “approximately 1500
cases with slightly over 1,000 deaths had been recorded since the virus
was discovered” in 1976.108
The long duration of the epidemics at Penrith and Eyam is due to the
same peculiar seasonal pattern. In both cases, the epidemics break out
in the autumn and after quite a short period of increasing activity they
suddenly begin to falter, subside and eventually almost completely dis-
appear in the coldest winter months, before the advent of spring brings
warmer weather when the epidemic again breaks out and reaches its
106
107
www.who.int/inf-fs/en/fact103.html 2003: 2; www.who.int/inf-fs/en/fact103
.html 2003: 1–3.
108
www.who.int/inf-fs/en/fact103.html 2003: 2.
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642 chapter fifteen
pinnacle in late summer and early autumn and, then, again begins to
falter, subside and eventually disappear completely with the second
advent of cold weather.109 This seasonality of the plague epidemics at
Penrith and Eyam is representative, it has been observed all over Europe
from the time of the Black Death to the end of the plague period over
three hundred years later. In the chapter on plague seasonality, it was
shown that this pattern is a unique and therefore defining feature of
bubonic plague.110 No theory of the microbiological nature of historical
plague and its means of transmission can be accepted which does not
readily provide a well-founded explanation of this particular seasonal
pattern and demonstrate that this is not a defining feature of bubonic
plague, but is associated with an alternative microbiological theory.
It is a central and self-evidently true tenet of epidemiology that all
diseases spread by cross-infection, whether by droplets or other means
of direct interhuman dissemination and transmission, flourish in cold
weather for the simple reason that people tend to stay or huddle closer
together and stay more indoors in more crowded rooms to keep warm,
a behavioural strategy that reduces interpersonal distance and obvi-
ously facilitates the direct spread of microbiological agents by cross-
infection. This means that the seasonal pattern of plague epidemics is
incompatible with all diseases spread by cross-infection, also the filo-
viridal viruses of Ebola and Marburg haemorrhagic diseases which are
spread by “direct contact with the blood and/or secretions of an infected
person” or “direct contact with the blood, secretions, organs or semen
of infected persons.”111 Thus, also Ebola and Marburg haemorrhagic
diseases or possible variants of filoviridal diseases would tend to
exhibit stronger powers of spread in cold weather than in warm weather,
a pattern which is at complete variance with that of historical plague
epidemics.
In sharp contrast, the peculiar seasonal pattern of historical plague
epidemics can be easily explained according to the epidemiological
mechanisms of dissemination and transmission of bubonic plague.
There are two main factors which provide explanatory powers. Firstly,
cold weather will prevent or impede the reproductive process of fleas,
109
Scott, Duncan and Duncan 1996: 17; Scott and Duncan 2004: 154; Shrewsbury
1971: 523; Bradley 1977a: 87; Coleman 1986: 383.
110
111
.int/inf-fs/en/fact103.html 2003: 1.
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because the development of eggs and the survival and development of

larvae and cocoons are temperature-dependent and significantly or
seriously negatively affected by chilly or cold weather. The number of
adult rat fleas which enjoy a pleasant life in the fur of the rat with a
good microclimate and easy opportunity of feeding, will diminish as
some of them are scratched off or simply fall off, while their number
will not be replenished from the reproductive process.112 A diminish-
ing number of rat fleas will reduce correspondingly the potential inten-
sity of epidemic developments. Secondly, plague septicaemia in rats
falls sharply in temperatures below 10 °C, so that feeding rat fleas will
be much less infected and, consequently, will develop blockage at much
lower rates.113 Thus, the strong tendency of historical plague epidemics
in Europe to disappear or, especially in Southern Europe, continue in a
more or less sporadic endemic form in wintry weather, and corre-
spondingly the pronounced tendency of transseasonal epidemics can
be easily explained in relation to the epidemiological mechanisms of
bubonic plague and be established as a defining property of this dis-
ease. In contrast, it remains inexplicable in terms of epidemics caused
by filoviridal viruses (and by all other diseases spread by cross-
infection). Shrewsbury, Bradley and Coleman correctly point out that
the seasonal pattern and time-course of the epidemic at Eyam exhibit
the characteristic features of bubonic plague epidemics.114 In the words
of Coleman, for instance:
The timing of the outbreak in autumn, the transient decline during the
winter months and the peak in summer is also typical, and largely reflects
the influence of the weather, since the activity and survival of rat-fleas is
temperature-dependent.
The next stage in the process leading to Scott and Duncan’s alternative
theory of historical plague as filoviridal disease is the invention of a
purported long incubation time:
Three factors point to a long incubation period for the disease. (i) The
duration of the summer epidemic in phase three, as explained above.
(ii) In both Penrith and Eyam (Chapter 10) the epidemic began with the
death of a stranger or visitor who had taken up lodgings and was living,
albeit temporarily, in the town. He must have been infected elsewhere,
112
For a detailed discussion of these matters see Benedictow 1993/1996: 160–70.
113
Lamb 1908: 88–90; Hirst 1953: 271–82, 340–5; Seal 1969: 288–9. Above: 397.
114
Shrewsbury 1971: 524–7, 529; Bradley 1977a: 70–1; Coleman 1986: 382.
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644 chapter fifteen
perhaps some considerable distance away, and brought the disease into
the community whilst still not showing any symptoms […]. The death of
the first victim, the incoming stranger, was followed by an interval of 15
(Eyam; see Chapter 10) or 22 (Penrith) days […].
The early stages of these outbreaks, whilst the epidemic was being
established, that we have studied in detail, are much more informative
than are the confusing events in mid-summer when the infection spread
with devastating rapidity. We have analysed a number of these outbreaks
(see following chapters) and have determined from a number of sources
the following epidemiological parameters:
Latent period: 10–2 days.
Infectious period before symptoms: 20–2 days.
Period of symptoms: 5 days.
Total infectious period: 25–7 days.
Total time from point of infection to death: 37 days, a very long time
[…].115
The first part of the citation relating to the first epidemic events in
Eyam and Penrith is obviously central to the argument, and this part
will therefore be discussed first. As shown above, the course of the
summer epidemic and the whole course of the epidemic are entirely
compatible with the seasonality of a bubonic plague epidemic which
arrives in the autumn, is arrested by chilly and cold weather and forced
to retreat into a smouldering existence in the rat colonies, revealing its
presence with the occasional plague death (one in February), and
then recrudesces with the advent of warmer spring weather, finally
to explode with summer warmth. Viral diseases spreading by cross-
infection have in common that they spread more efficiently in cold
weather when people keep closer together, whether the disease is spread
by aerial transmission with droplets or by direct physical contact and
transmission of living cells (if we exclude transmission via contami-
nated hypodermic needles). Also, droplets drift longer in chilly, cold
and moist air which increases their probability of reaching other per-
sons. Scott and Duncan attempt to get around this problem by seeking
arguments to the effect that for this specific filoviridal disease this was
not the case, without presenting the general problem and informing
their readers why the mechanism of interhuman transmission or diffu-
sion should be different in this case and not follow the general
pattern.116
115
116
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The first plague victim in Eyam died 6 September 1665, on the third
or fourth day of his illness,117 and was buried the next day. Presuming
that the disease was bubonic plague, the time of incubation would be
three to five days, which indicates that he was infected in the period 30
August–1 September. According to the oral tradition among the inhab-
itants of Eyam conveyed by W. Wood, the local historian who lived
there and published a history of the epidemic in 1842, he was a tailor
who had received a box with cloth from London where the last plague
epidemic was raging. This story reflects the fact that people in the Early
Modern Period recognized the dangers in times of plague of shipments
of cloth or of second hand clothing left by plague victims, which have
also been confirmed by modern plague research on more concrete
grounds, incriminating rat fleas as the great “villain” hiding in such
matter.118 In this respect, this account is quite similar to how plague was
shipped from Mumbai to London in a case of clothes early in the plague
epidemic in India.119
As pointed out by Bradley, after 176 years the oral tradition was no
longer entirely reliable,120 for instance, that the tailor fell immediately
ill after having opened the box. Source-criticism will indicate that this
part of the account must be presumed to be a reflection of the typical
feature of folkloristic oral dramatization by compression of the
sequence of events. At the time, it would also have been inspired by
miasmatic epidemiology that does not draw on notions of microbio-
logical agents and has at best only hazy ideas about incubation, much
like Boccaccio’s hogs which rooted with their snouts in the ragged
clothing of a pauper diseased from plague and almost immediately fell
dead to the ground. Thus, the process of oral (and literary) dramatiza-
tion has led to a compression of the time between the time of arrival of
the box of cloth and the time the tailor fell dramatically ill (a few days
later) so that the connection between the events would be obvious and
dramatic. The details of local oral tradition can be left out here; it suf-
fices to point out that this account of how plague reached Eyam from
London is easily compatible with the usual mechanism of spread of
bubonic plague over a distance, namely of metastatic spread (spread
per saltum) by rat fleas, and that heavily infected rat fleas in a relatively
117
Bradley 1977a: 64–5, 68–9.
118
Hirst 1953: 310–1, 314–20.
119
Hirst 1953: 311. Cf. Simpson 2005: 201.
120
Bradley 1977a: 64, 68–9.
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646 chapter fifteen
humid climate can survive for many weeks under favourable condi-
tions of transportation as, for instance, in cloth, for at least fifty days in
temperatures under 15 °C.121 In this case, the traditional account relates
that the cloth was damp and the tailor therefore took it out of the box
to hang it out to dry in front of the fire, a detail which increases the
realism and trustworthiness of the history.
The subsequent rhythm of epidemic events is also compatible with
the pattern of bubonic plague. After having fed on the tailor, an infected
flea (or fleas) concealed in the cloth would seek out their normal host,
house rats. The second victim was interred 22 September, not fifteen
but sixteen or seventeen days after the death of the tailor and twenty-
two or twenty-three days after the beginning of the process of infective
transmission. As can be seen, this is a very fine match for the general
time structure of the two first cases of an epidemic of bubonic plague
comprising the epidemiological developments from infection of the
house rats and the course of the epizootic (ten to fourteen days), the
release of rat fleas and the period of starvation until they attack people
(three days) and the course of incubation and illness (six to ten days),
in all nineteen to twenty-seven days, as documented above.122 This is
also an excellent match with the subsequent epidemics events at Penrith
where the second plague burial followed twenty-two or twenty-three
days after the first. The difference is probably due to the fact that
Andrew Hogson was infected at the time he arrived at Penrith which
compresses the time horizon of the developments leading to the next
case, and variation in the time that the rat fleas they brought with them
took to find a rat host. In the case of the beginning of the epidemic at
Eyam, the process of spread in the rat colonies would begin whilst the
tailor was incubating the disease or was ill.
As pointed out in the chapter on latency, the observation of this
peculiar delay in the opening sequel of the two first deaths was made by
the early plague researchers, by Simond, Hankin, Sticker and the IPRC,
and was later underlined in all standard works of bubonic plague as
being a characteristic or distinguishing feature of this disease,123 what
here is called a defining feature or property. It is difficult to understand
121
Bacot and Martin 1914: 437; Hirst 1953: 322; C.Y. Wu 1936a: 260–1, 287. See for
instance Hirst 1953: 324, 330–1. See also above: 178–82.
122
123
IPRC 1907g: 764–5; Lamb 1908: 21, 51–2; Sticker 1910: 220; Wu Lien-Teh 1936c:
387. See above: 281–3.
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how Scott and Duncan can have missed this information. In their paper
of 1996 they refer to the excellent standard work on plague by Pollitzer
of 1954124 where this information is given in the opening pages of the
chapter on the epidemiology of bubonic plague.125 In Shrewsbury’s
monograph the concept of latent period is presented under the term
“lag interval” on pages 3–4; Scott and Duncan have used Shrewsbury’s
monograph extensively, referring to Shrewsbury by name 116 times.126
The plague epidemic at Eyam has been the subject of considerable
scholarly interest. In 1977, L. Bradley published an outstanding paper
on the epidemic at Eyam based on family-reconstitution of the parish
registers; M.P. Coleman’s fine paper of 1986 is at least partly also based
on this technique; and Shrewsbury discusses the epidemic quite thor-
oughly, over quite a number of pages. Cohn and Alfani maintain that
Scott and Duncan performed a family-reconstitution study of the
plague at Eyam, but this is not correct: only Bradley has done that, and
Coleman at least partially, but Scott and Duncan only use wording or
phrasing that could easily produce such an impression.127 They also
insert their assumption of the very long incubation period. Bradley,
Coleman, and Shrewsbury point out that the duration of the time lag
between the first and second plague victim is characteristic of the early
development phase of bubonic plague, and represents a defining prop-
erty and an important factor for the identification of the disease as
bubonic plague.128 This point has been comprehensively documented
above in the chapter on latency.129 One should note that Scott and
Duncan refer to Shrewsbury’s and Bradley’s works, but do not argue
why Bradley and Shrewsbury were erroneous on this point.
The second part of the citation can now be usefully discussed.
Crucially for their argument, Scott and Duncan assert that the normal
or average duration of the disease from infection to death was thirty-
seven days and that infected persons were infective throughout the
whole of this period. The incubation period can be estimated by sub-
traction of five days for the course of illness and lasted, consequently,
124
Scott, Duncan and Duncan 1996: 16.
125
126
See above: 285 and fn. 21.
127
Cohn and Alfani 2007: 181–4. However, Scott has performed a family-
reconstitution study of the plague in Penrith 1597–8, which is cited in Scott, Duncan
and Duncan 1996.
128
Shrewsbury 1971: 524; Bradley 1977a: 70–2; Coleman 1986: 382.
129
See above, chapter 8: 279–88.
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648 chapter fifteen
normally or on average thirty-two days. More specifically, they also

maintain that they used a computer model130 and the Reed-Frost
model131 to calculate that this disease had an incubation time of thirty-
two days132 and that “a person once infected had over a month in which
he could travel a considerable distance before the dreaded symptoms
appeared.” This crucial point can usefully be amplified and enlarged
upon by some passages from their monograph:
The key to understanding the epidemiology of the plague lies in the
lengthy incubation period and, because of this, apparently healthy infec-
tives could move around the country on foot or horseback covering con-
siderable distances before they were struck down.133
In contrast [to bubonic plague: my insertion], infectious diseases with
very long latent and pre-symptomatic infectious periods (as we suggest
for haemorrhagic plague) would allow widespread progressive, wave-like
dissemination (see the Black Death, Chapter 4) when movement through
the metapopulation was mainly on foot, or, in later centuries, more rap-
idly along the established communication corridors when travellers and
carriers [of the disease: my insertion] had time to move long distances
across Europe by horse.134
[…] the lengthy incubation period provided a long time during which
each victim could achieve onward transmission […].135
A symptomless infective could spread the infection widely.136
By parasitising healthy travellers, it crossed alpine passes into northern
Italy; it travelled enormous distances inland by the river systems; it
crossed the Mediterranean to Italy and Spain and the Atlantic to Portugal
and the northern Spanish coast; it crossed the Channel and North Sea to
England, Scotland and Iceland and the Baltic to Norway.137
Ignoring the evidence and the fact that all other scholars and the
Icelandic chroniclers agree that the Black Death did not reach Iceland
and that it is geographically impossible to cross the Baltic to Norway,
these citations contain important information on their theory. Clearly,
Scott and Duncan assert that the disease was haemorrhagic plague,
130
131
132
Scott and Duncan 2001: 128. Cf. above: 285, 288.
133
134
135
136
137
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that haemorrhagic plague was characterized by a very long incubation

period of thirty-two days and that persons infected by this disease were
highly contagious during this period and could travel about without
symptoms, contaminating towns and villages on their way. Such mys-
terious highly contagious persons, “infectives” in Scott’s and Duncan’s
terminology, play a crucial role in their outline of the mechanisms and
dynamics of the spread of historical plague.138 In their view, this consti-
tutes decisive evidence that historical plague really was some variant of
Ebola or Marburg haemorrhagic disease.
However, Scott and Duncan are conspicuously loath to test their
assertions with relevant and adequate information on the manifesta-
tions of filoviridal disease according to the accumulated knowledge of
modern medical science. One should note that, according to updated
modern medical science on these dise ases as cited by the leading med-
ical experts at the CDC (Centers of Disease Control, Special Pathogens
Branch) and WHO (World Health Organization), the “incubation
period for Ebola haemorrhagic fever ranges from 2 to 21 days, i.e., on
average, 9.5 days, not 32 days.139 According to the twentieth edition of
Manson’s Tropical Diseases, the incubation period is, on average, seven
to fourteen days,140 normally presumably around ten days. The medical
scientific knowledge of the incubation period of Ebola disease and
Marburg disease is incompatible with the result of their purported
computation and this cornerstone and necessary condition of their
alternative theory is therefore false. On the basis of ordinary scholarly
considerations this would constitute decisive proof that historical
plague was not caused by a filoviridal disease.
The CDC also indicates that “infections with Ebola virus are acute,
there is no carrier state,”141 which shows that Scott’s and Duncan’s
numerous assertions to the contrary are not based on medical evidence.
This is not accidental: Scott and Duncan portray the two types of haem-
orrhagic diseases as highly or rather extremely infectious, while,
according to the CDC and WHO, these diseases spread only by “direct
contact with the blood and/or secretions of an infected person”/or
“direct contact with the blood, secretions, organs or semen of infected
138
Scott and Duncan 2001: 108, 134, 361, 366, 371.
139
140
141
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650 chapter fifteen
persons”142 and this transmission occurs only by contact with a patient

“in the acute stage of the disease,” and only if the person becoming
infected has abrasions or cuts in the skin at the point of physical con-
tact permitting contagion to enter (before the time of syringes).143 An
outbreak of Ebola haemorrhagic fever in a locality in the Democratic
Republic of Congo was subjected to an intensive study comprising
twenty-seven households in which someone had been infected with
the Ebola virus. It transpired that none of “the 78 household members
who had no physical contact with a case during the clinical illness were
infected. Ebola Haemorrhagic Fever is transmitted principally by direct
physical contact with an ill person or their body fluids during the later
stages of illness.”144 Clearly, this is a highly restrictive condition for the
transmission of infection (compared, for instance, with air-borne
cross-infection by infectious droplets) which makes for weak, even
very weak powers of spread. This is the reason that filoviridal diseases
appear “in sporadic, small or mostly even tiny outbreaks” and explains
why there is “no carrier state.” Thus, all known and medically studied
outbreaks of this type of diseases are characteristically sporadic and
small even in their core areas in Western Africa. Contrary to Scott and
Duncan’s assertions throughout their monograph,145 filoviridal diseases
do not have the infectious properties necessary to explain the huge
mortalities caused by historical plague epidemics.
The reason that the references in this discussion are mainly to Ebola
haemorrhagic disease is that the overwhelming proportion of cases of
fioloviridal disease belongs to this category. Marburg disease is a rarity
among the cases of a quite rare type of disease, which means that the
constellation of necessary conditions allowing infection of human
beings are even more specific, rare and local.
Scott’s and Duncan’s dramatic accounts of extremely infective carri-
ers of the disease walking or travelling through the late medieval and
early modern countryside or towns disseminating the disease with
tremendous efficiency are imaginary and fictitious. However, these
accounts of mysterious “infectives” play a crucial role, for they are
called upon in order to explain the spread of historical plague
epidemics.
142
143
144
Dowell, Mukunu, Ksiazek et al. 1999: S87–S91.
145
See for instance Scott and Duncan 2001: 363, 376.
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According to Scott and Duncan, the duration of the course of illness

of historical plague disease normally is three to five days, and this
proves that this is the duration of the course of illness of haemorrhaghic
plague.146 However, they do not provide evidentiary support for this
view. This does not mean that there is not interesting evidence availa-
ble. In the study of twenty-seven households in a locality in the
Democratic Republic of Congo where at least one member had con-
tracted Ebola haemorrhagic fever (see above), it was discovered that:
the median duration of the early phase of illness at home was 4 days
(range 0–9). The median duration of the late (hospital) phase of illness,
from admission to death or discharge, was 6 days (range 2–13) […]. The
median duration of illness, defined as the time from onset of fever to
death, was 10 days.147
This shows that the median duration of the course of filoviridal illness,
the duration which occurs most often, is 2.5 times longer than observed
in historical plague. The outcome of this particular study corresponds
closely to the generalized information on this point given in the latest
edition of Manson’s Tropical diseases 1996 that “Death occurs most
commonly on the ninth day, but between the second and twenty-first
day.”148 Again, Scott and Duncan’s assertion on the characteristic or
defining features of haemorrhagic filoviridal disesase can be shown to
be fictitious or spurious. According to the general standard works on
bubonic plague, the normal or average duration of the course of illness
in bubonic plague is three to five days, which corresponds to the obser-
vations made in historical plague epidemics and therefore constitutes
evidence to the effect that these epidemics were bubonic plague.
As mentioned above, Scott and Duncan assert with respect to impor-
tant clinical manifestations that the “symptoms [of historical haemor-
rhagic plague] were violet and black spots and blotches […] or small
red spots, indicative of a haemorrhagic disease, the bubo and pus-
tules.”149 “Thus, when all the characteristic clinical features of bubonic
plague are observed by contemporaries,150 Scott and Duncan simply
declare that this is evidence of haemorrhagic plague without providing
any research-based support to the effect that this is the case. This does
146
Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1.
147
Dowell, Mukunu, Kalazek et al. 1999: S88–9.
148
149
150
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652 chapter fifteen
not mean that relevant information is not available: according to

Manson’s Tropical Diseases 1996, filoviridal disease does not display any
such clinical features but “on the fifth to seventh day a morbilliform
[measle-like] rash (never haemorrhagic) is visible on white but not
African skins.”151 Neither are any of these clinical cutaneous manifesta-
tions mentioned in the presentations of the CDC or WHO on filoviridal
haemorrhagic diseases, only the rash.152 Thus, haemorrhagic disease is
not characterized by cutaneous haemorrhagic manifestations, i.e., by
black, violet or red spots or blotches on the skin, contrary to what Scott
and Duncan arbitrarily maintain. Neither are pustules mentioned in
association with filoviridal diseases. Instead, all these features are, as
shown above, usual manifestations in cases of bubonic plague.
Scott and Duncan also assert, as mentioned previously, that the ordi-
nary clinical occurrence of buboes does not at all prove that a disease is
bubonic plague, but that buboes are also a characteristic feature of of
haemorrhagic plague and other infectious diseases and, consequently,
do not constitute a defining feature for a single specific disease.153
Centrally, they argue that it is a fact that
the victims of both diseases [bubonic plague and haemorrhagic filoviridal
diseases: my insertion] presented with enlarged glands and subcutane-
ous swellings […]
The characteristic (but not specific symptom) of bubonic plague is the
appearance of the bubo […] victims of haemorrhagic plague also some-
times presented with swollen lymph glands.154
These two assertions are obviously at variance with each other, since in
the first citation buboes are presented as a general clinical feature of
filoviridal disease, while in the second citation it is presented as an inci-
dental or episodic type of occurrence. It has been demonstrated above
as an indisputable fact that buboes as an ordinary clinical manifesta-
tion of an epidemic disease are a characteristic feature only of bubonic
151
152
Centers for Disease Control and Prevention, Special Pathogens Branch, www
.cdc.gov./ncidod/dvrd/spb/mnpages/dispages/marburg.htm; Centers for Disease
Control and Prevention, Special Pathogens Branch, www.cdc.gov./ncidod/dvrd/spb/
mnpages/dispages/ebola.htm, and same but ebotabl.htm. 2003. “Ebola Hemorrhagic
Fever and Table Showing Known Cases and Outbreaks, In Chronological Order,”
pp. 1–4 and 1–3; WHO Information: 2003. www.who.int/inf-fs/en,fact. “Ebola
Haemorrhagic Fever,” Fact Sheet No. 103.
153
Scott and Duncan 2001: 6–7, 306, 362, 380–1, 388.
154
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plague and as such a defining feature of bubonic plague. Scott and

Duncan’s crucial assertions to the effect that buboes are also an ordi-
nary and characteristic clinical feature of other infectious diseases and
of any or some form of Ebola or Marburg haemorrhagic disease are not
supported by any reference(s) in a footnote or in the text to studies
providing such clinical evidence, not in this context or anywhere else in
their monographs. When Scott and Duncan at the very end of their
monograph finally provide some systematic but deficient clinical and
epidemiological information on filoviridal types of disease, their pres-
entation does not contain a word about buboes.155 In the research lit-
erature published in the three decades following the discovery of
Filoviridae in 1976, not a single patient has been registered who pre-
sented with a bubo or “swollen lymph glands.” This is the reason Scott
and Duncan are unable to present a single case in support of their
assertions on this crucial point, despite the fact that presumably most
serious infectious diseases may occasionally infect a lymph node and
cause the development of a bubo when infection enters through cuts or
abrasions in the skin.
In their monographs Scott and Duncan regularly claim identity
between the incidence of buboes in cases of bubonic plague and in
“haemorrhagic plague,” but the formulation “sometimes presented
with swollen lymph glands” indicates episodic individual occurrence,
which they also are unable to document. However, even if incidental or
episodic occurrence had been registered, this would not have signifi-
cance for the present discussion, since incidental occurrence is quite an
ordinary feature of infectious diseases. The pivotal point is that bubonic
plague is the only epidemic disease that presents with buboes as a regu-
lar and ordinary feature of the clinical panorama and this is therefore a
defining feature of bubonic plague. It was shown above that this is
stated in Scott and Duncan’s main source of medical information on
bubonic plague, Christie’s textbook, where it is specified that buboes
are a “distinguishing feature” of this disease.156
The Significance of Autopsies
Finally, Scott and Duncan turn to autopsies of plague victims, compar-

ing and discussing one modern autopsy of 1900 and three historical
155
156
See above: 339.
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654 chapter fifteen
autopsies from around 1660. Inexplicably, they have succeeded in find-

ing just one modern report of an autopsy of a plague victim. This is a
description of an autopsy of a sailor who had been aboard a ship sailing
from Rosario in Argentina via Buenos Aires to King’s Lynn and died
from plague near Cardiff in 1900.157 This autopsy was performed by
two physicians, W.G. Savage and D.A. Fitzgerald, who had no prior
experience with plague patients or plague autopsies and who had no
background for deductive inference. It was also performed under dif-
ficult circumstances putting considerable restraints on their work: “The
post-mortem examination of the patient W.G. was made at the mortu-
ary attached to the crematorium […] owing to unavoidable conditions
a more complete examination could not be made.”158 This is the only
case of a modern autopsy of a plague corpse mentioned by Scott and
Duncan, although thousands have been performed and numerous
cases are described or reported in the standard works on plague. This
paper is not mentioned in any of the standard works on plague.
This calls for some methodological comments: a single specimen or
individual occurrence, or, in this case, an isolated autopsy cannot be
used for drawing generalized inference to fact or reality, it can only be
used for establishing working hypotheses. Only a broader and more
composite set of data including independent cases can constitute mate-
rial for deduction and inference to reality or fact. As such, it is falla-
cious to use the autopsy of the sailor for inference to reality or fact and
also introduce it as part of a comparison with historical autopsies for
the purpose of making possible empirical differentiation between mod-
ern and historical plague. However, Scott and Duncan state undeterred
and unreservedly:
The important point to note here is that there are only limited signs of
necrosis in this autopsy report, in stark contrast with the post-mortem
examinations of those who died from haemorrhagic plague.159
The concluding reference is to the three historical autopsies which will
be discussed immediately below; first some preliminary comments
on the modern autopsy are needed. Since Scott and Duncan have
named their alternative disease “haemorrhagic plague” and have iden-
tified it as a filoviridal disease, one must be permitted to presume that
157
Savage and Fitzgerald 1900: 1232–6. Cf. Walford 1900: 1232.
158
Savage and Fitzgerald 1900: 1235.
159
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haemorrhages would be the characteristic feature. Yet here suddenly

necrosis, not haemorrhages, is the crucial or decisive point, and this
sudden new crucial point and turn of argument is based on a single
autopsy by a couple of physicians who have never before seen a plague
corpse.
However, although Scott and Duncan seem to describe the autopsy
report in some detail, central points are not mentioned. Savage and
Fitzgerald emphasize that “All the cultivations made from the blood
remained quite sterile.”160 This signifies that this plague patient, in con-
trast to over half of bubonic plague patients, did not develop significant
secondary septicaemia.161 Consequently, “the solvent action of plague
bacillus and its glutinous toxins”162 had not broken down the walls of
veins or tissues of buboes to a degree permitting microbes to enter
directly into the blood circulation.163 Since there is often an initial tran-
sient septicaemia in plague cases, this indicates that the infection dose
(ID) in this case was small and the immune apparatus succeeded in
eliminating the plague bacteria circulating in the blood stream.164 In
septicaemic cases, the blood stream becomes the agent for the distribu-
tion of the plague bacilli to the organs of the body, and the plague tox-
ins will damage the walls of veins and produce haemorrhages and
necrosis in the internal organs and tissues, cutaneous haemorrhages
and petechial or ecchymotic manifestations reflecting the bursting of
damaged capillaries. This lack of (significant) septicaemia and, as it
seems, small ID in the patient, are shown also by the unusual duration
of the course of illness which began, according to the sailor’s wife, on
21 September and ended, according to the medical statement, with his
death 4 October, after fourteen days of illness,165 in sharp contrast to
the usual duration of three to five days. This is a strong indication of an
atypical case of bubonic plague, information which Scott and Duncan
neglect to pass on to their readers. It may seem that Scott and Duncan
endeavoured to find an autopsy of an atypical case without significant
septicaemia in order to be able to formulate a view on internal necrosis
as a pivotal differential feature of haemorrhagic filoviridal plague in
contrast to bubonic plague.
160
161
Benedictow 19993/1996: 243–58.
162
Simpson 1905: 235.
163
Simpson 1905: 227–34.
164
Pollitzer 1954: 204–5, 414.
165
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656 chapter fifteen
The question must now be asked: Why do Scott and Duncan believe
that the standard works on plague do not describe autopsies? In fact,
several of them do, and on the basis of thousands of autopsies pro-
duced by and presented by outstanding scholars who have had over-
whelming opportunities to perform autopsies on plague cases in India,
China and elsewhere. In his chapter “Morbid Anatomy and Pathology,”
Simpson provides over twenty-three pages of both generalized infor-
mation from a great mass of autopsies and detailed descriptions of thir-
teen individual autopsies of plague cases. These thirteen autopsies
could constitute an acceptable basis for generalized inference to the
manifestations of plague disease as observed in post-mortem examina-
tions at a significant level of tenability but represent in this case a rep-
resentative sample of a much greater number of autopsies. Scott and
Duncan’s approach to this question is so extraordinary that I found it
worthwhile to count the number of times Simpson uses the terms
“haemorrhage” and “necrosis” in the twenty-three pages. The tally was
that the term “haemorrhagic” or “haemorrhages” are used a total of
seventy-two times, and the term “necrosis” or “necrotic” sixteen times.
Summarizing the significance of these clinical manifestations, Simpson
states:
Haemorrhages are, in fact, one of the characteristics of the disease
[bubonic plague: my insertion]. There are haemorrhages in nearly every
organ of the body, on the serous and mucous coats of the cavities, and in
and around the specially affected lymphatic glands. The plague bacilli
and their toxins appear to have a peculiar coagulative and necrotic effect
on the wall of the smaller veins and minute capillaries, leading to
exudations.166
Bubonic plague, judged by the pathological changes observed in the dead
body, is a disease both of the lymphatic and vascular system, on which
the plague bacilli and its toxins when brought in contact with them in
large numbers and quantity exercise an inflammatory, coagulative and
necrotic effect. The microbic agent and its toxins thus acting lead to
enlargement of the external and internal lymph glands, necrosis of their
substance and often haemorrhage or infiltration into the surrounding tis-
sues, to dilatation of the veins and capillaries, to destruction of their
walls, to haemorrhagic extravasations into nearly every part of the
body.167
166
Simpson 1905: 235.
167
Simpson 1905: 239.
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This summary of observations made in post-mortem examinations or

autopsies of plague victims is in full accordance with the shorter
accounts in other later standard works on plague.168 It is bubonic plague
which is the true haemorrhagic plague, and this is manifested exter-
nally by petechiae and ecchymoses on the skin and occasional bleeding
from the nose and mouth,169 and internally by comprehensive haemor-
rhages in the internal parts of the body.170 There is often comprehensive
necrosis of the internal organs and the vascular system in cases of
bubonic plague.
Scott and Duncan use the isolated single modern autopsy for com-
parison with descriptions of three historical autopsies, again without
taking into account questions of historicity and source-criticism. First,
they cite a description of a single post-mortem examination made
clandestinely by George Thompson, the physician, during the last
plague in London in 1665,171 “in his time greatly daring.”172 This is the
only post-mortem which is known to have been performed in connec-
tion with English plague epidemics. Thus, Thompson was not only
without prior experience in performing an autopsy on a plague victim,
he had no formal anatomical training in post-mortem examinations of
dead persons on which he could base his examination and understand-
ing of what he observed. Consequently, his interpretations of what he
saw were dependent on and affected by his highly deficient knowledge
of human anatomy and its tremendous complexity. Scott and Duncan
also repeat Cipolla’s citations of two brief contemporary reports on
autopsies performed in Naples and Rome respectively in 1656–7173
which were originally published by P. Savio.174 These three historical
autopsies represent the neonatal phase of the development of European
anatomy by post-mortem examinations, and they are performed by
physicians without formal training in anatomical dissection and with
highly limited understanding of the functions of the various parts of
168
Pollitzer 1936: 158–62; Chun 1936: 311–2; Pollitzer 1954: 203–17.
169
Simpson 1905: 247, 265; Manson’s Tropical Diseases 1921: 268.
170
Cf. Manson’s Tropical Diseases 1982: 339: “The characteristic appearance of
plague in a necropsy is that of engorgement and haemorrhage, nearly every organ of
the body participating more or less.”
171
172
Bell 1951: 128–9. The complete description of the autopsy is cited by Bell 1951:
335–8.
173
174
Savio 1972: 139–40; Cipolla 1981: 95–6.
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658 chapter fifteen
human anatomy and what caused changes in the appearance of various

internal organs and tissues.175 Cipolla states the point tersely:
it must be conceded that the rudimentary technology and the inability to
distinguish between pathological and cadaveric conditions made the
post-mortem reports of the period in question practically useless.176
The second part of Scott’s and Duncan’s comparison disappears here
into thin air as useless, a victim of the poor level of development of
medicine at the time. However, in addition Thompson’s autopsy per-
formed on a body still lying in its coffin can only be used as evidence
on the beginning of the history of medical autopsies in early modern
Europe. In his account, Thompson is frank about his purpose: he did
the autopsy for his “own instruction, and the satisfaction of all inquisi-
tive persons.”177 Thus, both parts of the comparison are useless for the
application of comparative methodology. It is a fallacious circular
assertion when Scott and Duncan summarily conclude that these are
“post-mortem examinations of those who died from haemorrhagic
plague” as if this identification of the disease is self-evidently correct
and not the central problem to be resolved.
In their monograph, Scott and Duncan cite part of one of the Italian
autopsies and conclude: “The similarities between the foregoing and
the case reports, description of symptoms and autopsy reports of
plagues in England, particularly in London, are striking.”178 The use of
the plural form indicating that more than one autopsy was performed
in England at the time is confusing and must be a slip of the pen, as
there is only one. Clearly, the fact that there are similarities between the
English autopsy and the two Italian autopsies does not warrant any
specific conclusion as to the identity of the disease and does not affect
the identification with bubonic plague. When Scott and Duncan later
revert to the topic of autopsies, they refer first to Thompson’s autopsy
and maintain that it
shows conclusively that, in patients who died, these outward signs
[petechiae: my insertion] were accompanied by extensive internal necro-
sis in which “no organ was found to be free from changes” […] compara-
ble degradative and necrotic changes were found in the autopsies in
175
176
Cipolla 1981: 96.
177
See fn. 172.
178
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Rome and Naples in 1656–7 (section 11.3.2). These signs are all indica-
tive of a severe haemorrhagic illness.179
This crucial assertion that extensive internal necrosis proves the iden-
tity of the disease to be filoviridal haemorrhagic disease is based on two
erroneous assumptions:
(1) Scott and Duncan imply on the basis of the single modern British
autopsy of 1900 that bubonic plague cases do not present with external
comprehensive cutaneous haemorrhages and with comprehensive
internal haemorrhages and necrosis, which has been shown above not
to be correct, on the contrary, exactly the opposite is the case. The
choice of the British autopsy of 1900 serves the objective of allowing
them to maintain that the three historical autopsies with their probable
descriptions of necrosis cannot be bubonic plague and therefore must
be cases of filoviridal haemorrhagic disease. This is, then, an instruc-
tive example of the fallacious use of comparative methodology because
the modern part is not representative and the historical part of the
comparison is based on only three cases imbued with serious eviden-
tial weaknesses of quality, competence, and anatomical knowledge.
Crucially, it is fallacious because the identity of the disease studied in
the historical autopsies has not been clarified by comparison with rep-
resentative modern autopsies of bubonic plague cases and representa-
tive autopsies of victims of filoviridal disease.180
In their popularized monograph, Scott and Duncan cite and com-
ment on Thompson’s autopsy and the two Italian autopsies in purported
comparative perspective with modern autopsies of bubonic plague and
state this even more clearly:
The signs, symptoms and autopsy reports of victims of bubonic plague
are entirely different from these: they do not display God’s tokens, nor is
there widespread necrosis of the internal organs.181
Here Scott and Duncan erroneously assert that they have presented a
sufficient number of modern autopsies of bubonic plague cases to per-
mit generalized conclusions and also erroneously assert that autopsies
of cases of bubonic plague did not display petechiae or widespread
internal necrosis. On both of these points, Scott’s and Duncan’s argu-
ment must be considered misleading.
179
180
See also Cipolla’s valuable remarks on these problems in 1981: 94.
181
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660 chapter fifteen
(2) The other assumption which allows them to produce this autopsy-
based argument is their claim that comprehensive necrosis is charac-
teristic of cases of Ebola or Marburg haemorrhagic diseases without
presenting any evidence in support based on necropsies of victims,
despite the fact that some relevant evidence is available: the CDC make
a few relevant comments to the effect that a “rash, red eyes, hiccups,
internal and external bleeding may be seen in some patients.”182 The
WHO’s statement on the matter is quite similar: “rash, limited kidney
and liver functions, and both internal and external bleeding.” As can be
seen, in these works nothing is said about necrosis. However, in the last
edition of Manson’s Tropical Diseases it is stated that
The virus is pantropic183 and invades cells producing necrotic lesions in
all organs. The liver shows necrosis of single hepatocytes184 with fatty
degeneration and necrosis at the periphery of the lobules […]
Bleeding occurs in the majority of cases, appearing towards the end of
the fifth day with haematemesis185 and bloody diarrhoea. On the fifth to
seventh day a morbilliform186 rash (never haemorrhagic) is visible on
white but not African skins.187
According to Manson’s Tropical Diseases, the clinical features of the
Marburg form of filoviridal disease “are almost identical to Ebola virus
disease.”188 Thus, although Scott and Duncan have neglected to docu-
ment the main clinical features of filoviridal diseases, it can be con-
firmed on their behalf that such cases are, indeed, characterized by
internal and external bleeding and by widespread necrosis of internal
organs. However, since this is also the case with bubonic plague, these
features cannot serve as a base for differential identification of the
infection by reports of post mortems produced around 1660. It is
probable that there are differences which can serve the differential
182
www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebola.htm 2003: 3.
183
“Pantropic” means having an affinity for or indiscriminately affecting many kinds
of tissues.
184
Hepatocytes make up 70–80 per cent of the cytoplasmic (gelatinous mass that
“fills” most cells) mass of the liver. These cells are involved in protein synthesis, protein
storage and transformation of carbohydrates, synthesis of cholesterol, bile salts and
phospholipids, and detoxification, modification and excretion of exogenous and en-
dogenous substances. The hepatocyte also initiates the formation and secretion of
bile.
185
“Haematemesis” means vomiting of blood.
186
“Morbilliform” means resembling measles.
187
188
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identification exist and establishment of another defining feature, but

they can only be ascertained by modern pathologists or anatomists as
part of a project aimed at this objective.
The African Confinement
Importantly, with respect to Filoviridae “researchers believe that the

virus is zoonotic189 and is normally maintained in an animal host that
is native to the African continent.” A special study on the possible host
animal emphasizes that “Marburg and virulent Ebola viruses are main-
tained in hosts that are rare and have little contact with humans or do
not readily transmit the virus.”190 This point makes it rather impossible
to envisage outbreaks and spread in Europe or Asia of these diseases
where this (these?) animal host(s?) and microbiological zootic
reservoir(s) do(es?) not live. Instead of facing this problem, Scott and
Duncan start their discussion of the spread of the Black Death in
Europe with Sicily and must reject the possibility that the Genoese gal-
leys returning from the Crimea were the source of infection. They sup-
port or borrow an untenable view of Twigg191 to the effect that the Black
Death could have been shipped to European Mediterranean ports out
of Syria or the Levant.192 In reality and long established fact, the disease
arrived about the same time in Syria and the Levant as in England, long
after it had arrived and spread in large parts of Mediterranean Europe
and spread from Marseilles all the way to Bordeaux on the Atlantic
coast of France, whence the contagion was shipped to Rouen, Melcombe
Regis and north-western Spain (A Coruña?).193
In an effort to strengthen their effort to avoid having to address the
origin of the Black Death in the south-eastern Russian plague reservoir
and transportation by ship out of the Crimea and via Constantinople to
the European Mediterranean cities, and move closer instead to the
homeland of filoviridal viruses, Scott and Duncan arbitrarily add North
Africa:
189
Any infectious disease that is able to be transmitted (vectored) from animals,
both wild and domestic, to humans.
190
Monath 1999: S127.
191
Above: 581, 585–6. Benedictow 2004. 57–67, and map pages 1–2.
192
Scott and Duncan 2001: 317, 318, 328, 332, 370, 384.
193
Benedictow 2004: 62–5, 68–104, 126–30.
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662 chapter fifteen
The Great Pestilence most probably originated in the Levant or from the
ports of North Africa.194
This is simply impossible and is easily corrected.195 “Most probably” is
an assessment of tenability at the highest possible level which requires
maximum empirical documentation. Scott and Duncan have not con-
sulted the only and fine monograph on the spread of the Black Death
in the Middle East and North Africa by M.W. Dols, which would have
clarified the matter. Scott and Duncan maintain also that the plague
epidemics which came from overseas in the fourteenth and fifteenth
centuries
probably originated from the Levant and North Africa and entered via
the ports at Venice and Sicily, or from France via Genoa and Leghorn
[Constantinople: my insertion].196
Here the level of tenability is lowered to “probably,” which is much
higher than hypothetical or possible and requires a good empirical
documentation. However, they again offer no evidence.
It has been shown in the preceding discussion and analysis of the alter-
native theory of Scott and Duncan that it is not based on modern med-
ical research on Ebola or Marburg haemorraghic diseases and therefore
has an arbitrary character. This has led to their arbitrary assertions of a
strongly mutated variant of one these pathogens which should have
equipped it with greatly different properties from the genetic origin
and that miraculously were tailor-made to the needs of their alternative
theory. As noted above, to introduce the concept of evolutionary devel-
opments by mutation without presenting a functional principle of
selection is a fallacy of methodology. This mutated variant is arbitrarily
assumed to have disappeared at the cost of making it impossible to
satisfy the central requirement for all scientific work, namely testabil-
ity. However, the theory is too flawed to be rescued by such means. In
the popularized version of their monograph, they do not reject the filo-
viridal theory altogether but they also launch a theory of an unknown
194
Scott and Duncan 2001: 370, 317, 318, 328.
195
Benedictow 2004. 65–7.
196
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type of disease that also since has disappeared. This may suggest that
medical scholars have pointed out to them that the filoviridal basis of
their theory is at great variance with present knowledge on filoviridal
diseases. Scott and Duncan have invented a phantom disease that suits
their case for an alternative theory but does not fit the facts on the
ground.
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CHAPTER SIXTEEN
COHN’S ALTERNATIVE THEORY
Cohn concludes with absolute certainty that the Black Death was not
bubonic plague caused by Yersinia pestis but he is completely unable to
identify any known disease that could have been the cause of the Black
Death or later historical plague epidemics.1 Since he argues strongly
both in his introduction and in his concluding chapter that survivors of
the disease acquired good and lasting immunity, and that plague there-
fore soon took on the character of a child disease, he has clearly a viral
disease in mind:
after several strikes, it became domesticated as a disease largely of chil-
dren. By contrast, to repeat, modern Yersinia pestis is unusual: humans
have no natural immunity to it and cannot acquire it.2
He also has in mind a disease spread by cross-infection with high spread
rates as emphasized on the first page and repeatedly later.3
Considering that we are discussing an epidemic disease operating
with great formative powers on European society over several centuries
which wreaked havoc in over thirty large-scale waves across the
Continent and in innumerable local outbreaks between these waves,
and which therefore left much evidence of various kinds to posterity,
much more evidence than any other disease, this may seem a rather
puzzling outcome.
The bubonic plague theory represents a consensus based on ample
material evidence and studies by numerous fine and outstanding schol-
ars and researchers. It has been shown in Part 3 and elsewhere that
rejection of this huge corpus of fine scholarly work requires compre-
hensive breaches of the ordinary methodological and source-critical
principles of scholarly work and comprehensive negligence of the
1
Cohn 2002: 1, 247.
2
Cohn 2002: 2–3, 249, 212, 238, 249. As shown above, Yersinia pestis produces, as
usual for bacterial pathogens, only relatively weak and transient immunity in survi-
vors, and re-infection of survivors in the same epidemic is quite usual. See chapter
6: 212–7.
3
Cohn 2002: 1–3, 138–9, 209; Cohn 2005: 1354–5. Cohn and Alfani 2005: 203,
where the spread rates of historical plague is said to be similar to those of influenza.
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cohn’s alternative theory 665
primary research and standard works on bubonic and primary pneu-

monic plague. In order to clear the way for his own alternative theory,
Cohn shows himself willing in his Part I to employ extraordinary
means to disparage the work of all scholars in the field of historical and
medical bubonic-plague research who have made valuable contribu-
tions and confirmed the bubonic-plague theory, which means almost
every scholar in the field. The revealing character of these endeavours
is reflected in the titles of the chapters “Scientists Square the Circle”
and “Historians Square the Circle,” an accusation of prevailing incom-
petence and intellectual dishonesty which cannot be credible to anyone
as characteristics of the dedicated work of historians and physicians on
the subject. In fact it is only revealing of the sort of means his alterna-
tive theory requires. In Part 2, “How S.K. Cohn Makes Physicians and
Historians Square the Circle” it is shown that his assertions and pur-
ported material points are untenable and invalid.
Cohn’s monograph is therefore primarily characterized by a furious
attack on the bubonic plague theory of historical plague and only mar-
ginally by the development of an alternative theory, since he is unable
to identify and present in a testable form an alternative disease known
to modern microbiology or medicine. In this construction, his mono-
graph differs sharply from the monographs of Twigg and Scott and
Duncan and from Karlsson’s paper where the construction and estab-
lishment of an alternative theory stand squarely in focus. In these cases,
the attacks on the bubonic-plague theory serve the legitimate purpose
of being attempts at clearing the way for the alternative theories,
although in the practical implementation they have been shown to be
untenable and exhibit little respect for the limitations of the methodol-
ogy of historical, medical, and social science. The various central
aspects of Cohn’s frontal attack on the bubonic plague theory have also
been thoroughly discussed in various chapters of this monograph and
have been shown to be untenable for various methodological and mate-
rial reasons.4
Cohn concludes that historical plague must have been a viral disease
spread by cross-infection that since has disappeared, and that is all he
will say about the central matter of his monograph.5 This reveals that
4
Above: 26–69, 74–7, 84, 86, 93–7, 136, 144–5, 151–273, 289–301, 314–20, 324–5,
340–80, 386 fn. 20, 387, 411–5, 487–8, 562, 647.
5
Cohn 2002: 247–50.
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666 chapter sixteen
his monograph is an unsuccessful attempt to construct an alternative

theory without being willing to admit defeat. Against the broad back-
ground of the preceding discussions of Cohn’s principal arguments, it
can therefore be dealt with briefly.
It should suffice to refer to part 4, chapter 10, “Defining Feature 4:
DNA of Yersinia pestis Reclaimed from Skeletal Remains in Historical
Plague Graves” which presents the by now quite considerable material
on DNA and proteins of Yersinia pestis recovered in plague graves from
the first pandemic of plague, the so-called Justinianic pandemic of
541–766, and the second pandemic of 1346–722. The systematic iden-
tification of the DNA of Yersinia pestis in quite numerous studies of
dental pulp and also proteins of DNA in bone material taken from skel-
etal remains in plague graves of these periods situated in highly varied
locations and parts of Europe, represent a decisive breakthrough. These
by now quite numerous and geographically varied studies exclude acci-
dental findings and also exclude the possibility that there could have
been a concomitant incidence of some other disease that should have
been overlooked in all these studies.
Also, each of the other defining features presented and discussed in
Part 4 excludes Cohn’s at best rudimentary alternative theory, and the
collective impact is devastating. Bubonic plague is the only known epi-
demic disease that presents with buboes as an ordinary clinical feature:
it is a defining feature of bubonic plague. The only other disease which
normally presents with buboes is tularaemia, also a bacterial disease
which is also normally transmitted by insects. And this is not, as under-
lined above, a coincidence, but associated with how ectoparasites trans-
mitting contagion will often or normally deposit it subcutaneously in a
position suitable for drainage through lymphatic tracts to lymph nodes.
Epidemic occurrence of buboes is, nonetheless, a defining feature of
bubonic plague, since tularaemia has only an episodic or endemic type
of occurrence and only outside human cultivated areas, principally in
forests and other types of wilderness, and is highly associated with
hunters who in these environments will be at risk of being exposed to
specific ectoparasites (see above).
No epidemic viral disease is known that is clinically characterized
by the normal occurrence of buboes. In principle, this represents an
exception-free rule which also for all practical purposes excludes
chance. There must be a systematic massive reason producing sys-
tematic clinical reflections or lack of reflections in the form of an
exception-free rule. One could start by asking how contagion conveyed
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by droplets in cross-infection and inhaled into the lungs would spread

from there to lymph nodes with anything approaching normal or fre-
quent incidence? The lymph nodes are part of the body’s first line of
defence against invasion through the skin, which explains the exclusive
role played by ectoparasites in disseminating disease characterized by
buboes as a normal or ordinary clinical feature. Cohn’s assertion about
the microbiological viral nature of historical plague contagion contains
therefore also an unformulated assertion to the effect that the only viral
disease that ever presented with buboes as a normal clinical feature in
patients, has since disappeared. This unique feature could on scholarly
premises possibly be discussed in terms of the usefulness of speculative
ideas or, perhaps, of microprobabilities. Since Cohn does not even
attempt to explain how inhaled viral contagion could be spread (fre-
quently) to the lymph nodes, these suggestions should also rather be
excluded from consideration.
Viral diseases imply good and durable immunity in survivors and
Cohn argues energetically that this was the case in historical plague
epidemics. However, it has been shown above that his material is much
too deficient to be usable for such an evidentiary purpose. It has also
been shown that there are, in fact, quite numerous references in con-
temporary sources to re-infections of the same person, also in the same
epidemic, and even cases of persons who had been infected three times
in the same epidemic.
It has also been shown that the mortality rates caused by historical
plague epidemics and the long-term development of population size
depend on the absence of immunity so that the whole population is
susceptible to plague infection the next time an epidemic appears,
including survivors. One important aspect of mortality in the case of a
disease that does not provide lasting immunity in survivors and which
therefore affects the whole population next time it appears, including
the adult population, is that parents fall ill and cannot provide nursing
care for their children or each other, which causes considerable super-
mortality in the form of secondary catastrophic mortality, especially
among children, the most vulnerable part of the population. When the
adult population is also affected, economic work grinds to a halt; in the
case of historical plague epidemics this is often in late summer and
early autumn before the start of the harvest. Plague epidemics are
therefore often accompanied by and followed by malnutrition or star-
vation that cause further supermortality and also may unleash hunger-
related diseases in weakened and vulnerable populations.
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668 chapter sixteen
These are important arguments and perspectives for the understand-

ing of the huge mortality rates in historical plague epidemics and their
long-term demographic effects. This means that while a disease which
confers immunity in survivors in principle may have as serious an
impact as other types of infectious diseases in the first original onslaught
on a naïve population, it must be very unlikely that a disease which
confers long-term immunity and therefore mostly hits children when it
reappears could cause the dramatic long-term decline of the European
population which was observed in the Late Middle Ages. Arguably, it is
not possible according to quite mechanical demographic considera-
tions. In this perspective, it becomes highly unlikely that historical
plague could have been a disease conferring lasting and good immu-
nity in survivors.
Cohn is unable to explain why a viral disease spreading efficiently by
cross-infection should have a seasonality strongly associated with the
warmer seasons, a feature so easily explicable by a theory based on a
disease transmitted and spread by insects. The powers of spread of this
type of viral disease tend to increase with cold wintry weather when
people tend to crowd or huddle closer together in small(er) rooms
which can more easily and affordably be heated and is, therefore, the
best time for colds and influenza, for instance. Cohn does not attempt
to identify any argument that can serve to explain this seasonal feature
of historical plague as a reflection of a viral disease spreading by cross-
infection, which represents an independent reason for falsification of
this theory.
The unique feature of latency periods is also inexplicable in terms of
Cohn’s alternative theory or any other alternative theory based on
interhuman cross-infection. Scott and Duncan at least try to address
and resolve this particular and conspicuous feature of historical plague
instead of ignoring it. The pattern of latency periods in modern and
historical plague, which is easily explicable on the basis of the known
properties and developments of bubonic plague infection by rat fleas,
remains unexplained by all advocates of alternative theories, and there-
fore retains its status as a unique and consequently defining feature of
this disease.
Cohn does address the extraordinary and unique feature of bubonic
plague called the inverse correlation between population density and
mortality/ morbidity rates. His ferocious and unfair attacks on Hankin’s
pioneering observation of this phenomenon not only in contemporary
India but also in historical plague epidemics is a sad chapter in the
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historiography of plague, as is his willingness to ignore all later research

corroborating and enlarging upon Hankin’s original observation. This
feature is incompatible with the theory of a virus spreading by cross-
infection, which would enjoy increasing powers of spread with increas-
ing population density of susceptible populations.
Cohn appears to believe that no legitimate scholarly demand can be
made on him for explanation of the disappearance of his alternative
viral contagion. It is just presented as a magic act for naïve believers,
which on methodological grounds makes it legitimate to presume that
it disappeared into the thin air from which it was taken. One should
consider the fact that Cohn has invented a virus with great powers of
transmission and dissemination within the enormous variation of
social milieus and circumstances and societal structures in the broad
European experience over three centuries and two historical periods,
or if the Justinianic pandemic is included, two more centuries and
another historical period must be added. One should also consider the
fact that a pathogen with great powers of transmission and dissemina-
tion in such enormously varied social milieus and circumstances and
societies would have dynamic properties that would make it most
unlikely that it would simply disappear. As a minimum, the demand
must be made on Cohn, or rather he should have made this demand on
himself, to illustrate or demonstrate how such diseases historically have
disappeared in order to identify the social or physical conditions in
which this would occur and provide this part of his theory a deductive
basis, however slight. When Cohn does not fulfil this minimal demand
on his theory, it shows that his theory is just arbitrary.
This is a point in the discussion where a helpful hand could be use-
ful. It is not accidental that historically important or significant epi-
demic diseases have displayed strong dynamic properties and therefore
generally seem, as far as can be ascertained, to be around still today.
Only quite recently has it been possible to witness how historically
important epidemic diseases, through the efforts of modern medical
science and huge vaccination programs implemented by national gov-
ernments and in a global perspective by the UN, have been eradicated
or appear to be in the process of eradication, such as smallpox and
poliomyelitis, respectively. The extreme rarity of the disappearance of a
historically significant epidemic disease in the pre-scientific past can
be ascertained by a look at E.H. Ackerknecht’s monograph on the his-
tory and geography of the most important diseases: he does not present
a single case.
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670 chapter sixteen
However, there is actually one instance available for study. The only
historically known disease of some significance to have disappeared by
itself is the sweating sickness (Sudor Anglicus) which appeared in
England in the years 1485, 1506–8, 1517, 1528, and 1551,6 but spread
also abroad in 1529 reaching, for instance, Denmark, south-eastern
Norway and the Duchies of Schleswig and Holstein in northern
Germany.7 The long intermissions of this disease could be taken to
indicate some special problems or requirements of transmission or dis-
semination which made it susceptible to extinction and also indicate a
zootic reservoir. It can hardly have been a viral disease disseminated by
cross-infection since it primarily spread in the late summer and early
autumn,8 which may indicate an insect-borne or water-borne disease.9
The demographic effects of the epidemics of this disease appears to
have been quite small,10 “it had only minor effects on mortality in larger
communities,”11 which can also be taken to indicate an inefficient mode
of transmission. An important aspect of this point is that the course of
disease appears to have been extraordinary severe and brief, death
often occurring within twenty-four hours according to contemporar-
ies.12 According to the Norwegian and Danish Councillor of the Realm
Henrik Krummedike in a private letter to his daughter, people “die very
6
Shrewsbury 1971: 154–68, 180–5; Slack 1985: 70–1.
7
Christiansen 2005: 80–96; Benedictow 2002: 148–50. Ibs 1996: 126–7.
Christiansen 2005: 88–9, has not found Henrik Krummedike’s letter from Norway to
his daughter in 1529, mentioned by C.F. Allen 1870. It is published in Diplomatarium
Norvegicum, vol. IX, no. 644, 16 September 1529, and cited in Benedictow 1977: 132,
and 2nd ed. 1987, and is more comprehensively and better discussed in my Norwegian
plague history of 2002: 150–2. Allen is mistaken in assuming that it was written in
Oslo; it was written in the Danish port town of Varberg in the county of Halland on the
eastern side of Kattegat north of the Sound after Henrik Krummedike had returned
from Oslo where he was a leading member of Duke Christian’s entourage as a leading
member of the Council of the Realm and expert on Norwegian affairs. In this letter
Henrik Krummedike is thus referring to the sweating sickness in Halland, the north-
eastern Danish border province with Sweden which was not conterminous with the
Norwegian border province Båhuslen in the north, since a narrow band of land along
the estuary of R. Göta Älv was Swedish and separated Båhuslen from Halland. Other
sources associated with Henrik Krummedike (whose private archive is preserved)
show that the sweating sickness spread in a serious way also into Båhuslen where it
caused some desertion of tenancies. Benedictow 2002: 152.
8
Christensen 2005. 83; Slack 1985: 83–4. See also date of letter mentioned in pre-
vious footnote.
9
See above: 311.
10
Slack 1985: 70–1; Benedictow 2002: 152; Christensen 2005: 82–3.
11
Slack 1985: 71.
12
Slack 1985: 70.
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fast, so that when they get it, they could hardly stand it for half a day
or one day at the most.”13 This feature provides an explanation for its
disappearance, namely that it killed its victims too fast to allow suffi-
cient incidence of transmission to occur and assure its survival by
infection, so the probability of transmission of the infection from one
diseased person to a healthy person fell under one and the epidemic
faded away, and soon also the disease itself for ever.14 This is the pattern
or model of primary pneumonic plague which cannot sustain an
independent existence in continuous form because it is contagious on
average only in 0.8 day (see above), much the same as in the case of
the sweating sickness, but can arise anew from cases of bubonic
plague who develop septicaemia (note also the development of non-
contagious forms, see above).
Not a single case of an important epidemic disease with great powers
of spread in a great variety of social circumstances over centuries is
known to the history of medicine to have disappeared by itself as pre-
sumed by Cohn’s theory, which emphasizes its arbitrary character and
why it is very improbable. At the heart of Cohn’s alternative theory is
therefore an assertion of the unique occurrence of such a phenomenon,
so superbly unique that he is not able to exemplify its factual occur-
rence in history and its social premises. Methodology is turned on its
head when this serves the defence of his theory by providing a quasi-
explanation of why his theory is not testable and, as he seems to believe,
therefore not falsifiable. However, it must again be emphasized that
testability and falsifiability are indispensable properties of all scholarly
hypotheses compatible with the methodology of science, untestability
means falsification ipso facto as a tenable and valid assertion of any
aspect of (human) reality.
Cohn’s alternative theory of the microbiological nature of histori-
cal plague can be rejected or invalidated on a number of independent
grounds, since it is incompatible with methodological, medical, epide-
miological, microbiological and other types of ordinary empirical
premises. Some of his assertions or the central implications of his the-
ory must be deemed extraordinarily improbable or speculative. One
should consider that all margins of uncertainty relate to each other
13
Diplomatarium Norvegicum, vol. IX, no. 644, 16 September 1529, see also foot-
note 203. My translation from the original source.
14
See also above: fn. 5.
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672 chapter sixteen
multiplicatively, and the multiplicative effects of highly improbable or

speculative assertions are only observable in an intellectual electronic
microscope.
This reflects also the fact that Cohn’s monograph is primarily a fierce
attack on the bubonic-plague theory of historical plague, since he is
unable to identify and present an alternative disease known to modern
microbiology or medicine or, as it seems, identifiable by paleomicro-
biological analysis. Instead, his inability to identify an alternative dis-
ease and the extraordinary means he employs to do away with the
bubonic-plague theory reflects the fact that the bubonic plague theory
is solidly founded in good scholarly work.
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EPILOGUE
In this monograph, the alternative theories of the microbiological

nature of historical plague presented by the so-called revisionists
against the bubonic plague theory have been thoroughly discussed.
The central arguments against the bubonic plague theory have been
discussed in comprehensive separate chapters in Part 3 and shown to
be based on ignorance of the primary studies and standard works on
bubonic plague. On the basis of the scholarly literature, it has been
demonstrated that their central assertions are untenable; these tenets
include: (1) the assertion that bubonic plague spreads only contiguously
between conterminous rat colonies, (2) the assertion that the black rat
was not widespread and usual all over Europe, (3) the belief that the
relatively small mortality rates in India around 1900 compared with
historical plague epidemics were due to differences between the dis-
eases (rather than the availability of modern anti-plague techniques in
India), and (4) the assertion that survivors acquired persistent immu-
nity for which there is no evidence (instead there is much evidence to
the contrary which indicates a bacterial disease). All basic conditions
for the spread of bubonic-plague epidemics were present in Europe at
the time of the Black Death and bubonic plague has the properties
needed for spreading efficiently all over pre-Industrial Europe.
Next, in Part 4 it was shown on the basis of the medical and epide-
miological literature that bubonic plague is characterized by a number
of defining features which are common to modern bubonic plague
and historical plague epidemics, among them (1) latency periods,
(2) inverse correlation between mortality rate and population density,
(3) seasonality, (4) buboes as a normal clinical feature in epidemics,
and (5) the reclamation of the DNA and proteins of Yersinis pestis in
biological material taken from historical plague graves associated with
the Justinianic pandemic 541–766 and the late medieval and early
modern epidemic in the period 1346–1722. The correspondence
between defining features of modern bubonic plague and historical
plague constitutes definite proof, with several instances of independent
sufficient proof, that historical plague epidemics were bubonic plague.
In Part 5, it was demonstrated that all of the alternative theories
are impossible, are argued in methodologically and source-critically
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674 epilogue
seriously flawed ways and on epidemiologically, medically, and materi-

ally untenable grounds.
On these grounds, the tenability of the bubonic-plague theory of
historical plague epidemics is confirmed.
Criticism, objections and the ambition to construct new explanatory

models or new theories are at the heart of all good scholarly work. It
has been a central objective of this monograph to improve the stand-
ards of possible alternative theories of the nature of bubonic plague in
the future by a comprehensive presentation of the methodological and
material prerequisites or conditions which must be satisfied in order to
form serious academic propositions deserving of serious discussion in
this field of scholarly work and research.
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APPENDIX ONE
BLACK DEATH MORTALITY IN SIENA: THE MATERIAL

PROVIDED BY THE NECROLOGY OF THE MONASTERY
OF SAN DOMENICO IN CAMPOREGIO AND
SUMMARIZED IN TABLE 5
This appendix contains the demographic material used and systematized in

Chapter 6: 245–68 and serves the purposes of full documentation and testabil-
ity and supplementary presentation of source-critical principles.
The Necrology is written in Latin by scribes who were not trained in keep-
ing demographic records. They have no standard form in which they record
the information, and thus they provide varying types or pieces of information.
Scribes often give only very brief and incomplete information on social status,
occupation or profession, marital status (for women), and so on. They also
have varying personal knowledge of the persons they record as buried in the
cemetery. One scribe takes a strong interest, probably because he thought it
was responsibility to do so, in giving accurate descriptions of the location of
the place of interment within the cemetery or buildings.
One should note that the Necrology’s editor has numbered the burials, but
because more than one person was laid to rest in the same grave on a number
of occasions, the number of interred is somewhat higher than the number of
burials. In some cases, the bones of persons buried elsewhere are transferred
to a grave in the cemetery, and so on, burials that must be deleted from the
material. On two occasions in the Black Death, a number of unknown per-
sons, three and four to six persons respectively, are laid in the same grave
without specification of name or gender, namely 796–3, 839–4/6, which means
that the number of registered males and females are smaller than the number
of interred.
All human beings are either sons or daughters, whatever their age. The
Latin terms filius and filia are used to designate patronymics for identification
of fathers independent of age; one must, therefore, keep in mind that use of
these terms do not specifically denote a child, though they are also used to
designate children. The terms filius and filia are inaccurate terms for indica-
tions of age. The only certain identifications of non-adult age, i.e., below the
age fifteen, are the terms puer = boy (Nos. 843, 881, 896, 976, 996, 1176,
1212/1229, 1227, 1231, 1233, 1425, 1909), puella = girl, (Nos. 466, 913, 1189,
1224, 1234, 1427, 1450, 1839), and parvulis = boy (1116–2, 1550). The term
juvenis = youth (1054, 1070–2, 1071, 1667) denotes persons around age fif-
teen. For practical reasons, here the age category of child, ages 0–14, includes
all that are called filius or filia or iuvenis without indication of marital status or
other indication of adult age (for instance, no. 113; Lippa, bighina nostra, filia
domine angele), or no. 1138 (Iohanna filia Antonii et uxor […]), which may
produce a slight exaggeration in the number of children. In the years 1338–46
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676 appendix one
there are sixteen cases where the scribe(s) indicate(s) that the father is dead by
adding olim = “deceased,” to the father’s name; this happens in the cases of
seven males and nine females (551, 582, 597, 608, 611, 667, 892; 279, 294, 312,
633, 658, 1021). Since this practice is discontinued by subsequent scribes
(except for one case in 1351, no. 892, and one in 1360, no. 1021), and since the
father had died, at least some and quite likely most of these recorded as filii or
filiae presumably were adults, and for practical reasons all of these persons are
considered adults; the other option would be to delete these entries from the
material. In the presentation of the basic material of children, males are men-
tioned first under each period or year (M) and females next (F).
Children 1337–39: Nos. M (1337) 236; M (1339) 304; F (1337) 255.

Children 1340: Nos. M 333, 412, 417, 473, 492; F 378, 393, 413, 463, 465, 466,
472, 485.
Children 1341–47: Nos. M (1341) 515; M (1343) 577; M (1344) 609, 621;
M (1345) 638; M (1346) 664; M (1347) 703, 706, 720; F (1341) 508, 519,
530; F (1342) 546, 553; F (1345) 651; F (1747) 705.
Children 1348: Nos. M 779, 783, 792, 813, 837, 838, 840, 843; F 747, 782, 785,
791, 800–2, 807, 834.
Children 1349–62: Nos. M (1349) 873, 881; M (1351) 896; M (1359) 976, 996;
1008; M (1361) 1038, 1054, M (1362) 1070–2, 1072. F (1349) 871, 878;
F (1353) 913; F (1358) 953; F (1360) 1032; F (1362) 1071.
Children 1363: Nos. M 1078, 1083, 1084, 1086, 1089, 1094, 1099, 1100, 1115,
1116–2, 1117, 1119, 1131, 1143, 1152, 1154, 1161, 1164, 1167, 1174, 1176,
1178, 1179, 1196, 1206, 1207, 1211, 1212(/1229), 1215, 1217, 1218, 1220,
1223, 1227, 1231, 1232, 1233, 1235, 1238, 1239, 1245, 1250, 1261, 1268,
1273, 1282, 1287, 1289, 1290, 1296, 1297, 1300, 1302, 1309, 1310, 1328,
1329, 1334, 1337, 1339, 1340, 1342, 1344, 1346, 1347, 1350, 1356, 1359,
1360, 1365, 1371, 1379, 1380, 1383, 1389, 1393, 1394; F 1081, 1087–2, 1093,
1094, 1102, 1103, 1106, 1107, 1112, 1118, 1121, 1123, 1126, 1128, 1130,
1134, 1136, 1142, 1145, 1147, 1153, 1157, 1158, 1159, 1162, 1165, 1166,
1170, 1177, 1183, 1184, 1188, 1189, 1192, 1200, 1201, 1204, 1205, 1214,
1219, 1222, 1224, 1234, 1241, 1242, 1249, 1252, 1259, 1265, 1266, 1269,
1270, 1277, 1280, 1295, 1311, 1315, 1321, 1323, 1324, 1330, 1343, 1345,
1353, 1358, 1363, 1374, 1375, 1376, 1378, 1386, 1390, 1391, 1396.
Children 1364–73: Nos. M (1364) 1402; M (1365) 1425; M (1368), 1456, 1463;
M (1369) 1470; M (1370) 1491; M (1371) 1509, 1511, 1528; M (1372) 1537;
M (1373) 1550; F (1365) 1427; F (1367) 1450; F (1369) 1487; F (1371)
1522.
Children 1374: Nos. M 1563, 1568, 1571, 1585, 1587, 1593, 1596, 1597, 1601,
1606, 1609, 1615, 1617, 1624, 1625, 1632, 1633, 1636, 1638, 1639, 1640,
1642, 1643, 1644, 1648, 1650, 1651, 1654, 1656, 1665, 1670, 1673, 1677,
1679, 1689, 1696, 1697, 1699, 1700, 1704, 1705, 1708, 1710, 1711, 1713,
1716, 1718, 1720, 1722, 1723, 1724, 1725, 1726, 1728, 1730, 1731, 1732,
1735, 1736, 1737, 1741, 1744, 1746, 1755, 1756, 1757, 1758, 1761, 1764,
1766, 1767, 1771, 1777; F 1572, 1573, 1576, 1591, 1592, 1594, 1600, 1605,
1608, 1610, 1611, 1612, 1613, 1614, 1616, 1618, 1619, 1621, 1622, 1623,
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black death mortality in siena 677
1627, 1628, 1629, 1635, 1637, 1646, 1647, 1649, 1652, 1653, 1658, 1664,
1666, 1669, 1671, 1680, 1682, 1684, 1685, 1686, 1687, 1692, 1701, 1703–2,
1706, 1712, 1704, 1721, 1738, 1739, 1752, 1763, 1775, 1778, 1779, 1781,
1782, 1783, 1784, 1785, 1786.
Children 1375–78: Nos. M (1376) 1809; F (1375) 1791, 1792, 1793; F (1376)
1810; F (1378) 1839.
Adults 1337–39: Nos. M (1337) 212, 214, 217, 220, 223, 224, 226, 227, 228,
232, 233, 238, 239, 240, 246, 247, 248, 252, 253, 256, 257, 258, 260; M (1338)
262, 263, 264, 265, 266, 267, 268, 270, 273, 274, 275, 276, 281, 286, 287;
M (1339) 295, 297, 298, 299, 300, 302, 306, 311, 313, 314, 316, 317, 318, 320,
323, 325, 326, 327, 329; F (1337) 213, 215, 216, 218, 219, 222, 221, 225, 229,
230, 231, 234, 235, 237, 241, 242, 243, 244, 245, 249, 250, 251, 254, 259, 261;
F (1338) 269, 271, 272, 277, 278, 279, 280, 282, 283, 284, 285, 288, 289, 290,
291, 292; F (1339) 293, 294, 296, 301, 303, 305, 307, 308, 309, 310, 312, 315,
319, 321, 322, 324, 328, 330.
Adults 1340: Nos. M 331, 334, 335, 336, 337, 340, 341, 343, 346, 347, 348, 354,
355, 356, 357, 360, 361, 362, 363, 364, 366, 368, 370, 371, 375, 379, 380, 382,
384, 385, 386, 387, 388, 392, 396, 397, 398, 400, 401, 404, 408, 414, 418, 423,
424, 426, 428, 431, 435, 436, 441, 443, 444, 445, 450, 451, 452, 454, 460, 461,
468, 470, 471, 480, 484, 488, 489, 494, 497, 499, 503, 504; F 332, 338, 339,
342, 344, 345, 349, 350, 351, 352, 353, 358, 359, 365, 367, 369, 372, 373, 374,
376, 377, 381, 383, 389, 390, 391, 394, 395, 399, 402, 403, 405, 406, 407, 409,
410, 411, 415, 416, 419, 420, 421, 422, 425, 427, 429, 430, 432, 433, 434, 437,
438, 439, 440, 442, 446, 447, 448, 449, 453, 455, 456, 457, 458, 459, 462, 464,
467, 469, 474, 475, 476, 477, 478, 479, 481, 482, 483, 486, 487, 490, 491, 493,
495, 496, 489, 500, 501, 502, 505, 506.
Adults 1341–47: M (1341) 509, 510, 511, 512, 514, 517, 518, 520, 521, 523, 526,
527, 529, 533, 536, 537; M (1342) 538, 539, 540, 541, 542, 547, 551, 555, 559,
563, 566; M (1343) 569, 570, 571, 573, 574, 575, 576, 578, 582, 584, 585, 586,
588; M (1344) 595, 596, 597, 598, 600, 601, 602, 604, 605, 607, 608, 610, 611,
612, 613, 617, 618; M (1345) 622, 624, 625, 627, 629, 630, 632, 637, 639, 640,
641, 644, 647, 650; M (1346) 653, 654, 655, 657, 667, 669, 670, 672, 674;
M (1347) 679, 681, 685, 686, 687, 689, 694, 698, 699, 701, 702, 704, 707, 708,
714, 716, 717, 718, 719, 722, 723, 725, 726, 728, 729; F (1341) 507, 513, 516,
522, 524, 525, 528, 531, 532, 534, 535; F (1342) 543, 544, 545, 548, 549, 550,
552, 554, 556, 557, 558, 560, 561, 562, 564, 565, 567, 568; F (1343) 572, 579,
580, 581, 583, 587; F (1344) 589, 590, 591, 592, 593, 594, 599, 603, 606, 614,
615, 616, 619, 620; F (1345) 623, 626, 628, 631, 633, 634, 635, 636, 638, 642,
643, 645, 646, 648, 649, 652; F (1346) 656, 658, 659, 660, 661, 662, 663, 665,
666, 668, 671, 673, 675, 676, 677, 678; F (1347) 680, 682, 683, 684, 688, 690,
691, 692, 693, 695, 696, 697, 700, 709, 710, 711, 712, 713, 715, 721, 724,
727.
Adults 1348: Nos. M 730, 731, 732, 734, 735, 737, 738, 739, 740, 743, 750, 752,
745, 755, 763, 765, 766, 767, 772, 781, 784, 787, 788, 790, 801, 803, 805, 808,
809, 812, 814, 815, 816, 820, 822, 823, 824, 825, 826, 827, 829, 833, 835, 836,
841, 842, 844, 845, 846, 848, 850, 852, 853, 854, 859, 860, 861; F 733, 736,
741, 742, 744, 745, 746, 748, 749, 751, 753, 756, 757, 758, 759, 760, 761, 762,
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678 appendix one
764, 768, 769, 770, 771, 773, 774, 776, 777, 778, 775, 780, 783, 786, 789, 793,
794, 795, 797, 798, 799, 802, 804, 806, 810, 811, 816, 817, 818, 819, 821, 828,
830, 831, 832, 847, 849, 851, 855, 856, 857, 858, 862, 863, 864, 865. Burials
of unknown persons, three and 4–6 respectively, without indication also of
gender: 796–3, 839–4/6.
Adults 1349–62: Nos. M (1349) 866, 868, 872, 876, 877, 879, 880, 882;
M (1350) 884, 886, 888, 890; M (1351) 892, 893, 898; M (1352) 899, 900,
901, 901, 902, 903, 905; M (1353) 908, 909, 911, 916; M (1354) 917, 918,
919, 920, 922; M (1355) 927, 928, 929, 931; M (1356) 934, 935; M (1357)
939, 940; M (1358) 942, 943, 944, 945, 946, 948, 952, 954, 955, 956, 957, 958;
M (1359) 960, 961, 965, 966, 967, 968, 970, 971, 974, 975, 977, 978, 982, 983,
984, 986, 988, 989, 990, 991, 992–2, 993, 995, 997, 998, 999, 1000, 1001,
1002, 1003, 1004, 1005, 1010, 1011; M (1360) 1012, 1013, 1014, 1016, 1017,
1019, 1020, 1022, 1024, 1025, 1026, 1028, 1029, 1031, 1033, 1036; M (1361)
1037, 1039, 1041, 1042, 1044, 1047, 1048, 1049, 1050, 1051, 1053, 1055;
M (1362) 1058, 1060, 1063, 1064, 1066, 1067, 1068; F (1349) 867, 869, 870,
874, 875; F (1350) 885, 889, 891; F (1351) 894, 895, 897; F (1352) 904, 906,
907; F (1353) 910, 912, 914, 915; (1354) 921, 923, 924, 925; F (1355) 926,
930; F (1356) 932, 933, 936, 937; F (1357) 938; F (1358) 941, 947, 949, 950,
951; F (1359) 959, 962, 963, 964, 919, 972, 973, 979, 980, 981, 985, 987, 994,
1006, 1007, 1009; F (1360) 1015, 1018, 1021, 1028, 1027, 1030,1031;
F (1361) 1040, 1043, 1045, 1046, 1052, 1056, 1057; F (1362) 1059, 1061,
1062, 1065, 1069.
Adults 1363: Nos. M (1363) 1073, 1075, 1082, 1085, 1090, 1101, 1105, 1108,
1111, 1114, 1120, 1122, 1124, 1127, 1129, 1132, 1133, 1135, 1139, 1141,
1144, 1146, 1148, 1149, 1150, 1156, 1160, 1168, 1172, 1173, 1175, 1181,
1186, 1187, 1193, 1194, 1195, 1197, 1199, 1202, 1203, 1209, 1213, 1216,
1221, 1225, 1226, 1236, 1240, 1243, 1246, 1247, 1248, 1251, 1253, 1254,
1255, 1256, 1258, 1260, 1262, 1263, 1271, 1274, 1275, 1276, 1278, 1279,
1281, 1286, 1291, 1292, 1293, 1294, 1299, 1304, 1305, 1307, 1312, 1314,
1317, 1318, 1319, 1320, 1325, 1326, 1327, 1333, 1335, 1349, 1354, 1355,
1357, 1364, 1366, 1367, 1369, 1370, 1372, 1373, 1377, 1381, 1382, 1385,
1387, 1392, 1397, 1398, 1399; F (1363) 1074, 1076, 1077, 1079, 1080, 1088,
1091, 1092, 1095, 1097, 1096, 1098, 1104, 1109, 1113, 1125, 1137, 1138,
1140, 1151, 1155, 1163, 1169, 1171, 1180, 1182, 1185, 1190, 1191, 1198,
1200, 1208, 1210, 1232, 1237, 1244, 1257, 1264, 1267, 1272, 1283, 1284,
1285, 1288, 1298, 1301, 1303, 1306, 1308, 1313, 1316, 1327, 1331, 1332,
1336, 1338, 1341, 1348, 1351, 1352, 1361, 1362, 1368, 1384, 1388, 1400.
Adults 1364–73: M (1364) 1401, 1405, 1406, 1407, 1409,1410, 1411; M (1365)
1414, 1419, 1421, 1423,1426, 1428; M (1366) 1431, 1432, 1435, 1436;
M (1367) 1439, 1440, 1442, 1443, 1446, 1451; M (1368) 1458, 1459, 1460,
1461, 1462, 1464, 1468, 1469; M (1369) 1474, 1475, 1476, 1477, 1478, 1479,
1483, 1485, 1488; M (1370) 1489, 1490, 1492, 1498, 1499, 1500, 1501, 1503,
1504, 1505; M (1371) 1507, 1508, 1513, 1518, 1519, 1520, 1523, 1524, 1526;
M (1372) 1530, 1534, 1535, 1539, 1542, 1543, 1546; M (1373) 1548, 1549,
1552, 1553, 1555, 1556; F (1364) 1403, 1404, 1408, 1412; F (1365) 1413,
1415, 1416, 1417, 1418, 1420, 1422, 1424; F (1366) 1429, 1430, 1433, 1434,
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black death mortality in siena 679
1437; F (1367) 1438, 1441, 1444, 1445, 1447, 1448, 1449, 1452, 1453, 1454,
1455; F (1368) 1457, 1465, 1466, 1467; F (1369) 1471, 1472, 1473, 1480,
1481, 1482, 1484, 1486; F (1370) 1493, 1494, 1495, 1496, 1497, 1502, 1506;
F (1371) 1510, 1512, 1514, 1515, 1516, 1517, 1521, 1525; F (1372) 1529,
1531, 1532, 1533, 1536, 1538, 1540, 1541, 1544, 1545; F (1373) 1547, 1551,
1554, 1557, 1558, 1559.
Adults 1374: Nos. M 1560, 1562, 1565, 1566, 1575, 1579, 1580, 1581, 1583,
1584, 1586, 1589, 1599, 1604, 1620, 1626, 1631, 1645, 1660, 1661, 1662,
1668, 1672, 1675, 1676, 1681, 1683, 1693, 1694, 1695, 1698, 1709, 1715,
1717, 1727, 1729, 1733, 1734, 1740, 1742, 1745, 1747, 1749, 1750, 1754,
1759, 1760, 1762, 1770, 1772, 1773, 1774, 1787, 1789; F 1561, 1564, 1567,
1569, 1570,1574, 1578, 1582, 1588, 1590, 1595, 1598, 1602, 1603, 1607,
1630, 1634, 1641, 1655, 1657, 1659, 1663, 1674, 1678, 1688, 1690, 1691,
1702, 1707, 1719, 1743, 1748, 1751, 1752, 1765, 1768, 1769, 1776, 1780,
1788.
Adults 1375–78: M (1375) 1794, 1798, 1799, 1800, 1802, 1804; M (1376) 1805,
1806, 1807, 1808, 1811, 1813, 1815, 1817; M (1377) 1820, 1821, 1822, 1823,
1824, 1825; M (1378) 1830, 1831, 1835, 1836, 1840, 1841, 1843; F (1375)
1790, 1795, 1796, 1797, 1801, 1803; F (1376) 1812, 1814, 1818, 1819; F
(1377) 1826, 1827, 1828, 1829; F (1378) 1832, 1833, 1834, 1837, 1838,
1842.
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APPENDIX TWO
THE ACCOUNTS OF THE ICELANDIC EPIDEMICS OF 1402–4

AND 1494–5 GIVEN IN ICELANDIC ANNALS1
These Icelandic accounts are important in the discussion of Gunnar Karlsson’s

views in Chapter 13 above. The most informative accounts of the first epi-
demic are provided by the New Annal (Nyi Annáll)2 and the Lawman’s Annal
(Lögmanns-annáll); I translate here the account in the first version:
[1402] Came out there [to Iceland] such a great virulent pestilence [‘bráðasótt’]
that men died within the third night, until a vow was made to celebrate three
votive masses with prayers and burning candles. It was also vowed to practise
dry fast [i.e. only eat vegetable foods] until Candlemas [2 February] and, for-
ever, water-fast before Christmas. After this, most people had time to confess
before they died. In the autumn, the pestilence ravaged the southern regions
so terribly that holdings were left completely deserted widely around. In many
places, those who survived were unable to take care of themselves. Dominus
Ali Svarthöfdason was the first priest to die in autumn, and next Brother Grimus,
priest in the church of Skálholt, then one after another of the resident priests,
Councillor Dominus Höskuldar on Christmas Day itself. Then died in this
place [Skálholt] all the learned men and lay men, except the bishop himself and
two lay men.
[1403] The year of great mortality in Iceland. Died Abbot Pal in Videy and
Dominus Thorstein from Helgafell. Died Dominus Runolf from Thykkvabær
and six brethren, but six others survived. Died Abbess Halldora in Kirkjubær
and seven sisters, but six survived. Domina Gudrun Halldorsdottir was conse-
crated abbess. Three times all servants there died, so that in the end, the remain-
ing sisters themselves had to milk the cows. And most of them were very unskilled,
as should be expected, because they had never before done such work. To the
church were brought, according to the count, 675 dead persons. After that, the
count was given up, because of the multitude who died. Likewise, the same year,
all the servants at Thykkvabær also died three times, so that only two brethren
remained there and one male servant of the court. [Here follow the names of six
well-known dead persons, presumably victims of the epidemic.]3
[1404] Second winter of mortality. In Skálholt [the cathedral centre of one of the
two Icelandic dioceses] all the servants died three times. Three priests died and
most of the clerics. Two priests survived.
1
My translations from Icelandic Norse.
2
Cf. Steffensen 1974: 45.
3
Annales islandici posteriorum sæcolorum 1922–7: 9–11. Also the Icelandic
Vatnsfjarðarannáll hinn elzti relates to this epidemic but it is written so long after the
event and is so infested with source-critical problems that it is not mentioned by
Gunnar Karlsson (or Jón Stephenson) who in other works shows good knowledge of
these important types of sources to Icelandic medieval and early modern history.
Annales islandici postseriorum sæcolorum, 1933–8: 22.
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the accounts of the icelandic epidemics 681
The most informative account of the later plague of 1494–5 is found in the
Bishops’ Annals of Jón Egilsson (Biskupa-annálar Jóns Egilssonar), translated
below in the somewhat compressed version of the Fitjaannáll (Fit.), but it
should be noted that the Skarðsárannáll (Skar.) also contains some interesting
information.
[Fit. 1494] At that time, pestilence and a great plague visited all Iceland, except in
the [area of the] Vestfjords, from Holt in Saurbær. Then, local communities
widely around were deserted. That plague is said to have come out of blue cloth
which had come out to Hvalf jord [from abroad] (but some say to Hafnarfjord at
Fornubudir). And when it first came out of the cloth, it was like a bird to look at,
and from it smoke went up in the air. It reached all places in this country, except,
as has been said above, in the Vestfjords. Four farmsteads in the east are also
mentioned as not having been visited, those are […]. Where there were nine
siblings on a holding, only two or three survived. From Botnsa southwards to
Hvitskeggshvammi (that is the whole [district of the] moot of Kjalarness) there
were no more than two boys, eleven winters of age, alive, and none others of the
same age in the whole bailiwick. That was Björn Olafsson, who later was priest in
Krysuvik, and Jón Oddsson who lived in Njardvik. Both became old men […].
That mortality was in the summer [i.e., of 1494], and almost all local communi-
ties were desolated. And at most of the farmsteads not more than two or three
survived, in some places one, and in some places none, and in some places chil-
dren lying at the breast of their dead mothers. In Skálholt, one child remained.
Every day, three or four and sometimes more were brought to the church at the
same time, and when six, seven or eight brought the dead to the church, then did
not return more than three, at the most four. They died while bringing others to
the grave, and ended in it themselves. Women sat dead beside their buckets in the
stalls and in the sheep sheds, so that three or four ended in many graves. Much
property then came in the hands of many, almost everybody received inheritance
from relatives, third cousins or closer relations […].4
[Skar. 1495–96] Great pestilence and plague over the whole of Iceland except in
the Vestfjords, from Holt in Saurbær: wide areas were desolated. Abbot Asgrimur
and all the prominent men in the North died except twenty with the bishop.
Every priest had to have seven churches. Then poor, common people came from
the Vestf jords, married men with wives and children, because they knew that
there were abandoned holdings in the north of the country. They could choose
the land on which they would settle, and many northerners are descended from
them.5
4
Annales islandici posteriorum sæculorum 1927–32: 27–8. Cf. Safn til sögu Islands
1856: 43–4.
5
Annales islandici posteriorum sæculorum 1922–7: 74–5.
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APPENDIX THREE
THE EXTRINSIC INCUBATION PERIOD AND THE

STRUCTURE AND COMPOSITION OF THE LATENCY PERIOD
In order to understand and explain the defining feature of bubonic plague

designated the latency period, some technical aspects of the epizootic process
among rats and the functions of their fleas must be identified and clarified.
A.B. Christie states that the time that passes between when a species of fleas
becomes infected and when it becomes blocked and infective is twenty-one
days.1 Technically, this period is called the extrinsic incubation period or the
infection-infectivity interval and represents a highly variable property between
various species of fleas. Christie’s number of days cannot be correct since it is
at variance with the established duration of the (first) latency period of nine-
teen to twenty-seven days. Christie is here referring to the early research on
this subject carried out by C.R. Eskey and V.H. Haas seventy years ago. They
found that
the extrinsic incubation in X. cheopis varied from 5 to 31 days, with an average of
21 days, at a mean temperature of 66° F., while in the case of N. fasciatus [the flea
of the brown rat] this period varied from 6 to 116 days, with an average of 41 days
[…] the average length of the extrinsic incubation period of plague in X. cheopis
which were kept in an incubator at 72° to 80° F. was 15 days, or 6 days less than in
the case of this species kept at a mean temperature of 66° F. Therefore, it would
seem that an increase in temperature may reduce the length of the extrinsic incu-
bation period of plague in these fleas.2
The importance of the observation of the effect of temperature on the extrinsic
incubation period for X. cheopis is obvious, since it is a typical fur flea which
enjoys in rat fur a stable and favourable microclimate, a condition that would
not be well simulated under laboratory conditions. Since the temperature in
rat fur will be higher than in rat burrows, this indicates that X. cheopis would
tend to become blocked in one-third or less of the time required by N. fascia-
tus. These results were part of a large-scale study of fleas involved in plague in
the south-western U.S.A. which was published in complete form the following
year. Eskey and Haas make the following comments in relation to their find-
ings on extrinsic incubation period cited above:
In the case of fleas found capable of transmitting plague the length of time
required for the extrinsic incubation of the infection is believed to be the most
important of all factors in determining the efficiency with which the different
species acted as vectors. For instance, if one species transmits in half the time
required for another, then the first species will spread the infection twice as
1
Above: 626.
2
Eskey and Haas 1939: 1473.
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the extrinsic incubation period 683
rapidly as the second, provided infected hosts give rise to an average of one vector
each. But, if the flea infestation of the infected hosts is sufficient for them to con-
tinue to produce 2 or 3 transmitting fleas per animal or if each infected flea infects
more than one host, the dissemination will be by geometrical progression, and
the fleas with the short incubation will be many times more active vectors than
the fleas requiring twice as long before their bites become infectious […] the bites
of rat fleas, X. cheopis, were infectious in a shorter time after their infection than
any other species of fleas that transmitted plague in sufficient numbers for judg-
ing the average extrinsic incubation for the species. The ability of infected X.
cheopis to transmit plague after a shorter extrinsic incubation than all other spe-
cies undoubtedly accounts for their superiority as vectors.3
Clearly, Eskey and Haas emphasize the properties of Xenopsylla cheopis which
make it a superior vector of plague disease.
A few years later, A.L. Burroughs, the entomologist, published a special
study of “the vector efficiency” of nine species of fleas, among them Xenopsylla
cheopis, Nosopsyllus fasciatus, and Pulex irritans, the term “vector efficiency”
including all of the relevant factors affecting the capability and frequency with
which they would transmit plague, and concluded:
X. cheopis, in these experiments, proved to be the vector par excellence that it has
long been claimed to be.
Of the species studied under comparable conditions, Xenopsylla cheopis was
much the best vector. Nosopsyllus fasciatus was better than the others […].4
This shows that Burroughs mainly confirmed the consistent findings of previ-
ous studies of the ability of various species of fleas to function as vectors of
plague from the beginning of such studies. This does not mean that Nosopsyllus
fasciatus did not have significant ability to develop blockage and transmit
plague according to this study, since eleven out of forty-eight fleas blocked,
but only six of them transmitted plague. However, its ability to transmit
plague was much weaker than that of Xenopsylla cheopis, in fact only about a
third: “ratio of transmission to fleas used” was 0.660 in the case of X. cheopis
but only 0.213 in the case of N. fasciatus, which, nonetheless, compares well
with 0 in the case of P. irritans.5 The different blockage rates relate to differ-
ences in the physiology and anatomy of the different types of fleas, making the
rat flea the plague flea “par excellence,” a characteristic noted by several prom-
inent plague scholars.6 Or in the words of Perry and Fetherston, X. cheopis “is
considered the classic vector and is the standard against which all other fleas
are measured.” This point is highlighted in Pollitzer and Meyer’s conclusive
comment: “these findings confirm the paramount importance of highly effi-
cient vector species in the transmission of plague.”7
3
Eskey and Haas 1940: 43–4.
4
Burroughs 1947: 381.
5
Burroughs 1947: 384, 394.
6
C.Y. Wu 1936: 250; Girard 1943: 32; Burroughs 1947: 381; Brygoo 1966: 39, Perry
and Fetherston 1997: 51, 53.
7
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684 appendix three
One should note Burroughs’s use of the phrase “under comparable condi-
tions,” since it contains the potentially fallacious notion that formal equality of
conditions for various species of fleas in the laboratory, in incubators or test
tubes, means real equality of living conditions whatever the ordinary condi-
tions in the biotopes or ecological niches to which they were evolutionarily
adapted. In the context of the present discussion, this implies the unformu-
lated and untested hypothesis that this also means real equality with respect to
the conditions effecting the pace and relative incidence with which these spe-
cies of fleas would tend to become blocked in nature. This may not appear
obviously likely in relation to the difference between fur fleas and nest fleas,
for example. In this connection, one may usefully note Burroughs’s observa-
tion that Nosopsyllus fasciatus “apparently feeds better than Xenopsylla cheopis
under the conditions of individual feeding described.”8 At this point of the
discussion it is appropriate to cite Hirst’s warning: “Experience has shown that
deductions from laboratory experiments and observations are by no means
always applicable to natural conditions in the field.”9 Or as formulated by
Christie in his textbook on infectious diseases: “Experiment may imitate but it
cannot reproduce nature, and laboratory findings often do not tally with what
happens in the field.”10 This is clearly relevant in this case, as empirical testing
will show, as we will see. In all fairness, it must be added that Burroughs too
was aware of this problem in more general terms: “A knowledge of the vector
efficiency of a species of flea acquired experimentally in the laboratory is prob-
ably, at best, only an approximation of its natural vector efficiency. This is
inevitable because of ignorance of the ecology of most species of fleas pre-
cludes the duplication of natural conditions.”11 The gradually decreasing dura-
tion of the extrinsic incubation period of X. cheopis in scholarly studies may
be taken to suggest that researchers have gradually succeeded in reducing the
effects of laboratory conditions in this respect, which is not to suggest that
those conditions do not still affect the outcome significantly.
The IPRC showed the basis of the latency period, specifically that from the
time of the introduction of an infective rat flea into a rat colony it took about
10–14 days before the colony was so severely reduced that rat fleas leaving
dead rats had difficulties in finding a new rat host and after a few days began
to attack human beings in their proximity. This means that the extrinsic
incubation time must be considerably shorter, since one must also take into
account the time needed for the subsequent periods of incubation and illness
of infected rats and the extrinsic incubation time of their fleas that would
make them infective. This has been confirmed and accepted by the authors of
the other standard works on plague.12 In this connection, several factors must
8
9
Hirst 1953: 165.
10
Christie 1980: 755.
11
12
Wu 1936c: 387; Hirst 1953: 140–1; Pollitzer 1954: 485; Pollitzer and Meyer
1961: 452.
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be taken into account: the extrinsic incubation time or the infection-infectiv-

ity interval varies strongly with temperature and the degree of septicaemia in
the blood the fleas ingest, and also with the species of flea because there are
large differences in the propensity of fleas to develop blockage. Xenopsylla
cheopis, the flea of the black rat, develops this condition more easily and rap-
idly than any other type of flea: “X. cheopis, in these experiments, proved to
the be the vector par excellence that it has long been claimed to be.”13 These
factors affect also the proportion of fleas that becomes infective, which is cru-
cial for the intensity of epidemic developments. These are variables that make
the relationship between laboratory conditions and conditions in nature or in
the field of plague disease quite tenuous in this case.14 In the words of Pollitzer:
“Little doubt can exist that, under the climatic conditions prevailing during
the plague seasons, the extrinsic incubation time is short.” More attention
should therefore be paid to the finding that Xenopsylla cheopis could block in
only five days,15 and to the fact that Christie wisely repeats: “laboratory
findings often do not tally with what happens in the field.”16 These points
are important because they relate to the pace and rhythm of development
of plague epidemics which represent central defining features of bubonic
plague.
Subsequent research has tended to reduce further the extrinsic incubation
time in X. cheopis and therefore to increase its vector efficiency. In 1997, Perry
and Fetherston indicated the normal time from infection to blockage in the
range of three to nine days and, since I have not noted any objections,17 this
must be considered the present scholarly consensus on the matter.
However, the periods of extrinsic incubation time established by the ento-
mologists are clearly very much too long not only for Nosopsyllus fasciatus to
produce such a temporal pattern of development characterizing the latency
period, it is also too long for the species of fleas which exhibited much the
shortest extrinsic incubation time, namely Xenopsylla cheopis, and clearly this
must be our focus. The extrinsic incubation period recorded for this species of
flea has now, as mentioned, been established at three to nine days, presumably
with increasing proportions of fleas blocking in the higher reaches of this
range. This is problematic as the outline of a standard scenario of spread of
13
14
Pollitzer 1954: 351–5; Hirst 1953: 323.
15
Hirst 1953: 323.
16
Christie 1980: 754–5.
17
Perry and Fetherston 1997: 51. “Two days after an infected blood meal, the stom-
ach exhibits clusters of brown specks containing Y. pestis. These develop into cohesive
dark brown masses, containing bacilli, a fibrinoid-like material, and probably hemin
[…]. Between days 3 and 9 after the infected blood meal, the bacterial masses may
completely block the proventriculus [= “fore stomach”], extend into the esophagus
[= gullet], and prevent ingested blood from reaching the stomach […] as the hungry
flea repeatedly attempts to feed, the blood sucked from the mammalian host distends
the esophagus, mixes with bacilli and is regurgitated into the mammalian host when
the feeding attempt is terminated.”
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686 appendix three
plague contagion based on standard assumptions will readily show. The point
of departure is the introduction into a rat colony of a blocked X. cheopis which
after having ridden in clothing or luggage will soon after arrival at a new
human habitation infect a rat. It would normally take at least four to five days
before the rat developed sufficiently severe septicaemia18 to cause the heavy
infection of the fleas feeding on it necessary to produce blockage of their ven-
tricular systems. According to the average duration of the course of plague
illness for this species, the rat would die 7.2 days after infection.19 The substan-
tial majority of the about seven fleas leaving this dead rat would normally tend
to become blocked and infective about two days later when they could infect
two or more rats on which they had settled and then a new period of incuba-
tion and disease of 7.2 days would follow before these fleas were released from
their dead hosts and possibly or probably would have difficulties in finding
new rat hosts. After about three days of fasting they would be blocked and
would begin attacking human beings in their proximity, producing the first
fatality among them after a period of eight days on average. Summarizing the
time elements of this process, the most favourable assumptions for the most
efficient vector of plague would produce a latency period of 27.4 days, corre-
sponding quite accurately to the maximum duration of the standard latency
period. There would among the great numbers of such cases in a plague epi-
demic be a significant number of cases where the earlier reaches of the range
of extrinsic incubation time would tend to occur, however, for the epidemic
process as a whole this rather long latency period would appear to be perhaps
incompatible with the rapid pace of the epidemic developments.
There are two factors which can function independently at least as partial
explanations for this finding and together can provide a full explanation. The
first factor or explanation relates to the adverse circumstances for this species
of fleas under laboratory conditions, which was pointed out above; these
adverse circumstances tend to delay the process of blockage formation and the
relative incidence with which it will occur. Since the objective of this estimate
is to establish the normal rhythm of the process from the introduction of a
blocked rat flea in a rat colony to the first human fatality, it is quite likely that
in nature, in real life under normal circumstances in rat fur, X. cheopis would
tend to block quite often in the shortest time or in lowest reaches of the
recorded time of the blockage-developing process, namely in three or four
days. An extrinsic incubation period of three to five days would have to be
quite usual in order to bring the process within the perimeter of the empiri-
cally well established ordinary duration of the latency period of nineteen to
twenty-seven days when this flea is involved, albeit mostly in the higher
reaches of this range. Still it would be difficult to explain the lower reaches of
this range.
The second factor may resolve this problem. In a research project on the
sensitivity of fleas to temperature, it was shown that X. cheopis infected with
18
IPRC 1906c: 521.
19
IPRC 1907g: 759.
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Yersinia pestis after feeding on infected rats preferred an ambient temperature

up to 1.6 °C cooler than did non-infected fleas. Further observations indicated
that this change in thermal preference is important in the transmission of
plague from rat to human by X. cheopis for two main reasons: (1) rats have
core temperatures approximately 1.5 °C higher than human beings. (2) infected
rats would react with fever to the plague infection which would produce a
further increase in temperature.20 “In view of the preference for cooler tem-
peratures in plague-infected rat fleas, it is possible that the fleas would actually
prefer the human host. This being the case, temperature becomes an impor-
tant factor in the transfer of Y. pestis from rat to man.”21 In short, infected rat
fleas of the species X. cheopis would tend to leave the host in an early phase of
the febrile process which sets in after the end of the incubation period of about
three days and would leave the rat two to four days before it normally will have
died.
With this background, it appears possible to conclude that recent research
has enabled construction of a fully tenable explanation of the duration of
nineteen to twenty-seven days of the first latency period in plague epidemics,
the period from the introduction of a blocked flea in a colony of black rats
until the first human fatality. This latency period is only compatible with the
normal flea (Xenopsylla cheopis) of the black rat acting as the vector of trans-
mission of bubonic plague between rats and man. Clearly, this flea satisfies the
conditions of empirical testing.
20
Thomas, Karstens, and Schwann 1993: 209–13.
21
Brown 1995: 931; Perry and Fetherston 1997: 55.
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GLOSSARY
Abscess Local inflammation of body tissue with deep suppu-

ration [secretion of pus] caused by bacteria which
destroy the cells in the centre of the area and leave a
cavity filled with pus.
Bacteraemia Presence of bacteria in the blood stream. See sepsis,
primary and secondary septicaemic plague.
Blain Pustule or vesicle, see below, historical word.
Boil Hard inflamed lymph node which may suppurate,
often used in the past to indicate plague bubo.
Carbuncle Localized dead body tissue (gangrene) caused by
plague bacteria (or staphylococci), usually by bacteria
left in the site of a flea’s bite, in which case it is called
a primary carbuncle.
Case mortality rate See lethality rate.
Case fatality rate See lethality rate.
Cutaneous Affecting the skin (Latin cutis=skin) see also
subcutaneous
Ecchymosis The passage of blood from ruptured blood vessels
into subcutaneous (see below) tissue, marked by a
purple discoloration of the skin. See petechiae.
Endemic Sporadic cases of an infectious disease in a human
population, too few to be considered usefully desig-
nated an epidemic, but which show that a particular
type of contagion occurs in a population, is called an
endemic phase or situation.
Entomology The discipline of natural science which studies
insects.
Enzootic Sporadic incidence of contagious disease among ani-
mals, cf. endemic.
Epidemic Disease that spreads rapidly through a population or
community for a period.
Epidemiology Science of epidemics, especially how epidemics are
spread and transmitted.
Epitaxis Bleeding from the nose (in plague caused by weaken-
ing of local blood vessels by the action of plague
toxins).
Epizootic Disease spreading among animals, i.e., a term corre-
sponding to the term epidemic among human
beings.
Eschar A scab, the crustlike surface of a healing skin lesion,
or a slough, resulting from injury by gangrene, burn,
or caustics.
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glossary 689
Expectoration Eject from lung airways thrown up by coughing.

In the case of plague, this bloody expectoration
may contain plague bacteria from consolidated
ulcers formed in the lungs by plague bacteria trans-
ported there in the blood stream (see secondary
pneumonic plague), which can be inhaled by other
persons and give rise to primary pneumonic plage
(see below).
Fatality rate See lethality rate.
Haemorrhage/ Bleeding. See also Ecchymosis and Petchiae.
haemorrhaging
Incubation period The period from infection to the outbreak of disease.
Infection dose A measure of virulence usually expressed as ID50, i.e.,
the number of microorganisms or micrograms of
their toxin (see this term) with which human beings
(or animals) must be infected in order to cause a mor-
bidity rate of 50 per cent. See Lethal dose.
Lethality rate The proportion of those who contract a disease which
dies from it.
Lethal dose A measure of virulence usually expressed as LD50, i.e.,
the number of microorganisms or micrograms of
their toxin (see this term) with which human beings
(or animals) must be infected in order to cause a mor-
tality rate of 50 per cent. See Infection dose.
Life table Life tables are based on series of age-specific death
rates for each gender and, shows, thus, the probabili-
ties of dying within particular age intervals according
to various life expectancies at birth. Or, if focusing on
the probabilities of surviving, life tables show life
expectancies at each age level in societies with various
life expectancies at birth.
Mixed epidemic Epidemic of bubonic plague comprising substan-
tial proportions of cases of primary pneumonic
plague, occasionally also of primary septicaemic
plague.
Morbidity (1) The quality of being ill/morbid; (2) incidence of
an infectious disease.
Morbidity rate Proportion of a population which contracts a specific
disease.
Mortality The number of people who die within a particular
period of time or on a particular occasion.
Mortality rate The proportion of a population which die no matter
the causal factors. Plague mortality is the proportion
of a population which dies from this disease in an
epidemic.
Naïve population Population without experience with a disease or dis-
eases, all members being equally susceptible.
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690 glossary
Paleomicrobiology Study of DNA or specific proteins reclaimed from

biological material of the past taken from remains of
human beings or animals.
Pandemic (1) Disease spreading in a serious way over large parts
of the world; (2) series of waves of epidemics. In
European history, plague has ravaged populations in
three protracted series of waves of epidemics which
are called pandemics. The first plague pandemic
occurred in the period a.d. 541–767; the second
plague pandemic occurred in the period 1346–1722
in most of Europe, longer in Turkish Balkans and
Russia. The Black Death is the first gigantic, particu-
larly disastrous and notorious wave of plague epidem-
ics of the second plague pandemic. A third plague
pandemic broke out in 1894, but was stopped by
countermeasures based on modern medicine and
epidemiology around 1940.
Pathogen Microorganism than can cause disease.
Pathogenicity The ability of microorganisms to cause disease, cf.
virulence.
Petechiae/ Dark coloured spots in the skin due to invasion by
plague spots plague bacteria of the capillary vessels of the skin, i.e.,
consequent upon the development of septicaemia in
the blood stream. Plague toxin weakens the walls of
the blood vessels which tend to break and leak drops
of blood, haemorrhages, which presents through the
skin as dark coloured spots, also called plague spots,
by contemporary Englishmen often designated (God’s)
token, since their appearance heralded imminent and
certain death. See Ecchymosis.
Plague focus/ In many areas of the world where wild rodents live in
plague reservoir great density, in colonies or otherwise, plague circu-
lates continuously in the rodent population. Such a
rodent population is called a plague focus.
Plague pox/ Patients who presents with so numerous pustules or
plague variola vesicles that the clinical picture resembles smallpox.
Primary Patients with primary lung infections have been
pneumonic infected by way of the respiratory system. Droplets
plague containing plague bacteria coughed up by persons
that have plague infection in the lungs (pulmonary
plague) are the source of infection (rarely also
animals). (Cf. secondary pneumonic plague, and
expectoration).
Primary This form of plague occurs when a flea disposits
septicaemic plague plague infection directly into a blood vessel or it is
passed directly on into the bloodstream without
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glossary 691
stoppage in a lymphatic gland (and development of a

bubo). Characterized by dramatic and rapid course of
illness leading to certain death without development
of bubo(es).
Pulmonary plague Fulminant type of primary pneumonic plague, i.e.,
caused by plague infection through the respiratory
tract. Dissection of lungs of such cases do not show
pneumonic foci of plague bacteria which produce the
cough with bloody sputum but present with only
hyperaemic (an excess of blood) and oedematous
(accumulation of excessive fluid) changes in the lungs
as well as marked septicaemic (see Sepsis) features.
These cases are designated pulmonary plague because,
though they are anatomically similar to the septicae-
mic cases encountered in bubonic plague, they were
etiologically different from them, the infection having
entered through the respiratory tract.
Pure epidemics Concept referring to the hypothetical notion that epi-
of primary demics of primary pneumonic plague can arise
pneumonic directly from droplet contamination, for instance
plague from the skinning of a plague infected animal or from
cats who have contracted primary pneumonic plague
from the killing of plague infected rodents. This has
never been observed in the field or reality. All known
epidemics of primary pneumonic plague have origi-
nated in cases of bubonic plague who have developed
secondary pneumonic plague (see below). This form
is, nonetheless, the notional basis of two alternative
epidemiological theories of plague in the past main-
tained by C. Morris and G. Karlsson and discussed
extensively in this monograph, see also Index of
Subjects and Index of Names.
Pustules Resemble vesicles and are due to invasion of the skin
by plague bacteria through the blood-stream, i.e.,
consequent upon the development of septicaemia.
See also Blain and Petechiae/plague spots.
Secondary In cases of bubonic plague in which plague bacteria
pneumonic pass on into the bloodstream plague bacteria are
plague transported also to the lungs where they quite often
consolidate and develop ulcers that cause a frequent
cough with bloody expectoration. This condition is
called secondary pneumonic plague, i.e., a pneumonic
condition that is secondary to the primary infection
of buboes. These cases are almost invariably mortal.
Such cases are the origin of primary pneumonic
plague.
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692 glossary
Secondary In about half of all cases of bubonic plague, bacteria at

septicaemic some point manage to overwhelm the lymphatic sys-
plague tem and pass on into the blood stream, causing a
bacteraemia which is secondary to the primary
bubonic condition, cf. primary bacteraemic plague.
These cases are almost invariably mortal.
Sepsis, septicaemic The majority of cases of sepsis are due to bacterial
infections, infecting agents or toxins, which invade
the blood stream. This allows them to spread to almost
every organ of the body. In this book, the terms
bacteraemia and bacteramic are used in the same
meaning.
Subcutaneous Lying or situated under the skin. See also cutaneous
Toxin A poison produced by microorganisms. Each specific
type of pathogenic microorganism produces its own
toxin which causes a particular disease when present
in the system of a human or animal body.
Vector Carrier of disease, especially insect that conveys path-
ogenic organisms from one person or animal to
another.
Virulence This term is closely related to the term pathogenicity,
i.e., the ability of microorganisms to cause disease,
but introduces in addition the concept of degree in
order to make it possible to differentiate between the
disparate abilities of various pathogenic microorgan-
isms to produce disease and cause death in infected
persons. Virulence is measured in terms of the
number of microorganisms or the micrograms of
toxin needed to kill a given host when administered
by a certain route. This is called the lethal dose (see
this term).
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INDEX OF SUBJECTS1
Alternative microbiological theories of Cohn’s disease, (see fn. 1, point 5)

plague in the past 16–7, 205–73, 289–90, 340–1, 411,
Anthrax, Twigg’s alternative 415, 664–72
theory 17–9, 82 fn. 33, 284, 327, Viral disease spread by droplets 1,
331 and fn. 82, 411, 424, 464, 470, 6–7, 28, 43, 66, 200, 205–73, 340,
487–8, 495, 553–609 and fn. 230, 379–80, 411, 415, 664–70
611, 639 Immunity, see also Viral
Airborne anthrax, see miasmatic- disease 205–273
telluric theory Child disease, see also Viral disease,
Cutaneous anthrax 556–9, 563, Black Death, Child diseases
571–3, 578, 590 fn. 145 below 218– 273
Epizootics among domestic animals Buboes 340–80
in the past 566, 574–81, 608 Ebola and Marburg haemorrhagic
Gastro-intestinal anthrax 318, diseases 18, 207, 284–90, 334–40,
556–9, 572 464, 487, 610–663
Interhuman transmission, never Afrian Confinement 581, 586, 636,
observed 558, 563 650, 661–2
Miasmatic-telluric theory, see also Bubo? 334–40, 638
Epidemiological theories 562–6 Carrier state? 288, 649–50
Mortality rate of gastro-intestinal Clinical and epidemiological
anthrax 557 features: fiction and facts 284–90,
Murrain, see Epizootics 305–8, 632, 636–661
Pulmonary or inhalational anthrax Density dependence, see also the
(occasional incidence) 556–7, Inverse correlation 290,
563, 572, 578, 591 fn. 144 305–8, 632
Visceral anthrax, see gastro- Incubation period 285, 288,
intestinal anthrax 648–9
Woolsorters disease, see Cutaneous Latency period 284–8, 639–41
anthrax Reed-Frost theory and model, see
Zoonoses of domestic animals, see also Epidemiological
Murrain theories 633–6, 640, 648
1
(1) The Index consists of an Index of Subjects, Index of Geographical Names and
People and Index of Names.
(2) For medical and epidemiological terms see also the Glossary, pp. 688–692.
(3) German and Nordic personal names and geographical names may include
letters not used in English that are entered alphabetically in the Index according
to the following phonetic rules: Å, å = AA, aa; Ä, ä, Æ, æ = AE, ae; ü = y; Ø, ø, Ö,
ö = OE, oe; ǫ = oe; ð = D, d; Þ, Þ = Th, th.
(4) In order to make titles of annals and chronicles and similar types of sources
more immediately and generally comprehensible, many of them have been translated
into English in the text and are entered according to the English translation in the
Index.
(5) S.K. Cohn, Jr. claims to have identified historical plague as an unknown disease
which he does not name, it is therefore entered in the Index of Subjects under Cohn’s
disease.
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718 index of subjects
Symptomless (travelling) infectives?, 115, 536–52, 553–5, 558–65, 567–74,

construed, see also Carrier 576–608, 611–2, 618, 629–31, 640,
state? 648–50 642, 648, 661–2, 664, 673, 675–9, 690
Transmission 649–50 Mortality rates, inegalitarian
Unknown mutated variant, see also according to social class, age and
Evolutionary theory 17–18, 487, gender 218–73, 299
636, 662 Children 42–3, 218–35, 240–1,
Alternative epidemiological theories 254–73, 598
of the Black Death and plague Youth 222–4, 236–7
in the past2 Women/females 257–8, 262–3,
Human-flea theory (Blanc, Baltazard, 348, 602
Walløe) 5, 9–16 and fns. 28 and 35, Mortality according to social class
28–9, 67, 110–2, 395 fn. 42 Customary tenantry 241, 299, 466,
Low-intensity theory of bubonic 480–2, 602, 632
plague (Shrewsbury) 16–7, Poor and destitute 224, 229, 239,
489–91 241–3
Primary pneumonic plague in Iceland Rural proletarians: cottagers,
(Steffensen) 16, 493, 500–22, sub-tenants, garciones 241–3 and
526–32, 535–8, 540–2, 550–552 fn. 136, 299, 602
Pure primary pneumonic plague Tenants-in-chief 421–5, 596–7, 600,
(Morris and Karlsson) 320–1, 332, 604, 607 and fn. 224
410, 487–8, 490–1, 493–552 Mortality of English parish priests in
American physicians (Vietnam War), see the Black Death according to first
also Butler 44–6 institutions 436, 453–8 and fns.
Anglo-Saxon England 127–8, 130, 134 161, 163, 462–3, 470–1, 475, 479,
Annals, see Chronicles under Sources 603, 631
Anthrax, see Alternative microbiological Origin of name Black Death 571–4
theories Seasonality of spread of the Black
Astrological-miasmatic theory, see Death, see also Plague seasonality
Epidemiological theories an Winter epidemics 108, 330, 398,
Autopsies, see Plague, autopsies 400–7, 413–6, 418, 420–5, 432–9,
445–6, 463–83, 521, 642
Barber surgeons 334, 638 According to institutions of parish
Bastard feudalism 255, 349 priests (England) 463–83, 521,
Bastard statistics, see also Quasi- 642
statistics (Cohn) 255–7, 346–9, Winter epidemics? 108–9, 113,
354–6, 359 252, 330, 397–426, 428, 433,
Black Death (1346–1353) Map of spread, 435–7, 460, 463, 471, 474–6, 479,
p. 2, 14–8, 20, 27–32, 34–7, 39–43, 482–4, 521
56–7, 59–62, 74, 76, 79–80, 82, 84, 86, Spread rates of the Black Death, see
91, 98–9, 106–10, 113–6, 122, 126, also Plague, Spread rates 27–32,
135, 137, 139, 147–8, 151–2, 169–70, 113–5, 151–2, 172–3, 464–5, 467–
173, 177, 180, 185, 187–8, 191–2, 194, 77, 585, 589–93, 595
201, 207, 218–23, 226, 231–3, 235–73, Territorial origin of the Black
289–90, 292, 294, 269–9, 314–6, 308, Death 499–500 and fn. 17,
311–2, 321, 323–7, 329–32, 340–80, 571, 580–1, 585–6, 620–1 and
382–4, 386 fn. 20, 390–4 fn. 39, 398, fn. 34, 661
400–1, 403–6, 407, 410–1, 413, 415–6, Boil, see Plague, Bubo and Glossary 324,
418 and fn. 61, 420–5, 432, 436–84, 331–2 and fn. 82, 347, 353–4, 356, 358,
489–91, 493, 496, 498, 500 fn. 17, 519, 363–4, 368–9 and fn. 180, 372–3, 491,
521–2, 527, 530–1 and fn. 108, 534 fn. 511, 540–1, 548, 612, 688
2
See also Blanc and Baltazard, Shrewsbury, Morris, Karlsson, Walløe.
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index of subjects 719
Organization of anti-plague measures Demographic techniques and structures

In India 194–205 Family reconstitution 62, 66, 68, 202,
In Hong Kong 202 234, 647
Bronze Age 121 Household size 65, 67, 202, 517 fn. 68,
601
Cardinal feature, see Plague, Defining Life expectancy 52, 148, 229 and fn.
feature 92, 230–1, 424, 428, 595, 600
Camels and plague 624 Life tables 229–32, 424, 597–8, 689
Cats 124, 137, 513, 691 Mortality according to size of
Cattle, see also Anthrax 81, 555–7, family 62, 65, 68, 146, 202–4, 268
566–7, 575–7, 579, 590, 592, Mortality rates (pre-plague), see also
594, 608 Plague, mortality
CDC, see Centers of Disease Control Density dependence, see Plague, Inverse
Censuses, see Demographic sources correlation
Centers of Disease Control and Diseases, see specific entries on Anthrax,
Prevention (CDC), see Index Cohn’s disease, Ebola disease, and
of Names Plague
Child diseases 207, 212, 248–35, 240, Dysentery 65, 327, 489, 509, 618
252, 267–8, 664 Exanthematic typhus 64–5, 67, 145,
Concept of (infectious) child 311, 322, 339, 489–91, 498, 509–10,
disease 222, 224, 227–8, 231, 618, 634
233, 235 Foot-and-mouth disease, see also
Fulminant development of plague Alternative theories, Anthrax
disease 233, 268 562–3, 575, 580
Mortality of parents, effects on German measles/Rubella 634, 636
mortality of children 233–4, Influenza 17, 19, 64, 67, 145–6, 489,
268, 667 590, 664fn. 3, 668
Supermortality of children in Leprosy 322 and fn. 30
bubonic plague 222–3, 233–7, Measles 205, 308, 489, 619, 633–5,
240, 271, 667 660, 698
Chinese Imperial Encyclopaedia 620 Poliomyelitis 669
Chroniclers, see Sources Small pox 205, 214, 317–8, 322, 327,
Civilizations (and concept), 47, 49–50 373–4, 376
and fn. 61, 254, 568–9 Sweating sickness 311, 670–1 and
Cohn’s disease, see fn. 1, point 5 and fn. 7
Alternative microbiological theories Syphilis 322
Commensal rats, see Plague, black rats Tuberculosis 322, 540
Corrody/corrodians 427 and fn. 84 Tularaemia, see also Diseases 319–20,
361, 379, 622 fn. 37, 666
Defining feature, see Plague Disparaging views of historians and
Distinguishing feature, see Plague, physicians
Defining feature Cohn 21–2, 25–69, 136, 172, 179–80,
Demography, see also Population 211, 353, 359
Demographic sources, see also Black Cohn, disparaging views of
Death and Sources of religious Benedictow’s work 29–30, 56–60,
institutions 62–3, 67–8, 74–5, 148–50, 169–80,
Bills of mortality 304, 434 290–301
Censuses, Icelandic of 1703, Indian Scott&Duncan 83, 87–8, 287, 611–5
of 1911, Chinese of 1912 52, 221, DNA, see Genetic aspects, Plague
238, 515, 532 pathogen, Paleomicrobiology
Parish registers, see Sources relating to
religious institutions Early Modern Europe 3, 26–7, 35, 56,
Poll Tax 1377–1378 600 66, 74–5, 80–1, 84, 86, 100, 103, 109,
Cemetery populations 232, 254, 122, 124, 130, 194, 199–201, 203–4
261–3 and fn. 35, 220, 226, 228, 277, 281,
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301, 323, 350, 369, 416, 421, 502 fn. Evolutionary theory, evolution of species
23, 521, 569, 592, 607 fn. 24, 612, 615, by selection of properties 18, 116–122
621 fn. 34, 629, 631, 645, 650, 658, Adaptation and change of
673, 680 fleas 119–20, 141, 399
Ebola and Marburg haemorrhagic Adaptation of horses by change of
diseases, see Alternative size and rougher coat 118–19
microbiological theories of Adaptation of rats by change of size
historical plague and rougher coat 117–22, 131,
Ectoparasites (bloodsucking insects), see 135, 137–41, 399, 440–1
Fleas, lice, ticks 5, 11–5 and fn. 28, Selection of plague strains by
112, 320, 379, 666–7 blockage in fleas 210–1
Emunctoria, see also Galenic Fallacious mutational theories (not
universalism 356, 359, 366 based on evolution by selection), see
Enzootic, episodic spread among Methodology
animals, see also Epizootic 4, 191, Theory of Karlsson 16, 18, 77, 487,
203, 399, 622, 688 494–6, 535
Epidemiological theories of contagion Theory of Scott and Duncan 17–8,
and dissemination 636, 662
Astrological theory see Miasmatic-
telluric theory Filoviridae, see Ebola and Marburg
Evil eye, infection by (evil) look Fleas, development from egg to
84, 362 imago 112, 396–7, 642–3
Fomites, infection by contaminated Natural mortality rate 396
objects 54–5, 81, 358–9, 615 Fleas, Evolutionary adaptation, see
Hippocratic-Galenic epidemiology, Evolutionary theory
see Miasmatic theory Fur fleas and nest fleas 108, 397,
Miasmatic-telluric theory/miasmatic- 406, 682, 684
astrological theory 39, 79, 560, Species in the text. See also Plague,
562, 564–6 Flea vector, Types of spread
Miasmatic and miasmatic- Nosopsyllus fasciatus (flea of the
contagionistic theories, airborne brown rat) 12, 683–5
and contagious miasma 54–5, 64, Pulex cheopis, see Xenopsylla
81–4, 91, 111–2, 220, 326, 337, 350, cheopis
352–3, 355, 358, 361–2, 509, 547, Pulex irritans (human flea) 10–1,
560–5 and fn. 32, 589–90, 614–9, 13 and fn. 35, 28–9, 683
645, 681 Xenopsylla cheopis (flea of the black
Microbiological epidemiological rat), see also Plague, Flea
theory 4, 7–8, 18, 21, 80, 318, 380, vector 5–6, 10, 12–3, 28–9, 89,
395, 553, 642 103, 119, 141, 156, 166–7, 180,
Reed-Frost theory and model 63–6 279, 398, 582, 627–8, 634, 682–7
Religious theory of epidemic Vector capacity/efficiency 5, 9–14,
disease 79, 81, 356, 615 28–9, 46, 66–7, 180, 203, 375,
Epizootic, see Glossary, also under Rats 393, 395, 407, 555, 582, 634,
and Alternative microbiological 682–7, 692
theories Fomites, see Epidemiological theories
Epizootics among domestic animals in
England, see Murrain Galenic universalism 54, 359
Epizootics among domestic animals in Genetic aspects, see Evolutionary theory,
medieval Iceland 608 Mutation and Paleomicrobiology
Murrain (including zoonoses in God’s token, see also Petechiae 286, 369
sheep) 83, 555, 562, 573, 576–7, and fn. 180, 374, 638, 659, 690
579–80 Great Plague (in London), 1664–66, 83,
Evil eye, see Epidemiological 210, 286, 304, 373–4, 413, 549, 554,
theories 119–20, 140, 399 567–8
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Haemorrhagic disease/plague, see IPRC, see Indian Plague Research

Alternative microbiological theories, Commission
Ebola and Marburg
Hanseatic cities/league 332, 403, 405, Justinianic (first) pandemic (541–766
418, 506–7, 569 ce) 3, 27, 214, 283, 327–9, 388–91
Hanseatic congregations in Bergen 332 and fns. 29–31, 574, 621 fn. 34, 666,
House rats, see Rats, Black rats 669, 673
Heriots 241, 466, 481–2
Hippocratic-Galenic medicine, see Latency periods, see Plague, Defining
Epidemiological theories and Miasma feature, Epidemiology, see Appendix 3
Hospitals 48, 147–8, 162, 168, 198, 216, Lethal dose (LD) 73, 689, 692
279–80 fn. 3, 312, 316, 322, 364, 370, Lethality, see Demography and Plague
372, 414, 515, 518, 545, 651 Lice (human) 9, 12 and fn. 28, 64, 67,
Humanists 322, 343–4, 350, 361, 401 395 fn. 42, 634
Hunters 319, 513, 626, 666 License to marry, see Merchets
Little Ice Age 416–7
Ice Age, see also Little Ice Age 120 Lymph nodes and Lymph tracts/vessels,
Icelandic epidemics of 1402–04 see Plague, buboes
and 1494–95, see Chapter 13:
493–552, Alternative epidemiological Malthusian theory and analysis 269 and
theories under Gunnar Karlsson, fn. 178, 517
and Appendix 2 Manchurian epidemics of primary
Climatic specificity 528–30, 536 pneumonic plague, see Primary
Clinical descriptions 536–42 pneumonic plague, Wu Lien-Teh and
Provenance? 501–7, 511 Bibliography 31, 511–27, 534 fn. 115,
Mortality rate 530–3 535, 539, 626–7
Mutation?, see Evolutionary theory Marburg disease, see Ebola disease
Painfulness of buboes 542–50 Marriage 195 and fn. 5, 268–74
Pleuritic pain in cases of primary Marriage register, parish (Givry) 270
pneumonic plague? 537–42, Merchets (feudal license to
546, 550 marriage) 271
Pure primary pneumonic plague in Sterility 269
Iceland? 533–5 Marxism, see also Kosminskiy 604–5
Immunity, see Plague Medieval and early modern medicine,
Immunity, viral diseases 17, 145, see also Source criticism 81–2,
147–8, 205–46, 249–50, 252–3, 264, 215, 220, 233, 326, 346–59, 361–3,
267–8, 272–3, 313 fn. 1, 393, 664, 366–7
667–8, 673 Clinical observation and examination
Incubation, see Plague, clinical features, of patients, contemporary 346, 348,
and Ebola disease 351–6, 358, 361–3, 365–7
Indian Plague Commission 33, 38, 51, Medication, examples 353, 358
175–6, 203 fn. 35, 213, 703 Medieval mind 78–84, 219–21, 344,
Indian Plague Research Commission 3, 346, 348–51, 353–4, 358–9, 361–7,
33–5, 41, 47–50, 53, 56–9, 66, 74–6, 589–92
92–4, 102–3, 105, 108, 111, 118, 140, Metastatic spread, see Plague, types of
148–204, 277, 279–80 and fn. 3, 284, spread
291–3, 296, 301, 373–4, 396, 416, 419, Methodology, principles and fallacies
567, 599, 616, 619, 623–4, 646, 684, Anachronisms 82 and fn. 33, 83,
703–5 100–1, 103, 120, 130, 357
Inheritance, see also Wills 262 fn. 168, Anachronisms and the functions of
267, 269–70, 424, 443, 681 historical periodization 99–102,
Institutions of parish priests, see Black 120, 130, 192, 228, 631, 669
Death, Mortality, Seasonality and Analogies, use, see also Fallacious
Sources of religious institutions use 100, 521, 563–4
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Argumentum or inference ex silentio, Idée fixe (Cohn) 33, 61–2

see Fallacy of In pari materia, see also Fallacious use
Bastard statistics, see Quasi-material of Comparative methodology 31,
and Quasi-statistics 86, 192–3, 304, 362, 537, 570
Comparative methodology, see also Necessary and sufficient conditions 7,
In pari materia 31, 44, 86, 192–3, 19–20, 30–4, 37, 74, 76, 89, 103, 105,
194–6, 201, 304, 362, 537, 570, 615, 112, 152, 180, 222, 262, 265–6, 289,
657–9 301, 308, 339, 379, 416, 459, 490,
Contemporaneity of events, 501, 511, 514, 522, 524, 530, 535–6,
methodological implications 439, 554, 558, 613, 626, 649–50, 686
462, 575, 592 Quasi-explanation (Cohn) 67
Explanation, character and function Random distribution and
of 39, 116, 164, 207, 209–10, 219, randomness 64–5, 307, 365,
263, 269, 310, 319–20, 339, 359, 469, 368, 377
497, 529, 565, 569, 590, 604, 628, Representativeness 31, 126, 222, 263,
669, 671, 686 280 fn. 3, 315, 345, 348, 352, 421–2
Fallacious use of analogy 100–1, and fn. 68, 424–5, 427, 440, 442,
563–6 445, 455, 517 fn. 68, 542, 571, 580,
Fallacious use of comparative 597, 600–1, 629, 642, 656, 659
methodology 31, 86, 172, 192–4, Rule of regularity 307, 387 fn. 20
201, 262, 304, 362, 365, 399, 537, Selective reading 25, 57–9, 273, 294,
570, 659, 684 567, 571
Fallacious use of evolutionary theory Speculation 106, 174, 207, 529, 564,
and selection 8, 399, 494, 496, 535, 578, 593
575, 662 Tenability, level of 37, 57, 106–7,
Fallacious use of models 633–6, 640 117, 158, 244, 293, 299, 340–1,
Fallacious use of wills (Cohn) 36–7, 362, 364, 426, 511, 564, 617, 637,
225–6, 260–2 and fn. 168 656, 662
Fallacy of abduction (inference from Testability, see Fallacy of invalidability
single case to fact/ Valid samples 346, 348, 356, 362, 365
generalizing) 355, 528–9, 654, 657 Working hypotheses, see hypotheses
Fallacy of argumentum or inference ex Miasma, miasmatic theory, see
silentio, inference from silence 78, Epidemiological theories
85–91, 97, 342–4 Mutation, see Evolutionary theory
Fallacy of circular inference 30, 232,
334–5, 563, 576, 638, 658 Nestorian graveyeard at Issyk-Kul
Fallacy of distribution 347 (see Index of Geographical Names
Fallacy of invalidability and People) 571
(infalsifiability), see Testability 13, Naïve populations, see Glossary 206,
17, 58, 123, 183, 218, 221, 245, 212, 235, 305 fn. 40, 668, 689
247, 247, 293, 341, 357, 364, Necrology, see under Sources, religious
439, 484, 553–4, 564, 638, Norse3 and Norse populations 99, 134,
662, 671, 675 537, 540, 693
Fallibility, see Invalidability, Testability
Hypotheses, uses of 63–4, 100–1, Obituary, see under Sources, religious
105–6, 111, 117–8, 121, 145, 162–3,
235, 243, 267, 291, 296, 340, 355, Paleomicrobiology of plague, the study
364, 500, 528, 556, 563, 575, 612, of DNA and proteins of plague
637, 654, 671, 684
3
Language of the Scandinavian populations and in Iceland and Greenland in the
Viking Age and the High Middle Ages, hence Norse(-speaking) people and
populations.
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pathogen of the past 18, 115, 381–95, Evacuation 20

472, 487, 690 Isolation by local rejection of
Microbiological identity of plague strangers or travellers 310
pathogen Isolation 195, 510, 615
Yersinia pestis 381–95 Quarantine and trade embargo 55,
Yersinia pestis, Biovars Orientalis, 195, 209, 613–5
Antiquae, Medievalis 387–8, Anti-plague measures in
392–5, 487 (494) Australia 47–52, 175
Yersinia pestis Orientalis (in all three Anti-plague measures by colonial
pandemics) 387–8, 392–4, 487–9 authorities in Hong Kong
DNA and proteins, specific of bubonic 1894–: 90–1, 202, 277, 373–4,
plague 218, 278, 329, 381–5, 387–9 519, 570
and fn. 28 no. 6, 391–3 and fn. 36, Anti-plague measures in
535, 666, 673 India 1896–c. 1920 48–52, 95–6,
Pali plague epidemic (India), see also 175, 194–205, 372, 673
Pali 43 Anti-plague measures in
Pandemics of plague, 541–766, Manchuria 1910–22 497, 499,
1346–1722, 1894–c. 1940 CE, see also 517–9, 525–6
Justinianic (first) pandemic 27–8, 40, Autopsies, post-mortem examinations
110, 387–8, 394–5, 487, 612, 690 of bubonic plague cases
Pathognomonic feature, see Defining Contemporary autopsies 653–4,
feature 277–8 657–9
Physicians, contemporary, see also Modern autopsies 373, 525–6, 539,
Plague tracts, Medieval Medicine 654–6
Chalin de Vinario 233, 357 Buboes, normal clinical feature in
Giovanni da Santa Sofia 353–4 plague, defining feature 312–80
Guy de Chauliac 109, 534 fn. 115 Contemporary notions and
Plague, bubonic rat-borne observations of buboes 322–334
Historical terminology for bubonic Buboes: Cohn’s problems 340–59
plague epidemics 40, 322–34, 342 Buboes: Boccaccio and
Forms of bubonic plague. See also Cohn 359–80
Buboes, Clinical features and Buboes and Tularaemia
Glossary Intense painfulness, sharp pangs of
Bubonic plague, main subject of pain 40, 324, 331, 333–4, 537–51
monograph but see 3–9, and Part Suppuration 549, 688
Four 277–395 Buboes, anatomical sites, associated
Mixed epidemics 109, 420, 520–1, with lymph nodes or (infrequently)
534 fn. 115, 689 glands
Plague pox/Plague variola 376–7, All over the body (Cohn) 366
690 Axillas/arm pits 314, 319, 323, 326,
Primary septicaemic plague 7–8, 328–30, 332–3, 354–5, 347, 356,
313, 524, 624–6, 689–90 359, 363, 366–7, 369 fn. 190, 491,
Secondary pneumonic plague 8, 107 542–5, 547–9, 612
and fn. 120, 313 fn. 5, 330 fn. 77, Breasts, under (Cohn) 364
332, 491–3, 513, 528, 534 fn. 115, Femoral 314, 316–7, 328, 332, 356,
549–50, 552, 621, 625–6, 689–91 366, 545, 548
Secondary septicaemic plague 7–8, Groin/inguinal-femoral 40,
313, 449, 548 fn. 144, 624–6, 655, 153, 286, 314–16, 323–33,
688, 692 342, 347, 354–5, 359, 363–4,
Anti-plague measures 366–9, and fn. 180, 542–5,
Anti-plague measures in 547–9
contemporary Europe 48–52, 55, Neck 286, 314, 319, 328–9, 333,
92, 95–6, 194–5, 203–4 and fn. 347, 356, 359, 364–7, 542, 545–6,
35, 209–11, 306, 310–1, 352–3, 550, 648
362, 510, 519, 613–5 Nose (Cohn) 364
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Other (infrequent) locations 313, Petechiae, cutaneous haemorrhages,

328, 351, 364, 366, see also God’s token 333–4, 346,
Thigh, see Femoral 359, 368–70 and fn. 180, 373–8,
Buboes, causation and function 638, 651–2, 655, 657–9, 690
Infective flea bite 313, 625 Plague pox/Plague variola 376–7,
Lymphatic nodes and glands 313 690
and fns. 1–2, 314, 317–8, 320–1, Plague spots, see Petechiae
326, 328, 330, 335, 337–8, 366–8, Pustules 331–3, 359, 364, 368–78,
540, 542, 544–5, 548–9, 652–3, 491, 559, 571–3, 612, 638,
656, 666–7, 691, 699 651–2, 690–1
Lymphatic system 5, 7, 313, 317, Secondary septicaemia 499, 626,
545, 625, 656, 692 655
Lymphatic tissue broken down by Vesicles 373–8, 690
plague toxin 626 Clustering of cases 64–5, 67–8, 145–6,
Lymph tracts/vessels 5, 313, 317–8, 199–204, 268
320, 379, 540, 625 Defining clinical and epidemiological
Buboes, proportions of locations 312, features 277–484
314–6 Concept of defining feature 277–8
Case mortality rates, see Lethality Buboes as unique normal clinical
Clinical features of plague, see also feature 312–80
Glossary and Defining features Development of bubonic plague
Blains, see Pustules epidemic, temporal rhythm
Bleeding from the nose 277–81, (682–7)
(epitaxis)367, 657, 688 Inverse correlation between
Blisters, see Cuticles, Pustules mortality and population
Bloody expectoration/sputum and density 16, 20, 34–8, 273,
cough (from secondary 289–311, 632, 668, 673
pneumonia) 8, 330–2 and fn. 77, Latency periods, see also
334, 491–2, 534 fn. 115, 547–9 Epidemiology 6, 16, 43, 75,
and fn. 144, 552, 612, 626, 689 279–88, 402, 431, 433, 466,
Buboes, see above 628, 639, 641, 644–8, 668, 673,
Carbuncles 326, 330–6 and fn. 82, 682–7
353, 373, 375, 491 DNA or proteins of plague from
Cuticles, see Pustules historical plague graves, see
Duration of illness 279–80 and fn. Paleomicrobiology
83, 288, 331, 534 fn. 115, 549 Epidemiology, see also spread of the
Ecchymosis, ecchymotic spots or Black Death, and for the initial
patches 373 and fn. 188, 375, epizootic phases see Latency period
378, 655, 688 under Defining features and
Eschar 377, 688 Epizootic under Rats
Extreme brevity of illness (primary Endemic phase 6, 85, 247, 280, 304,
septicaemia) 7–8, 84, 313, 524, 452, 524, 688
625, 690 Epidemic phase 6, 247–8, 280,
Fever, sudden and high 157, 282, 401, 431
328–30, 334, 351, 544–5, 548–9 Duration of disease in human
Haemorrhages, cutaneous, see beings (incubation +
Petechiae illness) 279–80 and fn. 3, 282,
Haemorrhages, internal 655–7, 659 286, 313, 331, 534 and fn. 115,
Headache, extreme 330–4 and fn. 549, 625
84, 491, 545, 548–9, 612 Duration of plague disease in
Incubation period 279–80, 281–2, rats 686
286, 288, 645–6, 689 Duration of epidemics 398–420
Necrosis 18, 375, 638, 654–9 Flea vector of human plague par
Papules, see also Pustules 374, 377 excellence, X. cheopis (see also
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Evolutionary theory) 4–5, 12, Grain/farina/bran, see also rice 27,

119–20, 141, 151–93, 683 56, 101–2, 105, 115, 129–30,
Attracted to man 6, 156–7, 151 fn. 3, 159–62, 166–7, 171,
160–1, 166 178–9, 183–4, 193, 393, 401,
Blockage, development of 5, 418–9, 492, 582
627–8, 682–5 Gunny bags 162, 178, 183–4
Blockage, selection of virulent Hides 178, 183–4
strains 210–1 Luggage/Baggage 6, 27, 56, 104,
Extrinsic incubation period, see also 116, 158 fn. 24, 162, 165–8, 171,
Appendix 3 and Evolutionary 173–4, 176, 178–9, 181–4, 187,
theory 627–8, 682–7 412, 472, 476, 568, 593, 595,
Fur flea 108, 397–8, 406, 682, 615, 686
684, 686 Merchandise, commodities 6, 55,
Infection-infectivity interval, see 104, 153, 159–61, 164–8, 171,
Extrinsic incubation period 173–4, 178–9, 183, 187, 419, 472,
Sensitivity to temperature in 492, 590, 593, 615
surroundings and in the Rags 118, 183–4, 361
host 682, 686–7 Rice 113, 166, 168, 179,
Septicaemia in human beings and Stockfish 418–9, 502, 506
rats 5, 14 Textiles 27, 151, 159, 174, 286,
Septicaemia, level required for 645–6, 681
blockage 10–1 Woolens, wool packs 27, 179, 331,
Survival period of infected, unfed 502, 555, 614
fleas 167, 180, 582, 645–6 Means of communication transporting
Vector capacity/efficiency 11, 682–7 infective rat fleas
Forms of spread by infected rat fleas Horse, packhorse, horseback,
Contiguous spread between cart 105, 132, 165, 172, 174, 444,
conterminous rat colonies 6, 113, 447, 472, 476, 648
146, 151, 155, 165, 167, 179, 175, Human beings/travellers, see also
178, 182, 189, 191, 193, 280, 567 Clothing and Luggage 104,
Human-flea theory, see Interhuman 163–5, 173–181 and fn. 85,
transmission 183–5, 189–9, 196, 202, 310, 580
Interhuman transmission by Pulex Lorry 165
irritans (human flea) 9–16 Railway 41, 58–9, 162, 164–5,
Metastatic spread over various 168, 170–2, 174, 176, 178, 196,
distances 6, 27, 104, 116, 144, 151–93, 517, 519
202, 280, 286–7, 293, 401, 433, 465, Roads, main 114, 116, 173, 191
472, 488, 492, 553, 568, 582, 585–6, Sailing ships, boats, and barges 55,
593, 595, 645 132, 153, 165, 168, 180, 185–7,
Saltatory spread, spread per saltum, 191, 398, 405, 419, 472–3, 477,
see Metastatic spread 501–5 and fn. 26, 569, 582, 586–7,
Medium of transportation of infected 589–90, 594
rat fleas Steamships 170, 176, 185, 196
Bedding 55, 154, 159, 174, 181–4, Fatality rates, see Lethality
187, 528, 614–5 Immunity, see also Re-infection
Clothing, clothes actively worn Lethality rates, see also Virulence 9
6, 9, 13, 27, 55–6, 104, 116, and fn. 14, 142, 205, 208, 210–1,
145, 151 fn. 3, 153–4, 158–62, 218, 220–1 and fn. 69, 233, 268, 296,
166–8, 171, 173–6, 178–80, 302, 512, 520 fn. 78, 557–9, 572,
182–4, 187, 195, 283, 286, 314, 578, 591, 606, 689
317, 358, 361, 363, 427, 472, Mass graves 256, 266, 381, 383, 385,
476, 492, 528, 568, 593, 595, 388, 391 fns. 32 and 34
614–5, 645, 686 Morbidity rates 296–7, 300, 302,
Cotton 27, 56, 166–7, 178–9, 183–4 468, 689
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Mortality rates according to Rise from secondary septicaemic

occupation 39–40, 143–5, 264 and plague, see also Glossary 8, 499,
fn. 171, 558, 572 516, 523–4, 626, 691
Plague pneumonic, secondary, see Size of epidemics 8, 518–22
Bubonic plague, Forms Spontaneous decline 518–27
Plague reservoirs (foci) 203, 513, Plague tracts, see also Medieval and early
580–1, 621 fn. 34, 661, 690 modern medicine 350–9
Plague seasonality, see also Black Specific medical works mentioned in
Death and Winter epidemics 75, the text 350, 354–5, 357
141, 247–53, 335, 396–436, 474, Pleistocene 121
528–9, 640–2, 644, 668 Population developments, see also
Seasonality of plague in Demography and Malthusian
England 1340–1666 420–83 theory 209, 489, 558, 595–608,
Transseasonal or multiseasonal 629–30, 668
type 398–420 Population size 600–6
Re-infection, see also Price history 178, 269 fn. 178, 421
Immunity 212–17
Sociology of rat-based plague 142–50 Quasi-empirical material (Cohn)
Spread rates of bubonic plague, see 218–24, 230–2, 237–45, 246–61,
also Black Death, Koliwada and 267–8, 341–59, 364–5, 367–79
India 17, 19–20, 27–32, 57, 113, Quasi-statistics and bastard statistics
151–94, 170–6, 590, 639, 664 (Cohn), see also Quasi-empirical
and fn. 3 material 245, 255–7, 341–9, 354–6,
Koliwada 94, 170, 173, 176, 178, 359, 365, 367, 370
189, 198
India 151–94
Vaccine, Haffkine’s anti-plague of Racism, accusation of, see also
1896 196 Ashburton Thompson and
Virulence 43, 209, 360, 525, 527, 529, Hirst 46–54, 174–5
689, 692 Rats, see also Plague, Forms of spread,
Historical stability by selection of Evolutionary theory
virulent strains by Terminology on rats
blockage 210–1 Commensal rats, domestic rats,
Plague pneumonic (spread by peridomestic rats, see Black rat
cross-infection) Mus decumanus, Rattus norvegicus
Primary pneumonic plague 8 and see Brown rat 134
fn. 13, 12, 27, 31–2, 107–9 and fn. Rattus rattus, Mus rattus, see Black
120, 113, 167, 213, 313 fn. 5, 321, rat 134
332, 376 fn. 200, 416, 420 fn. 66, Vǫlsk mus, see Black rat 134–5, 137
491–552, 625 History and role in plague of rats
Communicability/diffusibility Black rats in Europe, Prehistoric
(low) 499, 518–28, 535 times 120–1
Duration of epidemics, see also Black rats in Europe, finds of bones
spontaneous decline 505, from Roman to early modern
518–27, 639–42 periods 122–42
Duration of illness 523–4, 533–4 Black rat (Rattus rattus), history in
and fn. 115, 548–9 and fn. 144, Europe 53–4, 73–150, 180–1,
552, 571 286–8, 301, 395, 406, 417, 419,
Mortality rates 519, (530–3), 535 488, 495, 618, 634
Pulmonary plague 525, 527, 563, Black rat, role in plague epidemics,
690–1 its rat flea X. cheopis, see under
Pure epidemics of primary Fleas, Plague-Flea Vector 3–4,
pneumonic plague? 8, 16, 77, 6–7, 20, 29–30, 73–5, 158,
394, 492–9, 511–4, 521–2, 527, 160, 168, 170–3 and fn. 55,
533, 691 180–1, 191, 197–201, 281,
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286–7, 300–1, 396–8, 406, 419, Annal of Fitja (Fitjaannáll) 681

488, 495, 634, 646 Annal of Skálholt
Black rat, relevant elements of (Skálholtsannáll) 531, 536–7,
modern history in 551, 680–1
Europe 1700–1950 138–40 Annal of Skarðsa
Brown/grey rat (Rattus norvegicus), (Skarðsárannáll) 681
history in Europe and role in Bishop’s Annals of Jón Egilsson 681
plague epidemics, rat flea The Brut 223
Nosopsyllus fasciatus, see under Cronica (by the Villani brothers) 243
Fleas 53, 73–5, 99–100, 119–20, fn. 136, 258, 323–5 and fns. 34
125, 129–30, 133–4, 138–40, 147, and 43–4, 344, 347, 360, 413, 531
417 fn. 108
Rats, behaviour of black rats Fragment of an Annal of
Black rats, burrowing 92–6, 101–2, Skálholt 536–7 and fn. 120, 551
123–5, 140, 149, 172, 180, 682 Grey Friars’ Chronicle 472
Cannibalism 93–4, 623 Lawman’s Annal
Colonies, defending territories 102, (Lögmannsannáll) 99 fn. 91, 401,
185–6, 200, 279–80, 287, 301, 536–7 and fn. 118, 547, 551, 680
582–3, 628, 684–7 New Annal (Nýi Annáll) 502, 680
Dying rats, hiding in inaccessible The Oldest Annal of Vatnsfjörðr
places 92–6 (Vatnsfjarðarannáll hinn
Environments/biotopes/ecological elzti) 502, 680 fn. 3
niches, habitats 53–4, 92, 119, Official registrations
124–5, 140, 172, 301 Calendar of the Close Rolls 223
Fertility 118–9 Compoix d’Albi 239
Houses and house rats 74, 76, 92, Florentine Books of Dead 235, 264
96, 120, 131, 168, 197, 301 Wills (non-religious) 36–7, 225–6,
Mortality, natural rate 92 260, 262 and fn. 168, 401, 413–4,
Rat falls 78, 80, 85, 92, 96–7, 112 430–2
Ship rats 92, 131, 135, 301, 705 Wills, Court of Hustings 36–7
Size, variation, see Evolutionary Literary and proto-scientific sources
theory Book of Nature, by Konrad von
Epizootic, course of Megenberg 355
developments 6–7, 66, 185, La Divina Comedia, by Dante
200–1, 279–81, 582–3, 627–8, Alighieri 343
646, 682–7 Il Decamerone,
Septicaemia in rats, level and by G. Boccaccio 201, 344,
temperature dependency 5, 10–1, 359–60, 379, 618 fn. 27
14, 397, 643 Libellus de judicio Solis in conviviis
Reed-Frost theory and model, see Saturni, seu de horrenda illa peste,
Epidemiological theories by Simon Couvin 39 fn. 37
Regular clergy, see Sources, religious Sources relating to religious institutions
Renaissance 68, 80–1, 146, 209, Bishop’s registers 440–1 and fn. 137,
262, 322, 343, 350–1, 353, 531 fn. 443, 445–6, 449–51, 455–6, 460–1,
108, 631 463, 468–9, 484, 603
Revisionists, see Alternative theories Bishops’ administrations and
co-travelling staffs 444–5, 447–8,
Selective reading, see Methodology 460, 462, 468
Sheep 555, 562, 573, 575–6, 579, 590, Bishops’ circulation of
592, 594, 608, 681 dioceses 444, 447–8
Ship rat, see Rats Bishop’s registers and institutions of
Small pox 205, 214, 317–8, 322, 327, parish priests, see also Black
373–4, 376 Death, Mortality and Seasonality
Sources (written), non-religious according to institutions 192, 434
Chronicles and annals fn. 111, 436–84, 379, 618 fn. 27
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Duration of vacancies in parish Books registrating endowments for

benefices 436–63, 467, 470–1, religious services
475, 483, 602–4 Calendars 238, 341–2
Institution of parish benefices in the Necrologies, see also below 341–2
hands of the king 440–5 Necrology of the Monastery of San
Lapses of parish benefices to the Domenico in Camporegio 218,
bishop 455, 461, 483 231–2, 245–68, 273, 325 and fn.
Mortality according to first 45, 675–9
institutions, see Black Death Obituaries, see also below 426, 429
Patronage and advowsons 443–4, Obituary of the Cathedral of
451 Lund 59–60
Pluralism and absenteeism 443, Obituary of Christ Church Priory,
447, 602 Canterbury 426
Vacancies by exchange, resignation, Obituary of Santa Maria Novella in
retirement 438, 443, 445–6, Florence 261
450–1, 456–7, 470, 602 Parish registers
Diocese of Bath and Wells Parish registers of Central
(Sommerset to the Europe 521
R. Avon) 449–50, 459, 463, Parish registers of Colyton 62, 66,
475–8 202, 234
Diocese of Coventry and Lichfield Parish registers of Devonshire 295,
(Shropshire, Staffordshire, 433–4, 474
Derbyshire) 192, 445, 449, Parish registers of Eyam 68, 410,
454–5, 460–1, 603 647
Diocese of Ely Parish registers of Givry 108, 114,
(Cambridgshire) 449–50, 455–6, 270
465, 603 Parish registers of Penrith 284, 647
Diocese of Exeter (Cornwall and fn. 127
Devon) 449–50, 453, 455, 463, Registers of monks 60, 224–5, 229 fn.
470–4, 603 89, 426–30 and fns. 87 and 93, 453
Diocese of Hereford (Herefordshire, Saints’ lives 364
Shropshire to the R. Severn) 449, Source criticism
456–8 Cohn, deficient or lacking
Diocese of Lincoln (Oxfordhsire, source criticism, see also
Buckinghamshire, Hertfordshire, Quasi-statistics and Quasi-empirical
Bedfordshire, Huntingdon, material 36–7, 39–40, 42–3, 55,
Rutland) 439–40, 449, 59–60, 67–8, 86, 144–5, 200–1,
451–2, 603 218–24, 230–2, 236–40, 242–5,
Diocese of Norwich 449 247–68, 341–58, 359–70,
Diocese of Salisbury (Dorset, 372, 380
Wiltshire, Berkshire) 437, 461, Source criticism and the Medieval
463, 465, 467–70, 474 mind 78–84, 85–91, 219–24,
Diocese of Winchester 235, 254–5, 259–67, 324–58,
(Hampshire, Surrey) 241, 359–70, 380
449, 463, 479–82 Soviet plague research(ers) 3, 10,
Diocese of Worcester 58, 210
(Worcestershire, Gloucestershire, Spread per saltum/by leaps, see Plague,
Warwickshire) 449, 458, spread
460, 475 Stalinist biological theory xv
Diocese of York (Nottinghamshire, Statistics, see also Quasi-statistics
Yorkshire to the R. Tees and Bimodal pattern 296
R. Humber, Lancashire (from the Binomial expansion 64
R. Ribble) 439–42 and fn. 137, Comparative statistical
446, 449, 603, 631 inference 345
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Extrapolation 247, 251 Tularaemia, see Diseases

Random distribution 64–5, 307
Sweating sickness, see Diseases Vietnam War, plague research 3, 44–6,
193, 233–4, 315, 377, 520–1 and fn. 82,
Ticks 319 524, 545, 566
Trading stations on the Black Sea Viking Period 125–6, 132–4, 140, 395
and the Mediterranean 588 Viral diseases, see immunity
Tudor and Stuart England 179, 294,
432, 615 Zoogeography 104–5
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INDEX OF GEOGRAPHICAL NAMES AND PEOPLE1
A Coruña 661 Assam, province (India) 148–9

Adriatic Sea 588 Astrakhan Guberniya (Russia, at Caspian
Africa(n), see also South Africa 9, 29, Sea) 520
87–9, 98, 188, 191, 386–7 fn. 20, 581, Atlantic Ocean, see also North
585–6, 637, 650, 660–2 Atlantic 404, 648, 661
Aix-en-Provence (southern France) 190 Atmour Mistigid, hamlet (Egypt, north
Akershus castle (Norway, Oslo) 404 of Aswan) 166
Akkerman, see Mauro Castro Aubagne (southern France) 190, 383,
Albi (southern France) 239 390
Aleppo (Syria) 214 Augst (Switzerland), see Augusta Raurica
Alessandria (Italy northern, Australia(ns) 51–2, 91, 93, 155, 174–5,
Piedmont) 190 186, 383
Alexandria 569, 581, 585–7 Augusta Raurica (Roman precursor of
Almería (Spain southern) 55 Augst) 127
Alps, Alpine113, 404, 411, 415–6, 648 Austria(n)(s) 127, 213, 371, 389–90,
Alverdiscott, parish of (England, North 404–5, 507
Devon) 472–3 Avignon (Papal city, Provence) 109, 147,
Ambala, district (India, province of 220–1 and fn. 68, 357, 521, 534 fn.
Punjab) 154 115, 593, 618 fn. 27
Americas 92, 167, 186 Avon R. (England south-western) 459,
North America(ns) 44–6 and fn. 52, 475, 477
58, 92, 120, 193, 513, 523, 541, 545 Aylesbury, parish (England,
South America(ns) 92, 167, 182, Buckinghamshire south east), see
376–7 Walton 127–8
Amsterdam, see also Jordan 127, 146,
226 Båhuslen (medieval Norway) 670 fn. 7
Amur R. (Manchuria) 515 Baden-Würtemberg (Germany south-
Andenes, bailiwick of (northern western) 404
Norway) 419 Balkan 195, 690
Anglo-Saxon (England) 127–8, 130, 134 Baltic Sea 99, 131, 133, 139, 394, 403,
Ansford, village (England, 405, 407 and fn. 45, 569, 648
Somerset) 476 Baltimore (U.S.A.) 103
Antarctic Continent, see Macqarie I. Bangladesh, Bengal
Apt (France southern) 190 Barnstaple (England, North
Arctic Circle 418–9 and fn. 61 Devon) 472–3, 478
Arctic regions, see also Polar regions and Barcelona 585
sub-Arctic 417–9 and fn. 61 Basle (Switzerland) 405
Argentina 654 Batcombe, manor (England,
Arthur Road (India, Mumbai), Somerset) 478
hospital 372 Bath and Wells, diocese of (England,
Ascheim (Bavaria, Germany) 329, Somerset) 449–50, 459, 463, 475
389–90 Bavaria (Germany) 329, 389–90, 507
Asia 166, 193, 520, 621 fn. 34, 661 Beddingham, Roman villa
Asia Minor, see also Turkey 586 (England, Sussex) 127
1
Regarding special letters, see introduction to the Index of Subjects, fn. 1, no. 3.
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index of geographical names and people 731
Bay of Barnstaple (England, Burgundy (France) 114, 270, 593

North Devon) 472 Burma = Myan Mar 98, 185
Belgaum (India) 94, 102–3, 118 fn. 150,
140 fn. 224, 161–2, 198 Cadbury North and South, manors
Belgorod(-Dnestrovskyi), (England, Somerset) 467
see Mauro Castro Caffa, see Kaffa
Bengal East (Bangladesh) 148–9 California 172
Bergen (Norway) 113, 115, 136, Cairo (Egypt) 571, 575, 585
140, 332 fn. 84, 385, 393, 400–3, Calais (France north-western) 594
406–8, 418–9, 435, 502, 504–6 Calcutta (India), see Kolkata
and fn. 41, 530, 536–7, 541–2, Cambridge, University of 35, 449, 517,
546–7, 550–2 566
Bergen, King’s Mansion Cambridgeshire, county of (England
[= Kongsgården] 502 and fn. 22, 506 south-eastern) 271, 430, 455, 465
Bergenhus castle (in Bergen) 506 Camporegio, monastery and cemetery
Bern (Switzerland) 10 (Siena, Italy), see also Necrology 218,
Berkshire (England) 140, 465, 469 231, 245–68, 325 fn. 45, 675–9
Bethesda (U.S.A., Maryland) 371 Canterbury (England south-
Bihar (India) 379 eastern) 224, 229 fn. 89, 426–9, 465
Birka (Sweden, west of Stockholm) 132 fn. 192, 479
Bishop’s Waltham, manor (England, Canton (Guangzhou, China) 90–1, 153,
Hampshire) 482 202, 568
Black Sea 586, 588 Carcassone, (France south-western
Bodmin (England, Cornwall) 475 and Mediterranean) 593
fn. 218 Cardiff (Wales) 185, 654
Bohemia 121 Cassis (France southern) 383, 390
Bohuslän, see Båhuslen Castlecary, village (England,
Bombay, see Mumbai Somerset) 476
Bombay City and Island, see Mumbai Catalonia (Spain) 294, 298
Bombay Presidency, see Mumbai Catania (Italy, Sicily) 548
Bordeaux (France south-western) 114, Cathedral’s parish (Norway,
393, 477, 584, 593–4, 661 Bergen) 406–8, 435
Botnsa (Iceland) 681 Central Provinces (colonial India) 35,
Brabant (Netherlands) 325 397
Brazil 120, 141 Cetatea Alba, see Trebizond
Brenner Pass (Switzerland eastern) 404 Ceylon, see Sri Lanka
Bridford, parish of (England, Chambery (County of Savoy/
Devonshire) 295 France) 241
Bridgewater (England, Somerset) 477 Channel Islands, see also English
Bridport, parish (England Dorset) 468 Channel 594
Bristol (England) 14, 146–7, 185, 415, Charybdis (mythological whirlpool) 363
459–60, 465, 472–3, 475, 477–8 Cheshire, county (England
Bristol Channel 478 central-east) 188, 287 fn. 28
Britain, British, see also Britain Roman Chester (Chestershire, England) 287
and England 36, 85, 101, 185, 210, China, Chinese 3, 13–4, 90, 94, 153, 166,
222, 243, 257, 336, 341, 371, 489, 182, 234, 291 fn. 4, 316, 334, 375,
491, 502–4 and fn. 26, 507–8, 553, 497–500 and fn. 17, 515, 517–8 and fn.
571, 584, 615–7 and fn. 21 69, 520, 523, 526, 534, 543, 566, 568,
Britain Roman 128 620–1 and fn. 34, 656
Brough of Birsay, island north west of Chios I. (Greek, on the coast of Asia
Orkney’s Mainland 129 Minor/Turkey) 588
Bruges (Low Countries) 104, 569 Christ Church, parish in Bristol 147
Brunswick (Germany) 216 Christ Church Priory (England,
Buckinghamshire (England) 127, 465 Canterbury) 224, 229 fn. 89, 426, 429,
Buenos Aires 654 465 fn. 192, 479
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732 index of geographical names and people
Church of Friars Minor at Bodmin Dnestr R., estuary of (Russia) 588

(England) 475 Dorset, county (England) 453, 465–71,
Clevedon (England, Somerset) 477 478–9, 483
Colchester (England) 407 Dreux (France) 390–1
Cologne (Germany) 127, 324, 326, 330 Dubrovnik, (Croatia), see Ragusa
Colombo (Sri Lanka) 95–6, 185–6 Durham, county (England) 271, 632
Colyton (England, Devonshire) 65, Durham priory 229 fn. 89, 428,
67–8, 142, 145, 202, 234, 295, 406 430 fn. 93
Comtat Venaissin (France, region ar.
Avignon) 190 East Anglia (England) 151, 405,
Congo, Democratic Republic 650–1 430 fn. 93
Constance (Switzerland) 404 Ecuador (South America) 376
Constantinople 82, 185, 323, 328, 331, Edinburgh (Scotland) 508, 510
393, 500 fn. 17, 562, 569, 577, 581, Egypt(ian) 58, 92, 94–5, 166, 182–4,
585–8, 661–2 214, 397, 520 and fn. 82, 585–6
Continent (Europe) 73, 181, 306, 319, Eisenach (Germany) 326
562, 579, 661, 664 Ely, diocese (England,
Copenhagen (Denmark) 59, 386, 409 Cambridgeshire) 449–50, 455–6
Corfu (Greece, Kerkyra) 588 England, English 16, 34, 36, 48,
Corhampton, manor (England, 77, 81, 85–6, 99, 111, 113–6,
Hampshire) 482 119, 125, 127–31, 134–5, 147–8,
Cornwall (England) 453–4, 471, 474–5 155, 169, 179, 185, 188, 195 fn. 5,
Coron, see Koroni 209–10, 214, 216, 223, 225–6,
Corsica I. (Genoa, to France 1768) 119, 234, 243, 255, 257, 269, 271,
140 289–90, 293–6, 299, 303–6,
Corone, see Koroni 309–11, 322 fn. 30, 325, 327,
Cottenham, manor (England, 331–3, 341–2, 346, 349, 352,
Cambridgeshire) 271 369, 372, 393, 401, 403–5, 407,
Couvin (Belgium) 39 and fn. 38 415–17 and fn. 59, 420–84,
Coventry and Lichfield, diocese 489–90, 500, 502–4 and fn. 26,
(England) 192, 445, 454–5, 460, 603 506–11, 513, 518–9, 530–1, 535,
Crete I. 121 540–1, 554, 557, 560, 562, 565–6,
Crimea 323, 331, 393, 500 fn. 17, 569, 571–2, 574–9 and fn. 69, 582–3,
581, 583–6, 661 585–7, 589, 593–6, 599–602, 605–7
and fn. 222, 611, 615–8, 629–32
Dalinor mines (Manchuria) 523 and fn. 76, 639, 648, 657–8, 661,
Dalmatia(n) (c. present-day 670, 690
Croatia+Albania) 346 English Channel 596, 648
Damerham, manor (England, Essex (England) 405, 480
Hampshire) 482 Europe(an) 14, 17, 20, 26, 30, 35, 40, 42,
Danube R. 128 48–50, 52–3, 56, 73, 75, 77, 87–9,
Dean Prior, parish (England, Devon) 295 97–8, 100, 104, 106–8, 111, 113,
Dee R. (England) 120–2, 126, 136, 140–1, 143, 148,
Denmark 60, 125, 133, 135, 173, 179–81, 194–6, 199, 201–4
322, 394, 403, 504, 507 and fn. 45, and fn. 35, 207, 214, 221–2, 258, 269,
550, 572, 670 277, 291–3, 296, 299, 301, 305 fn. 40,
Derbyshire (England), see also Eyam 77, 319, 323, 325, 327, 331, 340, 344–5,
188 fn. 101, 561 383–4, 392, 395, 397, 399, 415, 417,
Developing countries 210, 396, 622 420, 432, 434, 464, 488, 490, 492,
Devon(shire), county (England) 67, 119, 495, 501, 505, 507, 510–7, 527, 540,
287, 295, 433, 453, 466, 471–6, 478–9 554, 559, 562, 565, 568–70, 576–8
Dhund/Dhand, village and fn. 86, 580, 583–5, 592–3, 600,
(India, Punjab) 94 607, 611, 613, 621 fn. 34, 642–3,
Ditcheat, manor (England, 648, 657–8, 661, 664, 666, 668–9,
Somerset) 478 673, 690
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Europe Central 191, 392, 394, 521 Friuli (Italy) 330

Europe Eastern 195, 296, 331
Europe Northern 12, 73, 77, 98, Gabon (Africa West) 636 fn. 91
105–7, 116–22, 126–8, 131, 140, Gallia, see Gaul
181, 188, 191, 269, 290, 394–5, 398, Garhwali (India) 112
400, 406, 416, 506–7, 530, 535, Gascony (France south-western,
565–6, 607 fn. 224 region) 472, 477, 593
Europe North-western 107, 128, 131, Gaul (Roman province, Gallia) 128, 327
391, 393, 399, 507 and fn. 45 Gaza (Middle East, area) 586
Europe Roman 106, 128 Geneva (Switzerland) 121, 127
Europe Southern 73, 121–2, 124, Genoa, Genoese (Italy) 104, 191, 413,
209, 269, 398–9, 412–3, 581, 569, 586–91 and fn. 145, 594, 661–2
584–6, 643, 661 Germania, Germanic (Roman province,
Europe Western 77, 86, 106–7, 117, “Germany”) 127–8, 131
128, 131, 195 fn. 5, 269 and fn. 178, Germany, German 113, 121, 131,
399, 432, 607 fn. 224 134–5, 143, 216, 225, 322, 325–6,
Evercreech, village (England, 330–1, 342, 344, 346, 354–5, 371,
Somerset) 476 389–90 and fn. 28 no. 6, 392, 394,
Exe R. (England) 473 404–5, 411, 415, 503–4 and fn. 27,
Exeter (England) 295, 473 506–7, 569, 573, 670
Exeter, diocese of (England) 449–50, Ghent (Low Countries) 558
453, 455, 463, 470–1, 603 Gignac (France) 190
Eyam (England, Derbyshire) 68, 77, Gillingham (England) 466–7
188 fn. 101, 285–7, 410, 561–2, Givry (France, Burgundy) 108, 114, 270
614, 638, 641–7 Glasgow, Glaswegians (Scotland) 185,
364, 367
Faccombe Netherton (England) 140 Glastonbury Abbey (England) 241, 299
Faxeholm (Sweden) 133 and fn. 194 Gloucester, (England) 114, 460
Fingrith, manor (England, Essex) 405 Gloucestershire (England) 475
Finland 138–9 Godthåb (Greenland) 418
Finnmark (Norway) 418 fn. 61 Göta Älv (Sweden) 670 fn. 7
Flanders (Low Countries) 216, 569 Golden Horde (Mongol Khanate,
Florence, Florentine (Italy) 62, 68, 104, south-eastern Russia) 580, 588
146, 201, 209, 215 and fn. 47, 221, 232, Gorhambury (England) 127
235, 251, 261, 264–5, 271, 273, 323–6 Gotland I. (Sweden) 133
and fns. 33 and 45, 330, 344, 347–8, Gouda (Netherlands) 506–7
353, 359–61, 413, 531 and fn. 108, 558, Greece, Greek 82, 346, 563, 571, 588
591, 618–9 and fn. 27 and fn. 132
Fosen (Norway) 418 Greenland 98–9, 411, 415–6, 418
France, French, see also Provence and Grimsby (England) 465
Languedoc 9, 12 fn. 28, 29, 31, 39, 43, Guangzhou (China), see Canton
58, 86, 92, 101, 107–8, 134, 147–8 and Gudbrandsdalen, principal valley
fn. 244, 181, 188, 214, 217, 223–4, 226, (Norway) 137
236–7 and fn. 109, 239, 241–2, 269, Gudhem, monastery (Sweden) 133
281, 295–8 and fn. 19, 303, 305–6, 308, Guelders (Netherlands) 503 fn. 27,
324–5, 327, 329–30, 341, 352, 371, 506–7
381–6, 388, 390–5 and fn. 29, 400, 405, Gulf of Gdansk (Poland) 131
566, 573–4, 585, 593–4, 619, 630, Gulf Stream 139, 399, 404, 418
661–2
Frankfurt on the Oder (Germany) 326 Hälsingland (Sweden) 133 and fn.
Fremington, village (England, 193, 138
Devon) 473 Hafnarfjord at Fornubudir
Freston (England, Suffolk) 186 (Iceland) 681
Frome Braunch, manor (England, Haithabu (Germany)
Somerset) 114, 459, 476–7 131, 135
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Halesowen, manor (England, 616, 620–1 and fn. 34, 624, 645,
Worcestershire) 241, 271, 478, 598 656, 668, 673
Halland, Denmark2 135, 138, 403, 670 Indonesia, see also Java I. 3, 58, 91, 167,
fn. 7 520, 543
Halmstad, port town (see Halland and Innsbruck (Austria) 404
fn. 2) 403 Ireland 114, 128, 134, 306, 325–6, 465,
Hampshire (England) 140, 463, 479–80, 477, 503
482 Issyk-Kul L. (Ysyk-Köl)
Harbin (Manchuria) 515, 517–8, 523 (Central Asia, Kirghizistan) 571
Hardanger (Norway) 557 Istria (Italy)3 330
Harnai (India) 153 Italy 55, 185, 188, 191, 200, 209–10, 215
Harwich (England) 465 fn. 47, 226, 229, 234, 246–7, 293,
Heacham, manor (England, 295–8, 302, 322–5, 330, 341–6,
Norfolk) 575 350, 352–3, 391 fn. 33, 393, 411–4,
Hebrides Is. (Scotland, north-west of), 548, 569, 581, 585, 588, 591, 631,
see Shiant Is. 119 648, 658–9
Helgafell (Iceland) 680 Ivory Coast (Africa West) 636 fn. 91
Helgeland, bailiwick (Norway) 419
Hereford, diocese (England) 449, 456, Japan(ese) 25, 518
458 Jemtland (medieval Norway)4 418
Hertfordshire (England) 430 Jordan (quarter in Amsterdam) 67, 146
Hesse (Germany, region) 326 Jutland (Denmark) 403
High Ham, manor (England,
Somerset) 478 Kaffa (the Crimea) 331, 393, 577, 581,
Holt in Saurbær (Iceland) 681 585–90 and fn. 144
Hong Kong (China) 90–2, 185–6, 192, Kilkenny, monastery (Ireland) 332, 491
202, 213, 314, 316, 373–4, 626 King’s Lynn (England) 115, 393, 401,
Honiton (England, Devon) 472 654
Hubli (India, Deccan) 284 Kirghizistan, see Issyk-Kul
Hull (England) 185, 465 Kirkjubær (Iceland) 680
Hunan, province (China) 526, 528 Kjalarness, meeting place of moot
Hvalfjord (Iceland) 681 (Iceland) 681
Hvitskeggshvammi (Iceland) 681 Koliwada, northerly part of Sion 94,
170, 173, 176, 189, 198
Iceland(ers, -ic) 30, 77, 99, 118–9 and Kolkata, formerly Calcutta (India) 185,
fn. 153, 401, 416, 418, 493–552, 518, 192, 194, 196, 373
608, 648, 680–1 Koroni (Coron, Greece,
Icelandic waters 502–3, 506 Pelopponese) 588
India(n) 3, 13–4, 20, 33–8, 40–5, Krakow (Poland) 269 fn. 178
47–53, 58, 66, 74–5, 91–4, 98, 108–12, Kronstadt Fortress (Russia, by St
121–2, 149, 153–5, 158, 168, 174–5, Petersburg) 214
177, 179, 182–3, 185, 188, 194–204, Krysuvik (Iceland) 681
213, 217, 234, 277, 279–81 and fn. 3,
284, 289–91, 293, 295–6, 301, 303–7, Lambesc (France) 381 and fn. 3, 390–2
316, 322, 334, 364, 366–8, 370–5, and fn. 35
396–7, 399, 464, 488, 519–20, 543, Landshut (Germany, Bavaria) 507
553, 566–8, 570–1, 581, 599–600,
2
Halland is a region situated north of the Sound on the eastern side of Kattegat.
Halland was a Danish province until mid-seventeenth century, when it was conquered
by Sweden; see also Scania.
3
Now part of Croatia.
4
Present-day Sweden, Jämtland.
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Languedoc (France) 190, 236 and fn. Martigues (France) 383, 388–91 and fns.
109, 390 28 no. 4 and 34
Les Pennes-les Septèmes (France) 190 Mauro Castro, trading station
Levant (Middle East, region) 586, 588, (Russia)6 588
661–2 Mayrargue (France) 190
Liège (Netherlands) 326 Mecklenburg (Germany) 121
Lincoln, diocese (England) 439–40, 449, Mediterranean littoral 73, 98, 101,
452, 603 105–6, 117, 119, 128, 397, 415,
Liverpool (England) 185 562, 565, 577, 581, 583, 586–7,
Lofoten, bailiwick (Norway) 419 594, 648, 661
Lombardy (Italy) 121 Melcombe Regis7 (medieval England)
London(er) 36–7, 79 fn. 21, 83, 104, 114, 116, 437, 462, 465–6,
127, 144, 147, 186, 204, 215–6, 223, 468–9, 471–2 and fn. 209, 474,
286, 302, 304, 306, 308–10, 333, 476–7, 479, 483, 586–7, 593–4
335–6, 373–5, 378, 383–4, 390–1, and fn. 162, 661
393, 405, 409, 429, 432–5, 465 fn. Mells, manor (England, Somerset) 478
192, 479–80, 490, 531, 549, 554, 558, Mende (France) 307
567–8, 577–9, 645, 657–8 Meon R. (England southern) 480
Low Countries, see the Netherlands Messina (Italy, Sicily) 393, 548, 581,
Lübeck (Germany) 104 587–8, 590
Lund (Sweden), see also Scania5 59–60, Middle East 581, 583–5, 587–8, 590
132–3, 135, 403 Milan (Italy), see also Nonantola 66,
Lundegaard L. (Bergen, Norway) 332 fn. 147, 200
34 Milan, stalli, poor quarters 147
Lynn, see King’s Lynn Mirabeau (France) 190
Modena (Italy) 324
Madagascar 3, 13–4, 58, 92, 180, 182, Modon, harbour (Greece,
334, 520–1 and fn. 82, 566, 582, 619 Pelopponese) 588
Mälaren L. (Sweden) 132 Monemvasia, port town (Greece) 588
Mahlgahla (India, Punjab) 282 Montpellier (France southern) 39 and
Mainz (Germany) 216 fn. 39, 236, 326, 382, 390–3
Málaga (Spain) 588 Morocco 9–10, 13, 28–31, 58
Malang (Indonesia, Java) 168, 182 Moscow (Russia) xv, 148, 214, 604
Malpas (England, Chesire) Mumbai (Bombay in citations,
Manchester (England) 385 India) 74–5, 92, 94, 102, 140 fn. 224,
Manchouli (Manchuria) 517 153, 156–9, 161–3, 171, 176, 188–9
Manchuria 8, 31, 120, 141, 234, 497, and fn. 103, 192, 194, 196, 198, 203,
512, 514–20, 523, 534 fn. 115, 535, 213, 284, 291, 316, 364–5, 370, 372,
539, 626–7 399, 567, 599, 623
Mantua (Italy) 413 Munich (Germany, Bavaria) 329,
Macqarie I. (sub-antarctic, between 389–91, and fn. 30
Tasmania and Antarctica) 119, 140 Myanmar, see Burma
Marnhull, manor (England, Dorset) 478
Marseilles 12 fn. 28, 114, 188, 191, Namdalen (Norway) 418
220–1, 283, 305, 307–8, 381–3, Naples (Italy) 302, 574, 588, 657, 659
388–93 and fns. 28 no. 4 and 35, 577, Nauplion (port town Greece,
587, 591–3, 620, 661 Pelopponese) 588
5
Lund used to be the cathedral city of the Danish archbishop. See Scania and fn. 8.
6
The ancient Greek colony of Tyras, later called Akkerman, from 1946 with the
slavic name of Belgorod(-Dnestrovskyi), in Romanian Cetatea Alba.
7
Melcombe Regis was situated within the area of present-day Weymouth.
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Narbonne (France) 324 and fn. 38, 326 Örebro, county (Sweden) 133
and fn. 52, 330 Öland I. (Sweden, in the Baltic) 133
Navarre (medieval kingdom in Orient(al) 98
Spain) 294, 298 Orkney I. (Scotland) 129
Neston (England) 287 and fn. 28 Oslo (Norway) 10, 103, 111, 115, 124,
Netherlands 127–8, 135, 225–6, 403, 186, 225, 371, 393–4, 400, 403–4, 670
503–4 and fn. 27, 506 fn. 7
Newark (England) 452 Otter R. (England) 453, 466, 472
Newenham, Cistertian house of Ottery St Mary, collegiate church
(England, Honiton) 472 (England, Devon) 453, 466, 472
Nidaros, see Trondheim Oxford, town (England) 435, 508–9
Nile Delta (Egypt) 397 Oxford, University of 29, 385, 566
Njardvik (Iceland) 681 Oxfordshire, county of (England) 465
Nonantola (Italy northern) 66, 200
Nordic countries, see also Padua (Italy) 351, 353–4
Scandinavia 10, 30, 46, 57, 59–60, 63, Palatinate, Upper (Germany,
98–9, 102, 115, 124–6, 131–2, 134–9, region) 330
141, 216–7, 232, 301, 319, 322 fn. 30, Pale (medieval eastern Ireland) 114,
371, 395, 400, 406–7, 416–7, 512, 569, 465, 477
609 fn. 230 Pali (India) 43
Nordland (Norway) 472–3 Parel, village (India, near Mumbai)
Norfolk, county of (England south- 102–3, 153, 157, 159
eastern) 430, 432, 579 Paris 9, 39 and fn. 39, 113–4, 134, 221,
Norrköping (Sweden) 217, 313 fn. 4, 237, 242, 324, 326, 355, 371, 389–92,
549 586, 593 and fn. 158
Norrland (Sweden) 138 Parma (Italy) 326
Northam 472–3 Patiala State and city (India, the
North Devon, see Devonshire Punjab) 154
North Sea 405, 407, 507, 648 Penrith (England) 284, 287, 410
North America, see America and fn. 37, 608, 617, 631, 638–44,
North Atlantic 119, 404, 646 and fn. 127
494, 506 Persian Gulf 328
Northumberland (England) 632 Peru 397
North-West Passage 98, 112 Pfäfers (Switzerland) 404
Norton, manor (County Durham, Piacenza (Italy northern) 548, 589
England) 271 Piedmont (Italy, region) 201,
Norway, Norwegian(s) xv, 13–4, 298, 352
16, 30, 59–60, 99, 102–3, 113, 115 Pilton, manor (England, Somerset) 478
and fn. 145, 119, 131, 136–40 Pisa (Italy) 413
and fn. 213, 143, 195 fn. 5, 225, Pithay, parish, (Bristol, England) 147
269–70, 304, 322, 327, 332 fn. 84, Plymouth (England) 295
385, 393–5, 399–403, 416–20 Poitiers (France) 201
and fn. 61, 449, 464, 493, 501–7 Poland 7, 131, 269 and fn. 178, 331, 394
and fns. 22, 40–1 and 45, 510–1, Polar regions 41–7
527–31, 536, 538, 551–2, 576, Pompeii 124
608, 648, 670 and fn. 7 Poona, see Pune
Norwich (England) 304 Portishead (England, Somerset) 477
Norwich, diocese (England) 449 Portugal 648
Nottinghamshire (England) 452 Prato (Tuscany, Italy) 298
Novgorod (Russia) 364, 521 Provence (France) 190, 220–1, 298,
Nuremberg (Germany) 507 381, 383, 390–1 and
Ny-Varberg, convent (medieval fn. 32, 592
Denmark, Halland), see also Pune (India) 140 fn. 224, 162–3, 198–9,
Varberg 133, 135 399
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Punjab (India) 40, 58, 92, 94, 102, 118 Salisbury, diocese (England) 437, 461,
fn. 150, 154, 163–4, 171, 200, 282, 463, 465, 467
291–3, 297, 399, 520, 623 Salon (France) 383, 390
Puy-Sainte-Réparade (France) 383, Salten, bailiwick (Norway) 419
390–1 San Gimignano city (Tuscany, Italy) 298
Santo Spirito, quarter in Florence 68,
Ragusa (present-day Dubrovnik) 588 146
Ramundeboda (Sweden) 133 Saurbær (Iceland), see also Holt 681
Rangoon (Myanmar), see Yangôn Savoy, County of (now France) 241, 298
Ratnagiri Collectorate, colonial Scania (medieval Denmark)8 59–60, 133
term, (India, Maharashtra), Schleswig and Holstein, Duchies9 670
see Harnai 153 Scotland, Scottish 119, 201, 306, 310,
Regensburg (Germany) 355 416, 503 and fn. 26, 510, 530, 631, 648
Reims, see Rheims Seine R. (France) 114
Rheims (France) 324, 329–30, 400 Sens (France) 329, 389–91 and fn. 29
Rhenish region (Germany) 521 Sheffield (England) 307–8
Rhine R. 128 Shetland Is. (Scotland) 118
Rhône R. (France) 190 Shiant Is. (Scotland, Hebrides) 119
Ribe (Denmark) 403 Shropshire, county (England) 127
Riez (France) 190 Siberia(n) 517
Rødøy, parish (Norway) 419 Sicily I. (Italy) 364, 548, 574, 581, 586–7,
Rome 413–4, 574, 567, 659 590, 661–2
Roman Empire (Western) 106, 127–8, Siena (Italy), see also Camporegio and
343 Necrology 218, 231, 245–68, 270, 273,
Rosario, port (Argentina) 654 324–5, 675–79
Roskilde (Zealand I., Denmark) 409 Sigtuna (Sweden) 126, 132
Rostock, University of (Germany) 322 Singapore 168
Rouen (France) 86, 114, 585, 593–4 and Sion, village (India, near Mumbai), see
fn. 162, 661 also Koliwada 94, 157–8, 170–1, 173,
Russia(n)/Soviet Union xv, 3, 10, 176, 178, 189, 198 and fn. 13, 567
58, 134, 195, 210, 325–6, 394, 514, Skagen, part of Stavanger 136
518, 520, 523, 576, 580–1, 585, 604, Skálholt (Iceland, cathedral city) 531,
661, 690 536–7 and fn. 120, 551, 680–1
Slavic territories 131
Sahara(n) (Africa) 566 Smuszewo (Poland) 131
St Albans, town (England) 127 Solent strait of (England) 480
St Germanus Church (Stuttgart, Småland (Sweden)10
Germany) 389 fn. 28, no. 6 Söderhamn (Sweden northern), see
St Giles’ Church (London) 554 Hälsingland
St Martin’s monastery (Tournai) 237 Somerset, county (England), see also
St Olaves Church (London) 567 fn. 39 Bath and Wells 114, 450, 459, 466,
Sainte-Tulle (France) 190 474–80
Santa Maria Novella monastery and Sound (between Denmark and
cemetery (Italy, Florence) 261 Sweden) 59, 132–3, 135, 670 fn. 7
8
Scania was a Danish province until mid-seventeenth century when it was con-
quered by Sweden together with Halland and Blekinge and the Norwegian areas
Båhuslen and Jemtland.
9
The Duchies of Schleswig and Holstein were under the Danish Crown at the time.
10
Småland was Sweden’s southernmost province until the conquests of the mid-
seventeenth century.
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South America, see America Tiverton (England, Devon) 295, 473

South Africa(n) 87–9, 88, 191 Tolkmicko (Poland) 131
Southampton (England) 309, 480 Tønsberg (Norway) 136–7
South Wales (Australia, region) 46 Torridge R. (England, Devon) 472
Soviet Union, see Russia/Soviet Union Toulon (France) 382
Spain, Spanish 269, 294, 198, 303, 576, Tournai (Low Countries) 237, 242
648, 661 Trebizond (Asia Minor/Turkey) 588
Spalato (present day Split, Croatia) 588 Trøndelag (Norway) 428
Split, see Spalato Trondheim (medieval name Nidaros,
Sri Lanka (Ceylon) 52–3, 95–6, 185–6 Norway) 113, 115, 136, 400–2, 419,
Stad (Norway) 505 505
Stavanger (Norway), see also Tropical zones 120, 141, 396, 416
Skagen 136, 403 Tunis(ia) (Africa North) 569, 588
Stepney (in London) 554, 562 Turkey, see also Asia Minor 328
Stettin (Szczecin present-day Tuscany (region, Italy) 302, 353, 412–3
Poland) 131 Tyras, ancient Greek settlement 588 fn.
Stockholm (Sweden) 126, 132–3, 507 132
fn. 45 Tyrol(ese), see also Alps 404
Stour R. (England) 405, 465, 432, 480
Stuttgart (Germany) 389–90 and fn. 28, Uelzen (Germany) 143
no. 6, 392–3 Ugborough (England, Devon) 295
sub-Arctic regions, see also United Provinces (colonial India) 163
Arctic 416–8 and fn. 61 Uppsala (Sweden) 133
sub-Saharan Africa 636–7 U.S.A., see America
Sudan 636 and fn. 91 Uzbekistan 364
Sudbury (England) 465, 480
Suffolk, county (England) 405, 430, 432, Vadstena, convent (Sweden) 507
480 Värmland (Sweden) 138
Sungari R. (Manchuria) 515 Västergötland (Sweden) 133, 403
Surabaya (Indonesia, Java) 168 Valkenburg, village (Netherlands) 127
Surrey, county (England) 479 Valle Susa (Piedmont, Italy) 298
Sussex, county (England) 127, 479 Varberg (medieval Denmark, Halland),11
Swanick, manor (England, see also Ny-Varberg 133, 670 fn. 7
Hampshire) 481 Venice, Venetian 8, 104, 191, 216, 302,
Sweden, Swedish 11, 59–60, 99, 119, 349, 357 fn. 143, 404, 569, 587–9,
126, 133, 138–40, 216–7, 313 fn. 4, 594, 662
327, 394–5, 403, 407, 507 and fn. 45, Venice and Terrafirma (Italy) 302
531, 549–50, 572, 670 fn. 7 Verdun (France) 386
Switzerland, Swiss 127, 371, 404–5 Vestfjords, area of (Iceland) 510, 681
Sydney (Australia) 48, 51, 93 Videy (Iceland) 680
Syria(c) 328, 581, 585–6, 661 Vienna (Austria) 329, 388–391
and fn. 31
Tavastland, county (Finland), in Finnish Vietnam(ese) 3, 44–5, 193, 233–4,
Hämeen lään 139 315–6, 377, 520–1 and fn. 82, 524,
Taw R. (England, Devon) 473 545, 566
Thuringia (Germany, region) 326 Vikings 118, 131, 134
Thykkvabær (Iceland) Viking Period/Age 125–6, 132–4, 140,
Titchfield, manor (England, 395
Hampshire) 480, 482 Visby (Sweden, Gotland I.) 133, 140,
Tiveden, district (Sweden) 133 403
11
Varberg was Danish until the mid-seventeenth century when conquered by
Sweden.
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Vitrolle (France) 190, 383, 390 Winchester, diocese (England) 241, 449,
Vladivastok (Russia) 514 463, 479, 482
Wittenberg (Germany) 327
Wadhala, village (India, near Worcester, diocese (England) 449, 458,
Mumbai) 157–8 460, 475
Wales 364, 518 Worcestershire, county (England) 241,
Waltersdorf (Germany) 131 271
Walton, manor (England, Somerset) 478 Worli, village (India, near
Walton, hamlet (England, Mumbai) 157–8
Buckinghamshire), see also Wroxeter (England,
Aylebury 127–8 Shropshire) 127
Westminster (England, city of
London) 567 Yangôn, formerly
Westminster Abbey (England, Rangoon (Myanmar) 166,
London) 229 fn. 89, 428–9 168, 185–6
Weston-super-mare (England, York, city (England) 127, 151, 631
Somerset) 477 York, diocese (England) 152, 439–42
Westphalia (Germany, region) 326 and fn. 137, 446–7, 449, 603
West Chickerell, parish (England, Yunnan (China) 621 fn. 34
Dorset) 468
Weymouth, see Melcombe Regis Zadar (Croatia, Dalmatian coast),
Widworthy, parish of (Devon, see Zara
England) 295 Zara, Venetian port (present-day
Wiltshire, county (England) 465–7, Zadar, Dalmatian coast) 588
469–70, 474 Zealand I. (Denmark) 409
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INDEX OF NAMES1
Aboudharam M. 381, 392 fns. Bell W.G. 216, 310, 333, 374–5, 549, 569,
35–6 657 fn. 172
Aberth J. 56, 179, 450 Belletini A. 229
Abbey H. 634 Benedetti Alessandro, physician 350
Absalon Pederssøn Beyer, Norwegian Benedictow O.J. xv–xvi, 5 fn. 5, 8 fn. 13,
humanist 332 fn. 84, 401–2, 407 9–12 and fns. 14, 28–9, 16–7 and fn.
Ackerknecht E.H. 669 40, 19, 30–1, 37–8, 44–6 and fn. 52,
Adam of Murimuth, chronicler 223 50–2, 56–60, 62–3, 67–9, 74–5, 91,
Adelberg E.A., see Jawetz, Melnick and 96–9 and fn. 74, 103, 107–9, 111,
Adelberg 113–5 and fns. 142 and 145, 119 fn.
Advisory Committee for Plague 153, 124 fn. 164, 126–8 and fn. 167,
Investigation in India 108, 624 130, 135–7, 140 fn. 224, 146, 148, 152,
Agnolo di Tura, chronicler 247–8, 250, 169, 171–3, 176–7, 186–7 and fn. 98,
265, 276 191–2, 195, 199–201, 203 fn. 35, 210
Alfani G., see Cohn and fns. 18–9, 213, 215, 217, 219–20
Alfred the Great, King 131 and fn. 69, 225, 229 and fn. 89, 232,
Ali(Oli) Svarthöfdason, Icelandic 238, 240–1, 243, 246, 252, 259, 261,
priest 680 264 and fn. 171, 267, 269 fn. 178, 273,
Al-Maqrizi, Arab chronicler 586 279–80 and fn. 3, 287 fn. 28, 290, 294–
Allen C.F., Danish historian 670 8, 300–2, 307–8, 314–5, 322, 324 and
Andrew Hogson, plague victim in fn. 38, 330 fn. 77, 332 fn. 84, 334, 336,
Penrith 284, 639–40, 646 341, 349, 352 fn. 129, 358–9, 368 fn.
Arthur P. 482 176, 370, 377 and fn. 205, 385, 390 fn.
Asgrimur, Abbot (Icelander) 681 28, 393–4 and fn. 39, 396, 398, 400–2,
Audoin-Rouzeau F. 11–2 416, 418 fn. 61, 420 fn. 66, 432 fn. 104,
Audoin-Rouzeau F and Vigne F.-J. 126, 436, 438 and fn. 129, 441, 445 fn. 144,
129 fn. 178, 136 450 and fn. 150, 463–5 and fn. 192,
Axon W.E.A. 287 471 fn. 206, 478, 487, 490, 492–3,
495–501 and fns. 8, 11, 503–4 and fns.
Bacot A. 119 30–1, 506, 511–2, 516–21 and fn. 68,
Bailey M. 601 527, 529, 531–2, 534 fn. 115, 536–8
Baltazard M., see Blanc and Baltazard and fn. 118, 540–3, 545–7, 550, 554–5,
Bannerman W.B. 153–4, 159 fn. 28, 203 558 and fn. 14, 564, 567 and fn. 39,
fn. 35, 291 569, 578 and fn. 86, 584–5, 590 fn.
Baratier E. 220, 592 143, 593–4 and fns. 157, 160, 598–9
Barnes J. 560, 577 and fn. 188, 602–4, 607 fn. 224,
Bath and Wells, diocese of, bishop, see 609 fn. 230, 612, 629, 631 fn. 74,
Ralph of Shrewsbury 656, 670 fn. 7, 680, 685
1
(1) The Index of Names registers personal names and names of institutions in the
running text, also supplementary information and comments in fns. but not authors of
works referred to in the fns.
(2) Medieval and classical persons are entered according to Christian name, except
in the cases of persons who are normally or systematically known by surnames; mod-
ern persons are entered according to surname.
(3) Regarding special letters, see introduction to the Index of Subjects, fn. 1,
no. 3.
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Berglund J. 99 Chun J.W.T 90, 316, 375–6, 539, 543,

Bertrand J.B. 214, 217 567, 571, 619–20 and fn. 34, 622
Berthe M. 294 Ciano C. 209
Beverwijk van J., Dutch physician 333 Cipolla C.M. 60–1, 209, 226, 293–4,
Bibikova V.A. and Klassovskij L.N. 58 352–3, 658
Biraben J.-N. 333, 586 Clark Ronaldson W. 154
Biraben J.-N. and Le Goff J. 390 fn. Clot-Bey A.B. 214–5
29, 514 Cohn S.K., Jr. 16–9, 21–2, 25–69, 74–7,
Björn Olafsson, Icelander, later priest at 85–6, 93, 96, 98, 135–6, 144–5, 148–52
Krysuvik 681 and fn. 3, 154, 156, 164, 169–80, 182,
Blanc G. and Baltazard M. 9–15 and fn. 184, 186, 194, 196 and fn. 7, 200–1,
28, 29–31, 58, 110 204–5, 207–8, 211–68 and fns. 47, 136
Block G., Swedish physician 216–7, 313 and 168, 273, 283, 289–94 and fn. 17,
fn. 4, 549 297, 299, 314–7, 321, 323–6 and fns.
Boccaccio G., Italian author (1313– 33, 44–5, 333–4 and fn. 88, 340–80,
1375) 201, 344, 359–80 and fn. 180, 386–7 and fn. 20, 389 fn. 28 no. 6,
618 and fn. 27, 645 392–3 and fn. 35–6, 400–2, 410–5,
Brachman P.S. 556 464, 487–8, 490, 495, 541, 562, 608–9
Bradley L. 62–3, 67–9, 410, 561–2, 643, and fn. 230, 647, 664–72
645, 647 Cohn S.K. and Alfani G. 66, 200, 647,
Bridbury A. 273 664 fn. 2
Brossollet J., see Mollaret Coleman M.P. 410, 643, 647
Brygoo E.-R. 58, 619 Collie, Major 153
Burnet E.M. (and White D.O.) 289–90 Commander of Akerhus Castle (Oslo),
and fn. 410–1, 414 see Peder Hansen (Litle)
Burroughs A.L. 683–4 Commodus, Roman Emperor (180—192
Butler T. 10–1 and fn. 18, 25, 44–6 and ce) 343
fn. 52, 193, 315–7 and fn. 20, 319, Cooper A. 384–5, 387
377–8, 545, 612 Cosmacini G. 215 fn. 46
Byrne E.H. 588 Coulton G.G. 449, 472
Court of Hustings (London), see Wills
Campbell B.M.S. 577, 579 Cox J.C. 467, 567 fn. 39
Cantey J.R. 545 Creighton C. 36–7, 81, 242–3, 257 fn.
Cantor N. 56, 179 156, 309–10, 333, 335–6 and fn. 100,
Carmichael A. 54–5, 68, 84, 146, 231, 475 fn. 218, 507–10, 560 and fn. 21,
235, 264, 325 fn. 44, 359, 370–2, 400, 589–90, 615–9
584–5, 616 and fn. 14
Carpentier É. 237, 239–40, 584 Dang L.V. 387–8
Castiglioni A. 352 Dante Alighieri (1265–1321) 343
Cazelles M.R. 147, 236–7 and fn. 109, Davis D.E. 73–4, 76, 98–121 and fn. 47,
240, 242–4, 268 226, 234–5, 246–7, 250–1, 413–4
CDC, see Centers for Disease Control Davis R.A. 454 and fns. 162–3, 461
(and Protection) Defoe D. 83
Centers for Disease Control and Devignat R. 387
Protection 3, 11–2, 649, 652, 660 de Langen C.D. and Lichtenstein A. 58,
Chalin de Vinario 233, 357 96, 212, 543–4
Chandler A.C. and Read C.P. 627 Del Panta L. 209, 215 fn. 47, 226, 234–5,
Charlemagne 574 246–7, 250–1, 413–4
Chenot A. 214 Diocletianus, Roman Emperor
Christian, Prince of Denmark 670 fn. 7 (284–305) 343
Choksy K.B.N.H. 366, 624, 626 Dijkstra J.G. 67–8, 146
Christie A.B. 88–90, 388–9, 613, 621–8, Diemerbroeck I. 216–7
653, 682, 684–5 D’Irsay S. 572–3
Ch’uan, physician 516 Dörbeck F. 58
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Dohar W.J. 456–7 George Leene, plague victim, son of

Dols M.W. 56, 583, 585–7, 662 William Leene 287–8
Drancourt M. 12 fn. 28, 192, 381, 385–7, Gilbert M.T.P. 384–7 and fn. 20, 392
392 fn. 35–6, 395 fn. 42 Gillaume de Machet, poet 329
Dubois H. 226, 236, 330 and fn. 17, 400, Gille, see le Muisit
405, 514 Gillingham, Squire of 466
Duncan C.J., see Scott and Duncan Giovanni (di Pagnolo) Morelli,
Duncan S.R., see Scott, Duncan and chronicler 347, 413
Duncan Giovanni da Parma, chronicler 346
Dutour O. 381, 292 fn. 35 Giovanni da Santa Sofia, professor of
medicine (d. 1389) 353–4
Ecclestone M. 241 Girard G. 9–10, 58
Eckert E.A. 521 Giseler G.O. 216
Eldevik T. 139 fn. 213 Glénisson J. 240, 268
Engelsen R. 143 Gottfried R.S. 56, 225, 293–4, 296,
Eske Bille, Chancellor of the Realm, 430–2 and fn. 104
Denmark 404, 409 Grandisson, Bishop, diocese of
Eskey C.R. 376 Exeter 455
Eskey C.R. and Haas V.H. 682–3 Gras P. 108
Estrade F. 58, 180 Greenwood M., member of IPRC 3,
Evagrius 214, 217 33–4, 41, 58, 163–4, 227, 291–4 and
fn. 17, 296, 567
Fenyuk B.K. 58 Gregory of Tours, Bishop 283, 327, 329
Fetherston J., see Perry Grimus, Friar, priest in the church of
Ficino Marsilio, physician Skálholt, Iceland 680
(1433–1499) 215 and fns. 46–7, Guaineri Antonio, physician 357
350, 352, 357 Guy de Chauliac, papal physician in
Fitzgerald D.A. 654–5, see also Savage Avignon 109, 534 fn. 115
Fiumi E. 226, 619 Gudrun Halldordsdottir, Abbess
Fletcher J.M.J. 467–8, 470 consecrated at Thykkvabær,
Fracastoro G., Italian physician Iceland 680
(1484–1553) 322
Frost W.H., see Reed Hårding B. 126
Furness W. 617 Haas V.H., see Eskey
Håkon V, King of Norway 531
Gabriele de Mussis 548–9, 589–90 Haffkine W., see also Haffkine’s anti-
Galen(os), Greek physician plague vaccine 196
(c.130–c. 200 ce) 356 see also Index of Hallam E.H. 601
Subjects: Galenic Halldora, Abbess at Kirkjubær,
Galfrid le Baker, chronicler 332, 557 Iceland 680
Gallienus, Roman Emperor Hankin E.H. 34–44, 59, 112, 158, 236,
(253–268) 543 281–2, 289–96, 303, 646, 668–9
Gasquet F.A. 108–9, 438–9 and fn. 129, Harrod H. 561, 579
450, 454–60 and fns. 161 and 170, Harvey B. 229 fn. 89, 429, 432
466–7, 470–2, 477, 479, 553, 560–1, Hatcher J. 221, 224, 226, 229 and fn. 89,
565, 572, 583, 587, 589–90, 592–3 and 417 fn. 59, 422–3, 425–30 and fns. 87
fn. 158, 602, 605–6 and 93, 432, 474, 500 fn. 17, 508, 510,
Gatacre W.F., Brigadier-General 371–4 531, 561, 595–8, 600–1, 603–5, 607 fn.
Gatari, Galeazzo, Bartolomeo, Andrea, 224, 632
brothers and chroniclers of Hatcher J., Piper A.J., and Stone D 229
Padua 351–2 fn. 89, 428 fn. 87, 430 fn. 93
Genicôt L. 273 Hatcher J., see Miller
Geoffrey le Baker, chronicler 242–4, Hecker J.F.K. 560 and fn. 21, 572, 577,
332–3, 557 583 and fn. 104, 585–6
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Henry Knigton, chronicler 223, 272–3, Klein I. 49 and fn. 60, 179
480 Klimenko V.C. 58, 520
Henry of Hervordia, chronicler 242 Konrad von Megenberg, natural
Herlihy D. and Klapisch-Zuber C. 232 scientist 355–6
and fn. 97, 264 fn. 171, 273, 412–4, Kosminsky E.A. 604–5
619 Krummedike Henrik, Norwegian and
Hingeston- Randolph, Rev. Danish Councillor of the
Prebendary 450, 471 Realm 670–1 and fn. 7
Hirsch A. 109, 111–2 and fn. 132 Krummedike Sofie, daughter,
Hirst F.L., see also Philip 3, 9–10, 25–32, 670–1
35, 45–6, 50–5, 73, 75–6, 81, 95–6, 98, Krüger S. 355–6 and fn. 137
109–10, 112–3, 120–1, 166, 178–80,
183–7, 193, 196 fn. 7, 203 fn. 35, 234, Lamb G., Senior Member of IPRC 33
282, 286, 321, 375, 432 fn. 104, 491 fn. and fn. 24, 41, 48–9, 75, 94, 109, 158–9
8, 523, 540, 544, 564 fn. 32, 567, 571– and fn. 28, 161, 195, 203 and fn. 35,
2, 582, 612, 616, 619, 622–3, 625, 643 396–7, 623–4
fn. 113, 684 Langen de C.D. and Lichtenstein
Hodges N. 216 A.A. 58, 96, 212, 543–4
Hörnick von L. 216 Langer W.L. 584
Höskuldar, Councillor at Skálholt, Leclainche E. 573–4
Iceland 680 Leeuwenhoek von A. 80
Hollingsworth T.H. 596 Le Goff, see Biraben
Hufthammer A.K. 73 fn. 1, 136 Lepiskaar J. 133
Le Roy Ladurie E. 56, 179, 417
Ibn Khatimah, chronicler 55 Li C.C, see Pollitzer and Li
Lichtenstein A.A., see Langen de
James T.B. 119 fn. 154 Liston W.G., member of IPRC 3, 33, 41,
Jankibai, Indian 157 88, 90, 153, 156, 164–5, 567
Jawetz E., see Jawetz, Melnick and Livi-Bacchi M. 226, 246–7, 261
Adelberg Loghem van J.J., see also next entry 75,
Jawetz, Melnick and Adelberg 558, 78, 97
562–3 Loghem van J.J. and Swellengrebel
Jean de Venette, chronicler 80, 223, 236, N.H. 3, 58, 75, 78, 96, 111, 167–9,
268–9 176–7, 179, 182–3
Jehan de Blanzy, burgher of Rheims 329 Lomas T. 271
Joakim Beck, Chancellor of the London, diocese of, bishop, see Ralph
Exchequer, Denmark 409 Stratfort
John Clyn, Friar of Kilkenny, Lopez R.S. 104, 107, 588
chronicler 332, 491–2, 557, 612 Lunn J. 439, 449–52, 474 fn. 163, 457,
John of Reading, chronicler 223 461, 463, 467–8, 470–2, 479, 483–4,
Jón Oddsson 681 603, 628
Lysenko T.D. xv
Kang-Hsi, Emperor (China) 620 fn. 34
Karlsson G. 16–9, 76–7, 194, 283, 290, Machiavello A. 180 fn. 78, 376
299, 312, 321, 394, 480, 487–8, 490– McArthur W.J. 3
552, 608, 665, 680 and fn. 3, 691 McCormick M. 119, 126–9 and fn. 178,
Karlsson G. and Kjartansson H.S. 493, 140
495 fn. 6, 501 McNeill W.H. 500 and fn. 17
Kinch J. 60 Magnus Eriksson, king of Norway and
Kirchoff G. 213, 217 Sweden 327
Kitasato S. 25 Maia J. 633–4
Kjartansson H.S., see Karlsson Malmborg G. 133 and fn. 192, 140 fn.
Klapisch-Zuber C., see Herlihy D. 233
Klassovskiy L.N., see Bibikova Mansa F.V 504
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Marchionne (di Coppo) Stefani, Petrarch Francesco (1304–1374) 618

chronicler 265, 326 and fn. 27
Marcus Aurelius, Roman Emperor Petrie G.F. 58, 95, 166, 182
(161–180 ce) 343 Pettenkofer M. von 619
Martin C.J. 109–10 Philip W.M. and Hirst L.F. 625
Martinez Dr. 376 Pickard R. 438 fn. 129, 450, 453–4 and
Massaria A. 215 fn. 161, 471, 475, 603
Matheson C. 128 Piper A.J., see Hatcher, Piper and Stone
Mead R. 561 and fn. 24 Planck? 112
Melnick J.L., see Jawetz, Melnick and Pollitzer R. 3, 7 and fn. 8, 9–10, 13 and
Adelberg fn. 35, 31–2, 45, 75, 90, 101–3, 113,
Meyer K., see also Pollitzer 212 and fn. 118–20, 142, 181–7 and fn. 85, 193,
26, 512 207–8, 212–3, 280 fn. 3, 314–6, 321,
Michele da Piazza/Michael of Piazza, 375–6 and fn. 200, 378, 525, 539,
Franciscan friar 333 fn. 88, 360 fn. 544–5, 554, 567, 571, 612, 619–20 and
155, 548–9 fn. 34, 622, 647, 685
Miller E. and Hatcher M. 601 Pollitzer R. and Li C.C. 526, 528
Mollaret H.H. and Brossolet J. 56 Pollitzer R. and Meyer K. 177–80, 184,
Mompesson W., Rector of Eyam 614 529, 683
Morony M.G. 328 Postan M.M. 226, 596, 588
Morris C. 16–7, 19, 312, 321, 332, 410, Pounds N.J.G. 220 fn. 68, 588
487–93, 496–9, 512–4, 518–9, 533–5 Prat G. 237, 239–40, 242, 244
and fn. 115, 691 Procopius, Byzantine physician 328
Muisit le G. 236–7, 242 Pusch C.M. 389 fn. 28 no. 6, 392
Narajan Laxuman, Indian, 157 Ralph Shrewsbury, bishop of Bath and

Nash A.E. 147 and fn. 243 Wells (1329–1363) 459
Naso I. 352 Ralph Stratford, bishop, diocese of
Nikephoros Gregoras, historian/ London (1340–1354) 465 fn. 192,
chronicler 82 479–80
Nohl J. 321, 333 fn. 88, 369 fn. 180 Ramji Motiram, Indian 157
Noordegraaf L. and Valk G. 226 Raoult D. 12 fn. 28, 192, 381, 38–7, 392
Nybelin O. 138 fn. 35
Ravensdale J. 27
Odysseus (Ulysses) 363 Razi Z. 241, 271, 478, 598
Ohlin G. 596, 599 Read C.P., see Chandler
Orosius, Roman historian 131 Reed L.J. and Frost W.H. 633–6,
Orraeus von G. 214 and fn. 37 640, 648
Orrman E. 516–7 and fn. 68 Rees W. 577–8
Ottar, Norwegian Viking merchant and Roux V. 387–8
explorer 131 Runolf, Friar of Thykkvabær 680
Russell J.C. 226, 421–6, 429–30, 432,
Pál, Abbot in Videy, Iceland 680 435–6, 438, 460, 475, 479, 596–602,
Palmer R.J., see also Zitelli 43, 349–51 605–7 and fn. 224, 630
and fn. 124 Russell P. 214
Peder Hansen (Litle), Commander of
Akerhus Castle (Oslo) Sabine E.L. 579
(1536–1551) 404 Samoilowitz D. 214
Perroy E. 237, 239–40, 244 St Germanus 389
Persson B.E.B. 11 St Remi 329
Perry D.P. and Fetherston J. 11, 683, 685 Savage W.G. and Fitzgerald D.A. 654–5
and fn. 17 Savio P. 657
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Schofield R. 62–9, 45–6, 202–3, 226, 331, 363 fn. 159, 369 fn. 180, 504, 507,
234, 406–7, 415 520, 548, 554, 567, 570–1 and fn. 50,
Scott S. 207, 610 574–5, 612, 619, 622, 646
Scott S. and Duncan C.J. 16–9, 66, 76–7, Stone D, see Hatcher, Piper and Stone
82–4 and fn. 33, 87–91, 98–9, 127–30, Sudhoff K. 341
151, 156–8, 164, 172, 178–91, 194, Sutherland I. 356–7
199–200, 205–14, 217–8, 221, 284–5, Swellengrebel N.H., see also Loghem
287–8 and fn. 28, 290, 293, 298–9, van 58, 96, 111, 167–9, 176–7, 179,
301–11, 321, 334–40, 385–6 and fn. 182–3
20, 398, 407, 410–1, 415–7, 419–20, Swinnas W., Dutch physician 333
436–7, 439, 442, 445–6, 462–5, Sydenham T. 619
468, 470–2, 474, 482–4, 487–8, 490,
495, 499, 503, 554, 562, 581, 584–6, Taylor J. 435
590–1, 595, 600, 608, 610–63, Thomson G.M 98
665, 668 Thompson Ashburton J. 46–53, 93–5,
Seebohm F. 438, 602, 605–6 111, 155–6, 174–5
Segal A.E., see Vasil’ev Thompson A.H. 151–2, 439–42 and fn.
Sellers M. 631 137, 446, 449, 452, 602–3
Shirk M.V. 294 Thorlak, ship owner, Icelander 536 fn.
Shrewsbury J.F.D. 16–7, 19, 30, 54, 128, 128
151, 223, 226, 278, 283, 285 and fn. 21, Thorstein, priest at Helgafell,
287 fn. 28, 333, 398, 407, 420, 433, Iceland 680
437–9, 449–51, 453–4, 457, 461–4, Titow J. 596
467–8, 470–1, 475, 479, 483–4, 487, Twigg G. 16–7, 19, 76, 78, 85, 87, 96,
489–92, 496, 498, 501, 503–4 and fn. 98–9, 103, 117, 119–23, 128–30, 138,
26, 507–10, 512–3, 552–3, 560, 562, 140, 151, 153–4, 156, 164, 170, 172,
572, 628, 631, 643, 647 177–8 and fn. 67, 180–6, 188, 191, 194,
Sigurðsson J.V. 516–7 fn. 68 205, 220–1, 283–4, 290, 292–3, 317–8,
Simon of Couvin 39–40 and fns. 38–9, 327–8, 405, 407, 411, 415–6, 419–20,
42, 236 422–3, 425, 435–9, 442, 445–6, 449,
Simond P.L. 43, 281–2, 646 461–5, 468, 470–1, 474, 482–4, 487–8,
Simpson W.J. 3, 40–1, 108–9, 153, 196, 490, 495, 553–611, 615, 621 fns. 34
202–3 and fn. 35, 366–7, 373–6, 378, and 36, 628–30, 661, 665
542–3, 545, 554, 567–8 and fn. 39, 570,
612, 656
Singleton C.S. 395 fn. 153 Ulsig E. Danish historian 60
Slack P. 56, 62, 68, 146–7, 179, 209–10
and fn. 18, 226, 287, 294–6, 304, 306, Vahtola J., Finnish historian 99
309–11, 322, 333, 415, 432–3, 435, Valk G., see Noordegraaf
508, 510, 614–5 Vasil’jev2 K.G. and Segal A.E. 58
Smith R.M. 601, 605–6, 632 Valerianus, Roman Emperor
Snorri Sturluson 137 (253–260) 343
Steffensen J. 493, 500, 502 fn.23, 504, Veale E.M. 578 and fn. 86
506–12, 514–5, 519, 522, 526–30, 532, Vigne F.-J., see Audoin-Rouzeau
535–8, 540–2, 550, 552 Vilar R. 294
Sticker G. 3, 143, 213–5, 221, 282, 284, Villani Filippo, chronicler 324
314, 322, 324 fn. 38, 326, 330 fn. 78,
2
The phonetical symbol l’ refers to the phonem palatalized l, phonetically
written lj.
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746 index of names
Villani Giovanni, chronicler 344, 347, Wood W. 561–2, 654

531 fn. 108 Wrigley E.A. 226
Villani Matteo, chronicler 243 fn. 136, Woodall J. 216
258, 323–5 and fns. 34, 43–4, 360, 413 Wood-Legh K.L. 450
Villani brothers 344 Wu C.Y. 166–7, 179, 539, 567, 620, 622
Viverius Jacobus, Dutch physician 333 Wu Lien-Teh 3, 31–2, 45, 75, 90, 97, 113
Vogel de, Dr 168, 182–3 and fn. 137, 142, 172 fn. 55, 208, 213,
321, 498–500 and fn. 17, 512–26 and
Wakil A.W. 58 fns. 66 and 70, 529, 534 fn. 115,
Walløe L. 12–15 and fn. 29, 400–2 and 538–9, 554, 567, 612, 619–22 and
fn. 18 fn. 34, 627
Weber M. 104
White D.O., see Burnet Yersin A. 25, 92, 314, 316, 337, 617 and
WHO, see World Health Organization fn. 20
Wigh B. 132 and fn. 186
World Health Organization 3, 11–3, 556
fn. 6, 558 fn. 15, 649–50, 652 and fn. Ziegler P 439, 441, 450 and fn. 150, 472,
152, 660 553–4, 572, 578, 584, 591–3 and fn.
William Dene, chronicler, monk of 158, 611
Rochester 448 Zinsser H. 490
William Leene, plague victim, see also Zitelli A. and Palmer R. 54, 449–51 and
George Leene 287–8 fn. 124
Woehlkens E. 68, 143–4, 146 Zouche William 452
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On the Controversy over the Microbiological

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This book is printed on acid-free paper.

Library of Congress Cataloging-in-Publication Data

Benedictow, Ole Jørgen.

Copyright 2010 by Koninklijke Brill NV, Leiden, The Netherlands.

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

List of Figures and Tables ........................................................................xiii

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The Question of the Presence of Rats and the

Ole Benedictow - 978-90-04-19391-8

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Shrewsbury: the Composite, Low-Intensity Theory ....................489

Ole Benedictow - 978-90-04-19391-8

15. The Alternative Theory of Scott and Duncan...............................610

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Ole Benedictow - 978-90-04-19391-8

Den som vill mitt fotspor fylgje

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

THE ISSUE AND THE PROBLEMS

Most of our knowledge of bubonic plague was established by medical

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

specifically the species Xenopsylla cheopis. Central to the process of

Ole Benedictow - 978-90-04-19391-8

All of the above-mentioned leading scholars and researchers of

Ole Benedictow - 978-90-04-19391-8

from the introduction of an infective rat flea into a colony of black

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

victims of a bubonic plague epidemic. Pneumonic plague introduces a

The Human-Flea Theory of Plague Epidemiology

The history of alternative theories of the transmission of bubonic

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

of interhuman transmission by the human flea leading to bubonic

Ole Benedictow - 978-90-04-19391-8

bubonic plague.31 It is therefore surprising that Walløe is silent on this

Ole Benedictow - 978-90-04-19391-8

environmental conditions found in a bed.”36 Fortunately, however,

Ole Benedictow - 978-90-04-19391-8

Ole Benedictow - 978-90-04-19391-8

for instance the inverse correlation of morbidity and mortality rates

The recent history of alternative theories began in 1971, when J.F.D.

Ole Benedictow - 978-90-04-19391-8

the character of a children’s disease, implying that adults were to a large

Ole Benedictow - 978-90-04-19391-8

paleomicrobiology, may provide the opportunity of testing genetic

Ole Benedictow - 978-90-04-19391-8

There is a curious and conspicuous fragmentation of the alternative