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Handbook of Food Engineering
Third Edition
Handbook of Food Engineering
Third Edition

Edited by
Dennis R. Heldman
Daryl B. Lund
Cristina M. Sabliov
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742

© 2019 by Taylor & Francis Group, LLC


CRC Press is an imprint of Taylor & Francis Group, an Informa business

No claim to original U.S. Government works

Printed on acid-free paper

International Standard Book Number-13: 978-1-4665-6312-4 (Hardback)

This book contains information obtained from authentic and highly regarded sources. Reasonable efforts have been made to pub-
lish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the
consequences of their use. The authors and publishers have attempted to trace the copyright holders of all material reproduced in
this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright
material has not been acknowledged please write and let us know so we may rectify in any future reprint.

Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any
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http://www.crcpress.com
Contents

Preface...................................................................................................................................................... vii
Editors........................................................................................................................................................ ix
Contributors............................................................................................................................................... xi

1 Linear and Non-Linear Rheological Properties of Foods............................................................. 1


Ozlem C. Duvarci, Gamze Yazar, Hulya Dogan, and Jozef L. Kokini

2 Advances in Nanotechnology of Food Materials for Food and Non-Food Applications........ 153
Rohollah Sadeghi, Thanida Chuacharoen, Cristina M. Sabliov, Carmen I. Moraru,
Mahsan Karimi, and Jozef L. Kokini

3 Reaction Kinetics in Food Systems.............................................................................................. 225


Ricardo Villota and James G. Hawkes

4 Phase and State Transitions and Transformations in Food Systems...................................... 485


Yrjö H. Roos

5 Transport and Storage of Food Products................................................................................... 551


M. A. Rao

6 Heating and Cooling Processes for Foods................................................................................... 597


R. Paul Singh and Gail Bornhorst

7 Food Freezing and Frozen Food Storage.................................................................................... 637


Dennis R. Heldman

8 Mass Transfer in Foods................................................................................................................ 683


Bengt Hallström, Vassilis Gekas, Ingegerd Sjöholm, and Anne Marie Romulus

9 Evaporation and Freeze Concentration...................................................................................... 705


Ken R. Morison and Richard W. Hartel

10 Membranes in Food Technology.................................................................................................. 765


Frank Lipnizki

11 Food Dehydration.......................................................................................................................... 799


Martin R. Okos, Osvaldo Campanella, Ganesan Narsimhan, Rakesh K. Singh,
and A. C. Weitnauer

12 Thermal Processing of Canned Foods........................................................................................ 951


Arthur Teixeira

13 Extrusion Processes...................................................................................................................... 985


Leon Levine and Robert C. Miller

v
vi Contents

14 Food Packaging........................................................................................................................... 1031


John M. Krochta

15 Engineering Considerations for Cleaning and Disinfection in the Food Industry............... 1125
Kylee R. Goode, David Phinney, Tony Hasting, and Peter Fryer
Index......................................................................................................................................................1175
Preface

The editors and authors of the Third Edition of the Handbook of Food Engineering hope the content will
continue to provide students and food engineering professionals with the latest information needed to
improve the efficiency of the food supply system. As the complexity of the system increases, the focus
on processes used to convert raw food materials and ingredients into consumer food products becomes
more important. As suggested in previous editions, there are three different audiences for the content of
this Handbook: (1) practicing engineers in food, beverage, and related industries; (2) students preparing
for careers as food engineers; and (3) other engineers and scientists seeking the latest information on unit
operations and processes needed for process design and development. Hopefully, practicing engineers
will use the content to improve processes throughout the food supply system. The Handbook should
become the primary reference for students as a supplement to textbooks during the study of unit opera-
tions and process design and development. Other scientists and engineers should be able to locate the
latest information and data needed when evaluating processes during development of new products or
for quality assurance considerations.
As with the previous editions, the Handbook of Food Engineering contains the latest information on
the thermophysical properties of foods and kinetic constants needed to estimate changes in key compo-
nents of foods during manufacturing and distribution. Illustrations are used to demonstrate the applica-
tions of the information to process design. Researchers should be able to use the information to pursue
new directions in process development and design, and to identify future directions for research on
physical properties of foods and kinetics of changes in food throughout the supply system. As in the
second edition, the Appendix provides tables of data and illustrations for many food-related properties.
The first four chapters of the Third Edition focus primarily on properties of foods and food ingredients
with a new chapter on nanoscale applications in foods. Each of the eleven chapters that follow focus on
one of the more traditional unit operations used throughout the food supply system. Major revisions and/
or updates have been incorporated into chapters on heating and cooling, membrane and extrusion pro-
cesses, and cleaning operations. Most of the chapters have been revised and updated.
The editors are dedicated to continuing the evolution of food engineering as an interface between
traditional engineering disciplines and food science. As the focus on a more efficient food supply sys-
tem continues to evolve, with a specific focus on reducing energy, fresh water, and waste, the need
for more efficient unit operations and processes is very evident. These needs, driven by the consumer,
have evolved as the demands for safe, high quality, nutritious, and health-enhancing foods continue to
increase. As the applications of molecular biology, nanoscale sciences, and metabolomics evolve and
begin to impact consumer food products, the design of processes used throughout the food supply sys-
tem will improve. The importance of unit operation and process design from bench-scale to pilot plant
scale-up to commercial scale becomes even more critical. Opportunities for optimization of processes
that ensure food safety while achieving maximum food quality and throughput should become more
evident when using the content of this Handbook. Finally, the incorporation of emerging technologies
and unit operations into the processes used throughout the food supply chain can be accelerated using
the background presented in this Handbook.
The editors wish to acknowledge the contributions of all contributors to the Handbook of Food
Engineering. Thirty-six authors have contributed to the 15 chapters in the Handbook. The content has
been greatly enhanced, broadened, and expanded through the contributions of each author. Each author
is a leading food engineer and scientist, and the co-editors are proud to include their contributions to the
Third Edition of the Handbook of Food Engineering.

Dennis R. Heldman
Daryl B. Lund
Cristina M. Sabliov
vii
Editors

Dennis R. Heldman was awarded a BS (1960) and MS (1962) degrees from The Ohio State University,
and a PhD (1965) from Michigan State University. In 1966, he joined the faculty at Michigan State
University, and began teaching and research in the area of food process engineering. He served as chair
of the Agricultural Engineering Department at Michigan State University from 1975 to 1979. He joined
the Campbell Soup Company in 1984, as the vice president of Process Research and Development. In
1986, he moved to the National Food Processors Association, as executive vice president of Scientific
Affairs, CEO for The National Food Laboratory, and president of The Food Processors Institute. In 1991,
he joined the Weinberg Consulting Group Inc, as a consultant on food regulatory issues.
In 1992, he was appointed professor of Food Process Engineering at the University of Missouri and
Leader for the Foods, Feeds and Products cluster in the Foods for the 21st Century program. Beginning
in 1994, he served as unit leader for the Food Science and Engineering Unit, and in 1997, as director for
the Office of Value-Added Agriculture Outreach. From 1998 to 2004, he was professor of Food Process
Engineering at Rutgers, the State University of New Jersey, and director of the Cooperative Research &
Development Program in the Center for Advanced Food Technology (CAFT). From 2004 to 2012, he
was a consultant involved in applications of engineering concepts to food manufacturing for educational
institutions, industry and government. In August 2012, he joined the faculty at The Ohio State University
as Dale A. Sobering Endowed Professor of Food Engineering. In 2016, he assumed responsibilities as
director of the Center for Advanced Processing and Packaging Studies (CAPPS).
He has received numerous recognitions, including the FIEI Young Researchers’ Award from the
American Society of Agricultural Engineers in 1974, elected fellow of the Institute of Food Technologists
(IFT) in 1981, the DFISAASAE Food Engineering Award in 1981, elected fellow of the American
Society of Agricultural Engineers in 1984, elected fellow in the International Academy of Food Science
& Technology in 2007, recipient of the Life Achievement Award from the International Association
for Engineering and Food, and the Frozen Food Foundation Freezing Research Award in 2011, the
Carl R. Fellers Award from the IFT and Phi Tau Sigma in 2013, the Harold Macy Food Science and
Technology Award from the Minnesota Section of IFT in 2017, and the Nicholas Appert Award from
IFT in 2018.

Daryl B. Lund earned a BS (1963) in mathematics and a PhD (1968) in food science with a minor in
chemical engineering at the University of Wisconsin-Madison. During 21 years at the University of
Wisconsin, he was a professor of food engineering in the food science department serving as chair of
the department from 1984–1987. He has contributed over 150 scientific papers, edited 5 books, and
co-authored one major textbook in the area of simultaneous heat and mass transfer in foods, kinetics of
reactions in foods, and food processing.
In 1988 he continued his administrative responsibilities by chairing the Department of Food Science
at Rutgers University, and from December 1989 through July 1995 served as the executive dean of
Agriculture and Natural Resources with responsibilities for teaching, research and extension at Rutgers
University. In August 1995, he joined Cornell University as the Ronald P. Lynch Dean of Agriculture and
Life Sciences. In January 2001, Dr. Lund became the executive director of the North Central Regional
Association of State Agricultural Experiment Station Directors located at UW Madison. In this position
he facilitated interstate collaboration on research and a greater integration between research and exten-
sion in the twelve-state region.
He has received numerous awards in recognition of personal achievements:ASAE/DFISA Food
Engineering Award, Irving Award from the American Distance Education Consortium (ADEC),
International Congress on Engineering and Food (ICEF) Lifetime Achievement Award, and Institute of
Food Technologists (IFT) International Award, Carl R. Fellers Award, and Nicolas Appert Award for

ix
x Editors

lifetime achievement. In 2016 he received the Lifetime Achievement Award from the International Union
of Food Science and Technology (IUFoST). He is an elected fellow of the IFT, IUFoST, and charter
inductee in the International Academy of Food Science and Technology (IAFoST).

Cristina M. Sabliov is the Richard R. & Betty S. Fenton LSU Alumni Professor in the Biological and
Agricultural Engineering (BAE) Department at Louisiana State University and LSU Agricultural Center.
She received a BS in Food Technology, two MS degrees in Agricultural Engineering and Chemical
Engineering, and PhDs in Food Science, and Biological and Agricultural Engineering. Currently, she
serves as a graduate coordinator in the BAE Department. is leading an international renowned research
program in the field of nanotechnology, specifically focused on polymeric nanoparticles designed for
delivery of bioactive components for improved food quality and human health. She collaborates exten-
sively across disciplines with colleagues from the US and abroad, to address complex research questions.
To date, she has published 56 papers and has been cited more than 1,000 times. She has been recognized
for the quality and impact of her work by LSU, as a recipient of Tiger Athletic Foundation Undergraduate
Teaching Award, and Distinguished Faculty Award. The American Society of Agricultural and Biological
Engineers awarded her the New Holland Young Researcher Award in 2011, and in 2016 She was inducted
as a Fellow of the American Institute for Medical and Biological Engineering.
Contributors

Gail Bornhorst Richard W. Hartel


Department of Biological and Agricultural Department of Food Science
Engineering University of Wisconsin
University of California Madison, Wisconsin
Davis, California
Tony Hasting
Osvaldo Campanella Tony Hasting Consulting
Purdue University Sharnbrook, Bedford, UK
West Lafayette, Indiana
James G. Hawkes
GLG, Inc.
Thanida Chuacharoen
Naperville, Illinois
Department of Food Science and Technology
Suan Sunandha Rajabhat University
Bangkok, Thailand Dennis R. Heldman
The Ohio State University
Columbus, Ohio
Ozlem C. Duvarci
Purdue University
West Lafayette, Indiana Mahsan Karimi
and Department of Food Science and Technology
Izmir Institute of Technology Islamic Azad University
Izmir, Turkey Kermanshah, Iran

Jozef L. Kokini
Hulya Dogan Purdue University
Kansas State University West Lafayette, Indiana
Manhattan, Kansas
John M. Krochta
Peter Fryer Department of Food Science and
Centre for Formulation Engineering, School of Technology
Chemical Engineering Department of Biological and Agricultural
University of Birmingham Engineering
Birmingham, UK University of California
Davis, California
Vassilis Gekas
Technical University of Crete Leon Levine
Chania, Greece Leon Levine & Associates, Inc.
Albuquerque, New Mexico
Kylee R. Goode
Centre for Formulation Engineering, School of Frank Lipnizki
Chemical Engineering Department of Chemical Engineering
University of Birmingham Lund University
Birmingham, UK Lund, Sweden

Bengt Hallström Robert C. Miller


University of Lund Consulting Engineer
Lund, Sweden Auburn, New York

xi
xii Contributors

Carmen I. Moraru Rohollah Sadeghi


Department of Food Science Department of Food Science
Cornell University Purdue University
Ithaca, New York West Lafayette, Indiana

Ken R. Morison R. Paul Singh


Department of Chemical and Process Department of Biological and Agricultural
Engineering Engineering
University of Canterbury University of California,
Christchurch, New Zealand Davis, California

Ganesan Narsimhan Rakesh K. Singh


Purdue University University of Georgia
West Lafayette, Indiana Athens, Georgia

Ingegerd Sjöholm
Martin R. Okos University of Lund
Purdue University Lund, Sweden
West Lafayette, Indiana
Arthur Teixeira
David Phinney University of Florida
The Ohio State University Gainesville, Florida
Columbus, Ohio
Ricardo Villota
M. A. Rao GKF Foods
Cornell University Glenview, Illinois
Ithaca, New York
Angela C. Weitnauer
Purdue University
Anne Marie Romulus
West Lafayette, Indiana
Université Paul Sabatier
Toulouse, France
Gamze Yazar
Purdue University
Yrjö H. Roos
West Lafayette, Indiana
University of Cork
Cork, Ireland

Cristina M. Sabliov
Department of Biological and Agricultural
Engineering
Louisiana State University
Baton Rouge, Louisiana
1
Linear and Non-Linear Rheological Properties of Foods

Ozlem C. Duvarci, Gamze Yazar, Hulya Dogan, and Jozef L. Kokini

CONTENTS
1.1 Introduction....................................................................................................................................... 2
1.2 Basic Concepts.................................................................................................................................. 3
1.2.1 Stress and Strain................................................................................................................... 3
1.2.2 Classification of Materials.................................................................................................... 4
1.2.3 Types of Deformation........................................................................................................... 4
1.2.3.1 Shear Flow............................................................................................................ 4
1.2.3.2 Extensional (Elongational) Flow.......................................................................... 7
1.2.3.3 Volumetric Flows.................................................................................................. 9
1.2.4 Response of Viscous and Viscoelastic Materials in Shear and Extension........................... 9
1.2.4.1 Stress Relaxation................................................................................................. 10
1.2.4.2 Creep....................................................................................................................11
1.2.4.3 Small Amplitude Oscillatory Measurements......................................................11
1.2.4.4 Interrelations between Steady Shear and Dynamic Properties...........................14
1.3 Methods of Measurement.................................................................................................................18
1.3.1 Shear Measurements........................................................................................................... 19
1.3.2 Small Amplitude Oscillatory Shear (SAOS) Measurements............................................. 24
1.3.3 Large Amplitude Oscillatory Shear (LAOS) Measurements............................................. 26
1.3.3.1 Time Dependency of Tomato Paste, Mayonnaise, and Soft and Hard
Dough in SAOS and LAOS.................................................................................41
1.3.4 Extensional Measurements................................................................................................. 44
1.3.5 Stress Relaxation................................................................................................................ 53
1.3.6 Creep Recovery.................................................................................................................. 57
1.3.7 Transient Shear Stress Development...................................................................................61
1.3.8 Yield Stresses..................................................................................................................... 63
1.4 Constitutive Models........................................................................................................................ 64
1.4.1 Simulation of Steady Rheological Data............................................................................. 66
1.4.2 Linear Viscoelastic Models................................................................................................ 67
1.4.2.1 Maxwell Model................................................................................................... 71
1.4.2.2 Voigt Model........................................................................................................ 73
1.4.2.3 Multiple Element Models.................................................................................... 76
1.4.2.4 Mathematical Evolution of Nonlinear Constitutive Models............................... 78
1.4.3 Nonlinear Constitutive Models.......................................................................................... 81
1.4.3.1 Differential Constitutive Models........................................................................ 81
1.4.3.2 Integral Constitutive Models.............................................................................. 84
1.4.3.3 Simulation for Large Amplitude Oscillatory Flow............................................ 89
1.5 Molecular Information from Rheological Measurements.............................................................. 91
1.5.1 Dilute Solution Molecular Theories................................................................................... 91
1.5.2 Concentrated Solution Theories......................................................................................... 94
1.5.2.1 The Bird–Carreau Model................................................................................... 94
1.5.2.2 The Doi–Edwards Model.................................................................................... 98
1.5.3 Understanding Polymeric Properties from Rheological Properties..................................101
1
2 Handbook of Food Engineering

1.5.3.1 Gel Point Determination....................................................................................101


1.5.3.2 Glass Transition Temperature and the Phase Behavior.................................... 105
1.5.3.3 Networking Properties...................................................................................... 109
1.6 Use of Rheological Properties in Practical Applications..............................................................111
1.6.1 Sensory Evaluations..........................................................................................................112
1.6.2 Molecular Conformations.................................................................................................115
1.6.3 Product and Process Characterization..............................................................................117
1.7 Numerical Simulation of Flows.....................................................................................................119
1.7.1 Numerical Simulation Techniques....................................................................................119
1.7.2 Selection of Constitutive Models.......................................................................................121
1.7.3 Finite Element Simulations...............................................................................................121
1.7.3.1 FEM Techniques for Viscoelastic Fluid Flows................................................. 122
1.7.3.2 FEM Simulations of Flow in an Extruder........................................................ 123
1.7.3.3 FEM Simulations of Flow in Model Mixers..................................................... 126
1.7.3.4 FEM Simulations of Mixing Efficiency........................................................... 128
1.7.4 Verification and Validation of Mathematical Simulations................................................133
1.8 Concluding Remarks..................................................................................................................... 136
References............................................................................................................................................... 138

1.1 Introduction
Rheological properties are important to the design of flow processes, quality control, storage and pro-
cessing stability measurements, predicting texture and learning about molecular and conformational
changes in food materials (Dealy and Wang, 2013; Davis, 1973). The rheological characterization of
foods provides important information for food scientists in ingredient selection strategies to design,
improve and optimize their products, to select and optimize their manufacturing processes and to design
packaging and storage strategies. Rheological studies become particularly useful when predictive rela-
tionships for rheological properties of foods can be developed, which start from the molecular architec-
ture of the constituent species.
Reliable and accurate steady rheological data are necessary to design continuous-flow processes,
select and size pumps and other fluid-moving machinery and to evaluate heating rates during engineer-
ing operations, which include flow processes such as aseptic processing and concentration (Sheath, 1976;
Holdsworth, 1971), and to estimate velocity, shear and residence-time distribution in food processing
operations including extrusion and continuous mixing.
Viscoelastic properties are also useful in processing and storage stability predictions. For example,
during extrusion, viscoelastic properties of cereal flour doughs affect die swell and extrudate expan-
sion. In batch mixing, elasticity is responsible for the rod climbing phenomenon, also known as the
Weissenberg effect (Bird et al., 1987). To allow for elastic recovery of dough during cookie making, the
dough is cut in the form of an ellipse which relaxes into a perfect circle.
Creep and smal‑lamplitude oscillatory measurements are useful in terms of understanding the role of
constituent ingredients on the stability of oil-in-water emulsions. Steady shear and creep measurements
help identify the effect of ingredients that have stabilizing abilities, such as gums, proteins or other
surface-active agents (Fischbach and Kokini, 1984).
Dilute solution viscoelastic properties of biopolymeric materials, such as carbohydrates and protein,
can be used to characterize their three-dimensional configuration in solution. Their configuration affects
their functionality in many food products. It is possible to better predict and improve the flow behavior of
food polymers through an understanding of how the molecular structure of foods affect their rheological
properties (Liguori, 1985). Examples can be found in the improvement of the consistency and stability of
emulsions by using polymers with enhanced surface activity and greater viscosity and elasticity.
This chapter will review recent advances in basic rheological concepts, methods of measurement,
molecular theories, linear and nonlinear constitutive models and numerical simulation of viscoelastic
Linear and Non-Linear Rheological Properties of Foods 3

flows. In this edition we have updated the new and emerging topics related to large Amplitude Oscillary
Measurements (LAOS)

1.2 Basic Concepts
1.2.1 Stress and Strain
Rheology is the science of the deformation and flow of matter. Rheological properties define the relationship
between stress and strain/strain rate in different types of shear and extensional flows. The stress is defined as
the force F acting on a unit area A. Since both force and area have directional as well as magnitude character-
istics, stress is a second order tensor and typically has nine components. Strain is a measure of deformation,
or relative displacement, and is determined by the displacement gradient. Since displacement and its relative
change both have directional properties, strain is also a second order tensor with nine components.
A rheological measurement is conducted on a given material by imposing a well-defined stress and
measuring the resulting strain or strain rate, or by imposing a well-defined strain or strain rate and by
measuring the stress developed. The relationship between these physical events leads to different kinds
of rheological properties.
When a force F is applied to a piece of material (Figure 1.1), the total stress acting on any infinitesimal
element is composed of two fundamental classes of stress components (Darby, 1976; Chhabra, 2010;
Campanella, 2011):

1. “normal stress” components, applied perpendicularly to the plane (τ11, τ22, τ33),
2. “shear stress” components, applied tangentially to the plane (τ12, τ13, τ21, τ23, τ31, τ32).

There are a total of nine stress components acting on an infinitesimal element (i.e. two shear and one
normal stress components acting on each of the three planes). Individual stress components are referred to
as τij, where i refers to the plane the stress acts on, and j indicates the direction of the stress component (Bird
et al., 1987; van Vliet, 2014). The stress tensor can be written as a matrix of nine components as follows:

é t11 t12 t13 ù


ê ú
t = ê t21 t22 t23 ú
êë t31 t32 t33 úû
In general, the stress tensor in the deformation of an incompressible material is described by three shear
stresses and two normal stress differences:

Shear stresses: τ12 (=τ21), τ13 (=τ31), τ23 (=τ32)


Normal stress differences: N1 = τ11 − τ22, N2 = τ22 − τ33

22

12

21

23
11
1
13
1-plane
3

FIGURE 1.1 Stress components on a cubical material element.


4 Handbook of Food Engineering

1.2.2 Classification of Materials
Rheological properties of materials are the result of their stress-strain behaviors. Ideal solid (elastic) and
ideal fluid (viscous) behaviors represent two extreme responses of a material (Darby, 1976).
An ideal solid material deforms instantaneously when a load is applied. It returns back to its original
configuration instantaneously (complete recovery) upon removal of the load. Ideal elastic materials obey
Hooke’s law, where the stress (τ) is directly proportional to the strain (γ). The proportionality constant
(G) is called the modulus.
t = Gg
An ideal fluid deforms at a constant rate under an applied stress, and the material does not regain its
original configuration when the load is removed. The flow of a simple viscous material is described by
Newton’s law, where the shear stress (τ) is directly proportional to the shear rate (g ). The proportionality
constant (η) is called the Newtonian viscosity.

t = hg

Most food materials exhibit characteristics of both elastic and viscous behavior, and are called
viscoelastic. If viscoelastic properties are strain and strain rate independent, then these materials are
referred to as linear viscoelastic materials. On the other hand, if they are strain and strain rate–depen-
dent than they are referred to as nonlinear viscoelastic materials (Bird et al., 1987; Macosko, 1994;
Ferry, 1980).
A simple and classical approach to describe the response of a viscoelastic material is using mechanical
analogs. Purely elastic behaviour is simulated by springs and purely viscous behaviour is simulated using
dashpots. The Maxwell and Voigt models are the two simplest mechanical analogs of viscoelastic mate-
rials. They simulate a liquid (Maxwell) and a solid (Voigt) by combining a spring and a dashpot in series
or in parallel, respectively. These mechanical analogs are the building blocks of constitutive models, as
discussed in Section 1.4 in detail.

1.2.3 Types of Deformation
1.2.3.1 Shear Flow
One of the most useful types of deformation for rheological measurements is simple shear. In simple
shear, a material element is placed between two parallel plates (Figure 1.2) where the bottom plate is sta-
tionary and the upper plate is displaced in x-direction by ∆x by applying a force F tangentionally to the
surface A. The velocity profile in simple shear is given by the following velocity components (Chhabra,
2010; Chhabra and Richardson, 2011):

u x = g y, u y = 0 and uz = 0

The corresponding shear stress is given as:


F
t=
A

A
F

∆y vx
y

FIGURE 1.2 Shear flow.


Linear and Non-Linear Rheological Properties of Foods 5

If the relative displacement at any given point ∆y is ∆x, then the shear strain is given by

Dx
g=
Dy
If the material is a fluid, the force applied tangentionally to the surface will result in a constant velocity
vx in x-direction. The deformation is described by the strain rate ( g ), which is the time rate of change
of the shear strain:

d g d æ Dx ö dn x
g = = ç ÷=
dt dt è Dy ø dy
Shear strain defines the displacement gradient in simple shear. The displacement gradient is the rela-
tive displacement of two points divided by the initial distance between them. For any continuous medium
the displacement gradient tensor is given as:

é ¶u1 ¶u1 ¶u1 ù


ê ¶x ¶x2 ¶x3 úú
ê 1
¶ui ê ¶u2 ¶u2 ¶u2 ú
=
¶x j êê ¶x1 ¶x2 ¶x3 úú
ê ¶u3 ¶u3 ¶u3 ú
ê ¶x ¶x2 ¶x3 úû
ë 1
A non-zero displacement gradient may represent pure rotation, pure deformation or both (Darby,
1976). Thus, each displacement component has two parts:

¶ui 1 æ ¶u ¶u ö 1 æ ¶u ¶u ö
= çç i + j ÷÷ + çç i - j ÷÷
¶x j 2 ¶x j ¶xi ø 2 è ¶x j ¶xi ø
è   
Pure deformation Pure rotation

Then the strain tensor (eij) can be defined as:


æ ¶u ¶u ö
eij = çç i + j ÷÷
è ¶x j ¶xi ø
Similarly, the rotation tensor (rij) can be defined as:

æ ¶u ¶u ö
rij = çç j - i ÷÷
è ¶xi ¶x j ø
In simple shear, there is only one non-zero displacement gradient component that contributes to both
strain and rotation tensors.

é ¶ux ù
ê0 ¶y

é0 1 0ù
¶ui ê ú du ê ú
= ê0 0 0ú = x
ê0 0 0ú
¶x j ê ú dy ê
ê0 0 0ú ë0 0 0 ûú
êë úû

The time derivative of strain tensor gives the rate of strain tensor (∆ij):

¶ æ ¶u ö ¶n
Dij =
¶t
( eij ) = ¶¶t çç ¶¶xui + ¶x j ÷÷ = ¶¶xni + ¶x j
è j i ø j i
6 Handbook of Food Engineering

Similarly, the time derivative of the rotation tensor gives the vorticity tensor (Ωij):

¶ ¶n ¶n
Wij =
¶t
( rij ) = j - i
¶xi ¶x j
Simple shear flow, or viscometric flow, serves as the basis for many rheological measurement tech-
niques (Bird et al., 1987). The stress tensor in simple shear flow is given as:

é0 t12 0ù
ê ú
t = ê t21 0 0ú
êë 0 0 0 úû
There are three shear rate–dependent material functions used to describe material properties in simple
shear flow:

t12
Viscosity; m ( g ) =
g
t -t N
First normal stress coefficient; y1 ( g ) = 11 2 22 = 21
g g
t22 - t33 N 2
Second normal stress coefficient; y 2 ( g ) = = 2
g 2 g

Among the viscometric functions, the viscosity is the most important parameter for a food material. In
the case of a Newtonian fluid, both the first and second normal stress coefficients are zero and the material
is fully described by a constant viscosity over all shear rates studied. First normal stress data for a wide
variety of food materials are available (Dickie and Kokini, 1982; Chang et al., 1990; Wang and Kokini,
1995a; Chesterton et al., 2011; Ng et al., 2011; Torres et al., 2013). Well-known practical examples demon-
strating the presence of normal stresses are the Weissenberg or rod climbing effect and the die swell effect.
Although the exact molecular origin of normal stresses is not well understood, they are considered to be
the result of the elastic properties of viscoelastic fluids (Darby, 1976; Chhabra and Richardson, 2011), and
are a measure of the elasticity of the fluids. Figure 1.3 shows the normal stress development for butter at

100.0 sec–1
1.0

0.8

0.6
10.0 sec–1
11− 22)

11− 22)

1.0 sec–1
0.4 0.1 sec–1
(
(

0.2

0.0
0 20 40 60 80 100 120
Time (sec)

FIGURE 1.3 Normal stress development for butter at 25°C. (Reproduced with permission from Kokini, J.L. and Dickie,
A., Journal of Texture Studies, 12, 539–557, 1981.)
Linear and Non-Linear Rheological Properties of Foods 7

25°C. Primary normal stress coefficients versus shear rate plots for various semi-solid food materials on
log-log coordinates are shown in Figure 1.4 in the shear rate range 0.1 to 100 s−1.
The Weissenberg effect and the die swell effect are known to occur due to the difference in the first
normal force. Phan-Thien (2013) discusses the role of the first normal stresses in terms of how they affect
the flow down an inclined plane. A Newtonian fluid seems to have a flat surface during the flow down an
inclined channel, while a viscoelastic fluid shows a convex surface due to negative second normal force
difference.

1.2.3.2 Extensional (Elongational) Flow


Pure extensional flow does not involve shearing and is referred to as shear-free flow (Bird et al., 1987;
Macosco, 1994). Extensional flows are generically defined by the following velocity field:

1
u x = - e (1 + b ) x
2

1
u y = - e (1 - b ) y
2

uz = +e z

where:
0≤b ≤ 1
e is the elongation rate (Bird et al., 1987; Chhabra and Richardson, 2011).

There are three basic types of extensional flow: uniaxial, planar and biaxial, as shown in Figure 1.5.
When a cubical material is stretched in one or two direction(s), it gets thinner in the other direction(s) as

105 105
Strick margarine Strick butter
Mayonnaise Canned frosting
4 Apple butter 4 Mustard
10 10
Ketchup

103 103
(Pascal sec2)

102 102

101 101
1

100 100

1 1
10 10

10 2 10 2
0.1 1.0 10.0 100.0 0.1 1.0 10.0 100.0
–1
Shear rate (sec )

FIGURE 1.4 Steady primary normal stress coefficient ψ1 versus shear rate for semisolid foods at 25°C. (Reproduced with
permission from Kokini, J.L. and Dickie, A., Journal of Texture Studies, 12, 539–557, 1981.)
8 Handbook of Food Engineering

Undeformed
y

x
1

Deformed

y y y
.
(t2–t1)
1l l l =e 1l l

1l l
x 1

1l l
z x
.
(t1–t2) x
l =e .
(t2–t1)
z l =e
1l l
z
(a) (b) (c)

FIGURE 1.5 Types of extensional flows (a) uniaxial, (b) biaxial, (c) planar. (Reproduced with permission from Bird, R.B.,
et al., Dynamics of Polymeric Liquids, John Wiley and Sons Inc., New York, 1987.)

the volume of the material remains constant. During uniaxial extension, the material is stretched in one
direction which results in a corresponding size reduction in the other two directions. In biaxial stretch-
ing, a flat sheet of material is stretched in two directions with a corresponding decrease in the third
direction. In planar extension, the material is stretched in one direction with a corresponding decrease in
thickness while the height remains unchanged.
The velocity distribution in Cartesian coordinates and the resulting normal stress differences and vis-
cosities for these three extensional flows are given in Table 1.1 (Bird et al., 1987).
The concept of extensional flow measurements goes back to 1906 with measurements conducted
by Trouton. Trouton established a mathematical relationship between extensional viscosity and shear

TABLE 1.1
Velocity Distribution and Material Functions in Extensional Flow
Uniaxial Biaxial Planar
(b = 0, e >0) (b = 0, e <0) (b = 1, e >0)
Velocity 1 u x = +e x u x = -e x
distribution u x = - e x
2 u y = -2e x uy = 0
1
u y = - e y uz = +e z uz = +e z
2
uz = +e z
Normal stress s11 - s22 and s11 - s33 σ11 − σ 22 and σ33 − σ 22 σ11 − σ 22
differences
Viscosity s11 - s22 s11 - s33 s11 - s22 s33 - s22 s11 - s22
hE = = hB = = hP =
e e e e e
Linear and Non-Linear Rheological Properties of Foods 9

viscosity. The dimensionless ratio known as the Trouton number (N T ) is used to compare the relative
magnitude of extensional (ηE, ηB or ηP) and shear (η) viscosities:

Extensional viscosity
NT =
Shear viscosity
The Trouton ratio for a Newtonian fluid is 3, 6 and 4 in uniaxial, biaxial and planar extensions, respec-
tively (Dealy, 1984).
h h h
h= E = B = P
3 6 4

1.2.3.3 Volumetric Flows
When an isotropic material is subjected to identical normal forces (e.g. hydrostatic pressure) in all direc-
tions, it deforms uniformly in all axes resulting in a uniform change (decrease or increase) in dimensions
of a cubical element (Figure 1.6). In response to the applied isotropic stress, the specimen changes its
volume without any change in its shape. This uniform deformation is called volumetric strain. An iso-
tropic decrease in volume is called a compression, and an isotropic increase in volume is referred to as
dilation (Darby, 1976). In this case, all shear stress components will be zero and the normal stresses will
be constant and equal:

é1 0 0ù
ê ú
sij = s ê0 1 0ú
êë0 0 1 úû

The bulk elastic properties of a material determine how much it will compress under a given amount of
isotropic stress (pressure). The modulus relating hydrostatic pressure and volumetric strain is called the
bulk modulus (K), which is a measure of the resistance of the material to the change in volume (Ferry,
1980). It is defined as the ratio of normal stress to the relative volume change:

s
K=
DV V

1.2.4 Response of Viscous and Viscoelastic Materials in Shear and Extension


Viscoelastic properties can be measured by experiments which examine the relationship between stress
and strain and strain rate in time-dependent experiments. These experiments consist of (1) stress relax-
ation, (2) creep and (3) small amplitude oscillatory measurements. Stress relaxation (or creep) consists
of instantaneously applying a constant strain (or stress) to the test sample and measuring the change
in stress (or strain) as a function of time. Dynamic testing consists of applying an oscillatory stress (or
strain) to the test sample and determining its strain (or stress) response as a function of frequency. All
linear viscoelastic rheological measurements are related and it is possible to calculate one from the other
(Ferry, 1980; Macosko, 1994; Banks et al., 2011; Münstedt and Schwarzl, 2014).

V V′

∆V=V–V ′

FIGURE 1.6 Volumetric strain.


10 Handbook of Food Engineering

1.2.4.1 Stress Relaxation
In a stress relaxation test, a constant strain (γ0) is applied to the material at time t0 and the change in
the stress over time, τ(t), is measured (Darby, 1976; Macosko, 1994). Ideal viscous, ideal elastic and
typical viscoelastic materials show different responses to the applied step strain, as shown in Figure 1.7.
When a constant stress is applied at t0, an ideal (Newtonian) fluid responds with an instantaneous infi-
nite stress. An ideal (Hooke) solid responds with instantaneous constant stress at t0 and stress remains
constant for t > t0. Viscoelastic materials respond with an initial stress growth which is followed by a
decay in time. Upon removal of strain, viscoelastic fluids equilibrate to zero stress (complete relaxation)
while viscoelastic solids store some of the stress and equilibrate to a finite stress value (partial recovery)
(Darby, 1976).
The relaxation modulus, G(t), is an important rheological property measured during stress relaxation.
It is the ratio of the measured stress to the applied initial strain at constant deformation. The relaxation
modulus has units of stress (Pascals in SI):
t
G (t ) =
g0
A logarithmic plot of G(t) versus time is useful in observing the relaxation behavior of different
classes of materials, as shown in Figure 1.8. In glassy polymers, there is a little stress relaxation over
many decades of logarithmic time scale. Crosslinked rubber shows a short time relaxation followed
by a constant modulus, caused by the network structure. Concentrated solutions show a similar quali-
tative response but only at very small strain levels caused by entanglements. High molecular weight
concentrated polymeric liquids show a nearly constant equilibrium modulus followed by a sharp fall
after long periods of time caused by disentanglement. Molecular weight has a significant impact on
relaxation time, the smaller the molecular weight the shorter the relaxation time. Moreover, a narrower

Input Responses

Ideal fluid Ideal solid Viscoelastic

Solid
Fluid
t0 t t0 t t0 t t0 t

FIGURE 1.7 Response of ideal fluid, ideal solid, and viscoelastic materials to imposed step strain. (From Darby, R.,
Viscoelastic Fluids: An Introduction to Their Properties and Behavior, Dekker Inc., New York, 1976.)

Crosslinking
Glass
Rubber
G0 (concentrated
suspension)
log G Mw

Polymeric
Dilute liquid
solution

log t

FIGURE 1.8 Typical relaxation modulus data for various materials. (Reproduced with permission from Macosko, C.W.,
Rheology: Principles, Measurements and Applications, VCH Publishers, Inc., New York, 1994.)
Linear and Non-Linear Rheological Properties of Foods 11

molecular weight distribution results in a much sharper drop in relaxation modulus. Uncrosslinked
polymers, dilute solutions and suspensions show complete relaxation after short time periods. In
these materials, G(t) falls rapidly and eventually vanishes (Ferry, 1980; Macosko, 1994; Gallegos and
Martinez Boza, 2010).

1.2.4.2 Creep
In a creep test, a constant stress (τ0) is applied at time t0 and removed at time t1, and the corresponding
strain γ(t) is measured as a function of time. As in the case with stress relaxation, various materials
respond in different ways, as shown by typical creep data given in Figure 1.9. A Newtonian fluid responds
with a constant rate of strain from t0 to t1; the strain attained at t1 remains constant for times t > t1 (no
strain recovery). An ideal (Hooke) solid responds with a constant strain from t0 to t1, which is recovered
completely at t1. A viscoelastic material responds with a nonlinear strain. Strain level approaches a con-
stant rate for a viscoelastic fluid and a constant magnitude for a viscoelastic solid. When the imposed
stress is removed at t1, the solid recovers completely at a finite rate, but the recovery is incomplete for the
fluid (Darby, 1976).
The rheological property of interest is the ratio of strain to stress, as a function of time is referred to
as the creep compliance, J(t).
g (t )
J (t ) =
t0
The compliance has units of Pa−1 and describes how compliant a material is. The greater the compli-
ance, the easier it is to deform the material. By monitoring how the strain changes as a function of time,
the magnitude of elastic and viscous components can be evaluated using available viscoelastic models.
Creep testing also provides means to determine the zero shear viscosity of fluids, such as polymer melts
and concentrated polymer solutions, at extremely low shear rates.
Creep data are usually expressed as logarithmic plots of creep compliance versus time (Figure 1.10).
Glassy materials show a low compliance due to the absence of any configurational rearrangements.
Highly crystalline or concentrated polymers exhibit creep compliance increasing slowly with time. More
liquid-like materials, such as low molecular weight or dilute polymers, show higher creep compliance
and faster increase in J(t) with time (Ferry, 1980).

1.2.4.3 Small Amplitude Oscillatory Measurements


In small amplitude oscillatory flow experiments, a sinusoidal oscillating stress or strain with a frequency
(ω) is applied to the material and the oscillating strain or stress response is measured along with the
phase difference between the oscillating stress and strain. The input strain (γ) varies with time according
to the relationship

g = g 0 sin wt

Input Responses

Ideal fluid Ideal solid Viscoelastic

Fluid
solid
t0 t1 t t0 t1 t t0 t1 t t0 t1 t

FIGURE 1.9 Response of ideal fluid, ideal solid, and viscoelastic materials to imposed instantaneous step stress. (From
Darby, R., Viscoelastic Fluids: An Introduction to Their Properties and Behavior, Dekker Inc., New York, 1976 and
Findley, W.N., et al., Creep and Relaxation of Nonlinear Viscoelastic Materials, Dover Publications Inc., New York, 2013.)
12 Handbook of Food Engineering

Dilute Steady-state
solution
Polymeric
liquid
log J (t )
Mw Rubber
(concentrated
suspension)
Crosslinking
Glass

log t

FIGURE 1.10 Typical creep modulus data for various materials. (From Ferry, J., Viscoelastic Properties of Polymers,
John Wiley and Sons, New York, 1980.)

and the rate of strain is given by

g = g 0w cos wt

where γ0 is the amplitude of strain.


The corresponding stress (τ) can be represented as

t = t0 sin ( wt + d )

where:
τ0 is the amplitude of stress
δ is shift angle (Figure 1.11)
δ = 0 for a Hookean solid
δ = 90° for a Newtonian fluid
0 < δ < 90° for a viscoelastic material.

A perfectly elastic solid produces a shear stress in phase with the strain. For a perfectly viscous liquid,
stress is 90° out of phase with the applied strain. Viscoelastic materials, which have both viscous and
elastic properties, exhibit an intermediate phase angle, between 0° and 90°. A solid-like viscoelastic
material exhibits a phase angle smaller than 45° while a liquid-like viscoelastic material exhibits a phase
angle greater than 45°.
Two rheological properties can be defined as follows:

t0
G¢(w) = cos d
g0

t0
G¢¢(w) = sin d
g0
The storage modulus, G′, is related to the elastic character of the fluid or the storage energy during
deformation. The loss modulus, G″, is related to the viscous character of the material or the energy dissi-
pation that occurs during the experiment. Therefore, for a perfectly elastic solid, all the energy is stored,
i.e. G″ is zero and the stress and the strain will be in phase. However, for a perfect viscous material, all
the energy will be dissipated, i.e. G′ is zero and the strain will be out of phase by 90°.
By employing complex notation, the complex modulus, G*(ω), is defined as

G* (ω ) = G ′ (ω ) + iG ′′ (ω )
Linear and Non-Linear Rheological Properties of Foods 13

0
Input

= 0° Strain
Stress
Strain/Stress amplitude

0
Elastic
response

= 90°

Viscous
response

0< < 90°

Viscoelastic
response

Time

FIGURE 1.11 Input and response functions differing in phase by the angle δ. (From Darby, R., Viscoelastic Fluids: An
Introduction to Their Properties and Behavior, Dekker Inc., New York, 1976; Ahmed, J., Mathematical Modeling of Food
Processing, CRC Press, Boca Raton, FL, 2010; and Chhabra, R.P. and Richardson, J.F., Non-Newtonian Flow and Applied
Rheology: Engineering Applications, Elsevier Ltd., Oxford, 2011.)

or
G* ( w) = ( G¢(w) ) + ( G¢¢(w) )
2 2

Another commonly used dynamic viscoelastic property, the loss tangent, tan δ(ω), denotes the ratio of
viscous and elastic components in a viscoelastic behavior:

G¢¢
tan d ( w) =

For fluid-like systems, appropriate viscosity functions can be defined as follows:

G¢¢
h¢ =
w
and


h¢¢ =
w
where η′ represents the viscous or in-phase component between stress and strain rate, while η″ represents
the elastic or out-of-phase component. The complex viscosity η* is equal to

2 2
æ G¢ ö æ G¢¢ ö
h* = ç ÷ + ç ÷
èwø è wø
The quantities of G′, G″, η′ and η″ collectively enable the rheological characterization of a viscoelas-
tic material during small amplitude oscillatory measurements. The objective of the oscillatory shear
14 Handbook of Food Engineering

experiment is to determine these material specific moduli (G′ and G″) over a wide range of frequency,
temperature, pressure or other material-affecting parameters. Because of experimental constraints (e.g.
weak torque values at low frequencies or large slip and inertial effects at high frequencies), it is usually
impossible to measure G′ (ω) and G″(ω) over 3–4 decades of frequency. However, the frequency range
can be extended to the limits which are not normally experimentally attainable by time-temperature
superposition technique (Ferry, 1980; Miri, 2011; Rao, 2014).
Some rheologically simple materials obey time temperature superposition principles where time and
temperature changes are equivalent (Ferry, 1980). Frequency data at different temperatures are superim-
posed by simultaneous horizontal and vertical shifting at a reference temperature. The resulting curve
is called a master curve, which is used to reduce data obtained at various temperatures to one general
curve, as shown in Figure 1.12. The time-temperature superposition technique allows an estimation of
rheological properties over many decades of time.
Shift factor (aT ) for each curve has a different value, which is a function of temperature. There are
different methods to describe the temperature dependence of the horizontal shift factors. The Williams–
Landel–Ferry (WLF) equation is the most widely accepted one (Ferry, 1980). The WLF equation enables
the calculation of the time (frequency) change at a constant temperature, which is equivalent to tempera-
ture variations at constant time (frequency)

h(T ) -C1 ( T - Tref )


log = log aT =
h(Tref ) C2 + T - Tref
where:
η(T) and η(Tref ) are viscosities at temperature T and Tref, respectively
C1 and C2 are WLF constant for a given relaxation process.

1.2.4.4 Interrelations between Steady Shear and Dynamic Properties


Steady shear rheological properties and small-amplitude oscillatory properties of fluid materials can be
related. The steady viscosity function, η, can be related to the complex viscosity, η*, and the dynamic

Stress Temperature
+8 shift factor
Log shift

relaxation
factor

data
10
11 +4
Stress relaxation modulus

10
10 –80.8 0

–76.7
(dynes/cm )
2

10
9 –4
–74.1 –80 –40 –0 40 80

8
–70.6 Temperature °C
10
–65.4
7 –58.6
10 –49.6
–40.1
0
6
10
+25
Master curve at 25°C
5
10
+50 –80˚ –60˚ –40˚ –20˚ 0˚ 25˚ 80˚
4
10
–2 0 2 –14 –12 –10 –8 –6 –4 –2 –0 +2
10 10 10 10 10 10 10 10 10 10 10 10
Time (h)

FIGURE 1.12 Construction of master curve using time-temperature superposition principle. (Reproduced with permis-
sion from Sperling, L.H., Introduction to Physical Polymer Science, John Wiley and Sons, Inc, New York, 2001.)
Linear and Non-Linear Rheological Properties of Foods 15

viscosity function, η′, while the primary normal stress coefficient, ψ1, can be related to η′/ω. The Cox–
Merz rule (1958) suggests a way of obtaining a relation between the magnitude of complex viscosity with
the steady shear viscosity at corresponding values of frequency and shear rate (Bird et al., 1987):

η* (ω ) = η( γ ) 
γ =ω

Figure 1.13 shows data to compare small amplitude oscillatory properties (η*, η′ and η″/ω) and steady
rheological properties (η and ψ1) for 0.50% and 0.75% guar (Mills and Kokini, 1984). Guar suspensions
tend to have a limiting Newtonian viscosity at low shear rates, as is typical of many polymeric materials.
At small shear rates, η* and η′ are approximately equal and are very close in magnitude to the steady
viscosity η. At higher shear rates, η′ and η* diverge while η* and η converge.
When the out-of-phase component of the complex viscosity is divided by frequency (η″/ω), it has the
same dimensions as the primary normal stress coefficient, ψ1. Both η″/ω and ψ1 in the region where data
could be obtained are also plotted versus shear rate/frequency in Figure 1.13; η″/ω and ψ1 curves show cur-
vature at low shear rates. This is also consistent with observations with other macromolecular systems (Bird
et al., 1987; Ferry, 1980). Moreover, the rate of change in the magnitude of ψ1 closely follows that of η″/ω.
A second example is shown for 3% gum karaya, which is a more complex material (Figure 1.14). Both
steady and dynamic properties of gum karaya deviate radically from the rheological behavior observed
with guar gum. First, within the shear rate range studied, η* was higher than η. This is in contrast to the
behavior observed with guar, where η was either equal to or higher than η*. Second, none of the three
viscosities approached a zero shear viscosity in the frequency/shear rate range studied. Third, the steady
viscosity function η was closer in magnitude to η′ than η* and seemed to be nonlinearly related to both η′
and η*. Finally, values of ψ1 were smaller than values of η″/ω, in contrast to observations with guar where
ψ1 was larger than η″/ω (Mills and Kokini, 1984).

FIGURE 1.13 Comparison of small amplitude oscillatory properties (η*, η′, and η″/ω and steady rheological properties (η
and ψ1) for 0.5% and 0.75% guar. (Reproduced with permission from Mills, P.L. and Kokini, J.L., Journal of Food Science,
49, 1–4, 1984.)
16 Handbook of Food Engineering

FIGURE 1.14 Comparison of small amplitude oscillatory properties. (η*, η′, and η″/ω and steady rheological properties
(η and ψ) for 3% karaya. (Reproduced with permission from Mills, P.L. and Kokini, J.L., Journal of Food Science, 49,
1–4., 1984.)

There are several theories (Carreau et al., 1968; Spriggs et al., 1966; Chen and Bogue, 1972) which
essentially predict two major kinds of results for the interrelationship between steady and dynamic mac-
romolecular systems. These results can be summarized as follows:

h¢ ( w) = h ( g )
g = w

2h* ( w)
= y1 ( g ) 
w g =w

h¢ ( cw) = h ( g ) 
g = cw

h¢¢ ( cw)
= y1 ( g ) 
w g = cw

These equations are strictly applicable at small shear rates. At large shear rates, the Cox–Merz rule
applies. For guar in the range of shear rates between 0.1 and 10 s−1, η* is equal to η. Similarly, in the zero
shear region, 2η″/ω is approximately equal to ψ1. In the case of gum karaya, on the other hand, nonlinear
relationships are needed as follows (Mills and Kokini, 1984):
a
h* = c éëh ( g ) ùû
g = w


h¢ = c¢ éëh ( g ) ùû
g = w
Another random document with
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Spread of Influenza in 1889–90.

Month. 1889–90.
First (October) St. Petersburg, Moscow, Courland, Livonia, Finland.
Second Berlin, Paris, Vienna, Sweden, Denmark.
Third London, Holland, Belgium, Balkan States, North America.
Fourth Capetown, Egypt, Honolulu, Mexico, Japan, Hong Kong.
Fifth San Francisco, Buenos Ayres, India, Sierra Leone, Scilly Islands.
Sixth Chili, Kamerun, Zanzibar, Basutoland, Tasmania.
Seventh British Bechuanaland, Barbados.
Eighth Gold Cost, Natal.
Ninth Trinidad.
Tenth Iceland, Madagascar, China, Senegal.
Eleventh Kashmir, Katunga.

Between the years 1889 and 1893 according to Leichtenstern there was no period
altogether free from influenza. Here and there individual cases or small epidemics
sharply localized were observed. In 1893 another epidemic appeared in many places and
became quite widespread. There was not, according to this author, the definite
geographic progression that had been observed in 1889. This was but a recrudescence, a
lighting up from endemic foci remaining after the first wide spread. In the first half of
1893 there was a light spring epidemic, and in November of the same year a larger
epidemic swept over the whole of Europe. The height of the latter was reached chiefly in
December.
The influenza incidence subsequent to 1893 will be discussed later.
TABLE I.
Influenza epidemics previous to 1889.
Date. General Site of origin. Direction of Localities Rapidity of
features. spread. affected. spread.
1173 Rather meagre Unknown. Described in Not known.
description. Italy, Germany,
England.
1239 Described by Described in Invaded all of
1311 Zeviani. France. France.
Records not
definite. Not
generally
accepted.
1323 Mentioned by
Hirsch, Gluge
and Zeviani.
Most believes
it was a
typhoid
epidemic.
1327 Mentioned by Described in
Zeviani, Italy.
Hirsch and
Gluge. Rather
doubtful.
1358 Described by Savoy, Germany,
Zeviani. Not France,
generally Catalonia.
accepted.
1387 (Zeviani, Italy. Italy, France,
Schweich, Strasbourg,
Gluge, Hirsch Southern
and Germany.
Ripperger.)
Characteristic
description.
1403 A very short France. Described in
epidemic. France. In 1404
(Gluge, it invaded
Ripperger, Flanders and
Pasquier.) Germany
(Hirsch).
1411 Described only Described only Described by
in Paris. in Paris. Pasquier as in
Extent Paris.
unknown.
1414 Characteristic In Italy and
description. France in
February and
March. In the
Danube district
between
January and
April.
1427 Very Described in
characteristic France.
description.
1438 Cited only by Described in
Zeviani. Italy.
1482 Very limited
description
by Mezeray.
1510 Widespread Malta (?) Generally, from Malta, Sicily,
over all of (Webster and South to Spain and
Europe. Hancock North. Portugal, Italy,
report that it France,
began in Hungary,
Africa). Germany,
Holland,
England,
Norway.
1557 All of Europe. Conflicting General direction Asia, 4 months from
information from South to Constantinople, Italy to
(Asia?). North in Sicily, Italy, Netherlands.
Europe. Spain, Sicily in June.
Dalmatia, Nimes in July.
Switzerland, Italy in August.
France, Madrid in
Netherlands, August.
England. Dalmatia in
September.
Netherlands in
October.
1562 Uncertain Only small
1563 information. epidemics at
most.
1580 True pandemic Orient (Hirsch) From Asia to Orient, North France in May.
covering the Africa and Constantinople Africa, Germany and
Orient, Africa Malta and in Europe Constantinople, Hungary in
and Europe. (Pechlin). from South to Malta, Venice, August.
North. Sicily, Italy, England and
Spain, Hungary Rhine Valley in
and Germany September.
to the Baltic, Saxony in
Bohemia, October.
France,
Belgium,
England,
Denmark,
Sweden.
1587 Apparently Described in Italy
quite and Germany.
localized.
1591 High mortality.
Indefinite
information.
1593 Spread over a Said to have Uncertain.
wide area in commenced
Europe. in Belgium,
“following a
violent
earthquake,”
and gradually
extended over
all the cities of
Europe.
1626 Local. Described in
Italy.
1627 In America. Spread from
North America
to West Indies
and Chili.
1647 In America
(Webster).
1658 Local. England (?). Described in
England and in
Treptow near
Stettin.
1675 Over Western Germany (?). Germany, Germany in
Europe. Hungary, September,
England, England and
France. France in
October and
November.
1688 Apparently England(?). Described only in
localized in England and
Great Britain Ireland.
and Ireland.
1693 England and Dublin(?). Dublin, Oxford, One month from
the adjacent London, Dublin to
continent. Holland, London.
Flanders.
1709 A period of In 1712, onset in 1712, spread Italy, France, Six months from
1712 extensive Germany. from Germany Belgium, Germany to
endemics. to Holland and Germany, Italy.
Italy. Denmark.
1729 First epidemic Usually Russia through Moscow, Sweden, Moscow in April,
said to have designated as Sweden, Poland, Silesia, 1729. Sweden
originated in Russia Poland, Austria, in September,
Russia and (Moscow). F. Germany, etc. Hungary, England in
first Hoffman to Italy and England, November.
described as claimed to perhaps North Switzerland, Paris in
entering have seen the America. France, Italy, December.
Europe from epidemic in Iceland. Rome in
the Northeast Halle in February,
rather than February, 1730.
the 1729.
Southeast.
First spread.
Pandemic
period.
1732 Second spread. Over Europe and Germany in
Pandemic America. November.
period. According to France in
Pelargus it January, 1733.
again followed Spain and Italy
the route from in February.
Russia through
the North of
Europe and
then South.
1737 Not generally England, North
recognized. America,
Barbados,
France.
1742 Slow spread Began either on Occurred in Germany, Germany in
1743 from the shores of Germany in Switzerland, January, 1742.
Germany. the Baltic Sea Jan. and Feb., Italy, France, England in
Recurrences or in single 1742, and then Holland, April, 1743.
in Germany cities in disappeared to Belgium,
up until 1745. Germany. reappear in England.
Switzerland in
the spring.
1757 A period of Began either France, Scotland, Barbados, Villalba states
1758 related first in North America, Germany, that the
1761 epidemics America and Finkler states Austria, epidemic in
1762 with spread thence that in 1762 Hungary, 1767 had
1767 complicated to Europe or influenza first Denmark, traveled over
geographic else began started in England, the whole of
pictures and spontaneously Germany and Ireland, Alsace. Europe in a
without clear in both spread thence period of two
cut direction hemispheres. in a very months.
of spread. irregular way
over Western
Europe. Gluge
and Hirsch
state that in
1767 the
disease
appeared
simultaneously
in Europe and
North
America.
1775 Slow spread First First spread to Germany, Italy, Invaded Vienna
1776 through appearances Vienna, and Austria, in June. Made
Western in Autumn of after a England, appearance in
Europe. 1775 in village quiescence Ireland, France. Italy in
of Clausthal in broke out in September. In
the Harz France and England and
mountains. England and France in
possibly October,
spread to November and
America and December.
China.
1780 Western January, 1780 in Spread to Alsace, Three months
1781 Europe and France. Germany and from France to
possibly Italy, and in Brazil.
Brazil and March
China. reported in Rio
de Janiero.
Appeared in
Sept. 1780 on
Southern coast
of China.
1781 One of the most China and Through Siberia China, India, Moscow,
1782 widespread perhaps India and Russia to America, January, 1782.
pandemics. in Autumn of Petrograd, Russia, Riga, Riga,
Abundant 1781 (Hirsch). Finland, Riga, Germany, February.
literature. English Germany, etc. England, Germany,
writers Scotland, March.
connect onset Netherlands, England, April.
with Ireland, France, Scotland, May.
occurrence of Italy, Spain. Ireland,
influenza in France and
the British Italy, June.
Army in India, Spain, August.
Nov., 1781.
Wittwer and
others begin
its history in
Petrograd in
January, 1782.
1788 Throughout all Russia, in West and South. Russia, Germany, Seven months
1789 of Europe. March, 1788. Spread in Hungary, required to
One year “Apparently America in Denmark, cover this
later in independent 1789 England, territory.
America. origin in throughout Scotland,
America in United States France, Italy,
Sept., 1789.” from New York Switzerland.
North and
South and
finally
touching the
West Indies,
South America
and Nova
Scotia.
Recurrences in
single cities of
U. S. in 1790.
1799 Local epidemic Origin in Russia. Spread West and Russia, Galicia,
1800 confined to South. Poland,
Northeastern Germany,
Europe. Denmark.
1802 Local endemic First reported in No clear cut France, Germany,
1803 outbreaks France. direction. Italy, England,
covering Recurrences Switzerland,
considerable until 1805–08. Central Europe.
territory General
which follow dissemination
the last throughout
period by a North America
quiescence of in 1807.
five months.
There
appears to
have been an
unassociated
epidemic
early in 1800
in China and
one in Brazil.
1811 Several 1807, onset in Usually from North and South 1815, one month
1815 epidemics in Massachusetts New England America. from Boston to
1816 North in February. West and New York, and
1824 America and 1815, onset in South. five months to
1826 to some Boston in South Carolina
extent in September. and Brazil.
South 1824, onset in 1824, three
America. Boston in months from
October. Boston to
Georgia.
1827 Widespread
epidemics
throughout
Eastern
Russia and
Siberia.
1830 Extensive China in To Manila in Entire earth. Ten months from
1833 influenza January, September, China to
period made 1830. 1830. Later to Russia. Four
up of two or South Sea months from
three Islands and Russia to
pandemic India. Germany. Two
periods. Appearance in additional
Russia in months
October, 1830, through
with France,
subsequent England,
spread West Scotland,
and South and Sweden,
on to North Belgium,
America (Feb., Switzerland.
1832). Six months
from Germany
to Italy.
1833 Second Probably Asia. After an interval Europe. (America Petrograd in
pandemic in of one year appears to have January.
above period. Europe was escaped this Berlin and
again visited second Constantinople
with an epidemic.) in March.
extensive Denmark and
plague which Sweden,
attacked the France and
same countries Great Britain
in about the in April, Italy
same order. in May.
1836 Third spread in Origin rather West and South Europe, Faroe Almost
1837 above period. obscure, as previously. Islands, simultaneous
possibly in Mexico,(?) invasion at
Russia. India, Java. Petrograd,
Sweden,
Denmark,
Germany and
England;
Egypt, Syria,
France,
Ireland,
Holland, and
Switzerland
one month
later. Italy,
Spain and
Portugal yet
another month
later.
1838 Every year in 1838, February;
1847 this period Island of
with the Bourbon and
exception of Iceland.
1840 showed, 1838,
according to November;
Hirsch, some Australia and
local New Zealand.
epidemic. 1839,
Abyssinia.
1841, Germany,
Hungary,
Ireland.
1842, Belgium,
England,
France, Egypt,
Chili.
1843, Germany,
England,
Iceland,
France, Siberia,
the United
States.
1844, Germany,
England,
Switzerland,
Cayenne.
1845, Germany
and
Switzerland.
1846–1847,
France, Russia,
Constantinople,
Brazil,
England,
Denmark,
Belgium,
Switzerland.
1847 Epidemic Origin Spread not All of the
1848 period uncertain. definite, North countries of
throughout America in Western
Europe 1848. Europe, West
without clear Indies, New
cut direction Zealand,
of spread. Newfoundland,
Sandwich
Islands, Egypt,
Algiers, West
Coast of Africa.
1850 Epidemics 1857, began in 1850–51, 1855, only one
1889 covering August in particularly month
larger or Panama and throughout the between
smaller spread to West whole Western Petrograd and
territory Indies and up coast of South Italy.
every year, and down the America with
but none to Pacific Coast. later spread to
compare in Prevailed in California &
intensity with Europe in Europe.
those of 1831, December. 1852, Australia,
1833, 1836 Tasmania,
and 1847. South America.
1853, Faroe
Islands.
1854, Bavaria.
1855, Europe,
spreading
rapidly West
and South from
Petrograd.
Later in same
year, Brazil.
1857–58,
widespread
epidemic in
both
hemispheres.
1860–70, very
irregular
appearances in
Australia,
Tasmania,
Philadelphia,
the Bermudas,
Holland,
California,
France,
Switzerland,
Africa,
Germany,
Belgium,
Russia,
Denmark,
Sweden and
Turkey.
1874–75,
Extensive
spread in
America,
Germany and
France, with
recurrence one
year later in
eleven areas of
the United
States.
1879, America.
1885–88, Re-
appeared each
year in
Petrograd.
1889, (Spring)
Greenland and
Hudson Bay
territory. (May)
Bokhara in
Turkestan from
where the great
pandemic of
1889–90 is
usually said to
have taken its
origin.
Table I shows that prior to 1510 the information was so limited as to be not entirely
conclusive. We must rely upon the fragmentary descriptions of writers located usually in
or near the intellectual centers who described the disease as they saw it in their city or
country. We have no way of ascertaining what other countries were invaded, and we
possess no method by which we may enumerate the “silent areas,” countries which in
the absence of a chronicler have not been able to transmit their story.
There have been fourteen very widespread epidemics since 1510, all of which might
appropriately be designated as pandemics. They are those of 1510, 1557, 1580, 1593,
1729, 1732, 1762, 1782, 1788, 1830, 1833, 1836, 1847, 1889 and 1918. Some of these have
spread farther than others according to the records, but in nearly all we have reports of
influenza being present in practically every country provided with a historian. We may
find from the table another group in which there have been more or less extensive
epidemics, apparently related, but without any general direction of spread. Such are the
epidemics of 1709–12, 1757–67, 1802–03, 1838–47 and the period 1850–59. Finally,
there are at least ten periods during which relatively small areas have been affected with
epidemic influenza. Such for instance is the year 1688 when the disease was apparently
localized in Great Britain and Ireland; in the year 1693 when England and the adjacent
continent were involved, with little spread elsewhere; and again in 1742, when there was
a slow spread through Germany into adjacent countries with recurrences in the former
up until 1745.
In England the following epidemics have been recorded, some of them in great detail:
1510 and 1557, described by Thomas Short; 1658 by Willis; 1675, by Sydenham; 1729–
1743 by Huxham; 1732–33 by Arbuthnot; 1758 by Whytt; 1762 by Baker and Rutty; 1767
by Heberden; 1775 by Fothergill, who collected observations from many physicians; in
1782 by Gray, Haygath and Carmichael Smith; 1803 by Pearson and Falconer, and a
great number of others; 1833 by Hingeston and others; 1837 by Streeten, Graves, and
Bryson, etc.; 1847 by Peacock, Laycock and many others; also those of 1855 and 1889–
93.
According to Stallybrass, epidemic crests have been reached in England in 1789–90,
1802–03, 1830–32, 1840–41, 1848–51, 1854, 1869–70, 1879, 1890–91, 1898 and 1918
to 1920. The periodicity in multiples of ten years in this latter group is remarkable.
The disease appears to have visited North America in the years 1627, 1647, 1729, 1732,
1737, 1762, 1782, 1789, 1811, 1832, 1850, 1857, 1860, 1874, 1879, 1889, 1900, 1915–1916
and 1918–20. Abbott speaks particularly of the years 1647, 1655 and 1697–98, 1732,
1762 and 1782 and 1889 as being years of especial epidemic prevalence in this country.
Clinical and Epidemiologic Identification.
Up to the present time we have discovered no one characteristic by which we may say
that a case or an epidemic is positively influenza. We have had to rely on the general
symptomatology, which indeed is sufficiently characteristic, although so nearly like the
symptoms of certain other diseases as to make us hesitate to make an absolute
diagnosis, and on the epidemic characteristics. The necessity of an absolute criterion in
the clinical diagnosis is particularly felt in the presence of an isolated interepidemic
case, or a small endemic outbreak. It is at this point that the opinions of epidemiologists
diverge, a divergence which results in two schools of thought in the explanation of the
endemic source of epidemic influenza. Are the interepidemic cases and the small
localized epidemics due to the virus which causes the great pandemics; are they
influenza vera, or are they entirely different diseases with similar symptomatology,
caused by some other microorganism and should they be designated by some other
name? Thus Leichtenstern remarks: “When we go over the records of the years 1173 to
1875, and particularly those of the last century, when the information has been more
extensive and more accurate, we find that scarcely a year has passed without news of the
epidemic occurrence of influenza at some point or other of the earth. Some of these local
and territorial epidemics are merely endemic recurrences of the great pandemics which
have left the germ deposited in the various localities. Others of these small epidemics
probably have nothing to do with influenza vera, but are local outbreaks of catarrhal
fever.”
Contrary to the usual belief, influenza is a disease of quite definite and distinct
characteristics, both clinical and epidemiological. The symptoms are clear cut, with
sudden onset, severe prostration out of all proportion to the clinical symptoms and to
the fever, headache and pain in the back, general body pains, and fever of greater or less
degree. There is usually a lack of leucocytosis or a true leucopenia. In uncomplicated
influenza there are as a rule no localizing symptoms. There may be a slight soreness of
the throat, or a slight cough, but these are at best mild. The fever lasts from three to five
days and disappears, while at the same time all of the symptoms clear up with the
exception of the profound prostration, which as a rule continues for some time,
rendering convalescence surprisingly slow. The pain in the back may remain for a week
or so. This is the description of uncomplicated influenza.
The manner of spread of epidemic influenza is constant in a primary epidemic and the
epidemic as a whole has certain features which render it characteristic. The sporadic
case has as a rule the same quite clear cut clinical symptomatology, but it fails to
manifest the one feature most characteristic of epidemic influenza—a high degree of
contagiousness. Further, although the symptoms in themselves are characteristic, there
is no one pathognomonic sign by which one may say, “this is a case of influenza,” and,
finally other disease conditions such as tonsillitis, frequently resemble it so much as to
cause error in diagnosis.
This becomes, then, one of the problems in the study of influenza epidemiology. It is a
matter of first importance to determine once and for all whether true influenza is with us
always, or whether it appears only at the time of the great pandemics. Upon the answer
to this question more than upon any other one thing rests our choice of methods of
eradication. Any procedures of preventive medicine that may be undertaken on the
assumption that the source of pandemic influenza is to be found in one or a few endemic
foci, such as the one supposed to exist in Turkestan, would fail utterly should the true
condition be that of a universal distribution of a relatively avirulent virus which from
time to time from some unknown cause assumes a highly increased virulence.
Before becoming involved in this very complicated question, let us familiarize
ourselves completely with the characteristics of the pandemic and epidemic variety of
the disease.
General Characteristics of Early Epidemic
Outbreaks.
We have described the symptomatology of uncomplicated influenza. It is rare that this
clinical picture is seen alone during the height of an epidemic. Complications, chiefly of
the respiratory tract, as a rule occur in such a large proportion of individuals that they
very nearly dominate the picture. Although caused by various microorganisms, all of
which appear to be secondary factors the results are so characteristic that in the past,
descriptions of influenza epidemics have usually been descriptions of the complications
of epidemic influenza. Most influenza epidemics are complicated. But we do know from
the experience of recent years as well as from history that relatively uncomplicated
epidemics of influenza have occurred, and that when they do so occur a predominant
characteristic has been the extreme mildness.
It is a fundamental characteristic of pandemic influenza that early cases in widespread
epidemics, as well as in “pre-epidemic increases” are very mild, with a minimum of
respiratory complications and with exceedingly low mortality. It is because we are better
acquainted with the more severe variety that, when these mild precursors appear we are
always in doubt for a time as to their true identity.
In spite of our 20th century erudition, the influenza when it first appeared in mild
form in the American Expeditionary Forces in 1918, for a lack of better knowledge as to
its cause was called “three-day fever.” In Italy in the same year the designation of the
disease progressed from pappataci fever through “Spanish grip” and “summer
influenza,” until finally it was designated influenza, pure and simple. Sampietro in Italy
particularly discussed the possibility of the disease being pappataci fever.
Belogu and Saccone, who wrote in May of 1918, decided that the epidemic was not
influenza in spite of the manifest clinical similarity, chiefly because of the absence of
signs of secondary invasion, such as nervous symptoms, gastro-intestinal symptoms,
and pneumonia, and especially because of the rapid recovery after defervescence. They
also considered the possibility of pappataci fever and dengue, and ruled out both. They
discussed calling the condition “influenza nostras,” but reached no definite conclusion.
Trench fever was also considered by some. United States Public Health Reports for 1918
record that dengue was reported prevalent at Chefoo, China, during the two weeks
ended June 15th, 1918. One week later there was a paragraph stating, “Prevalence of a
disease resembling dengue and affecting about fifty per cent. of the population was
reported at Shanghai, China, June 15, 1918.” It is not impossible that this was influenza.
Zinsser reminds us that Hayfelder, when he saw the influenza as it spread in
Petrograd in November of 1889, remarked its close clinical similarity to the description
of an epidemic of dengue which had prevailed in Constantinople during the preceding
September. Hayfelder, in studying the 1889 epidemic at its onset in Russia and the East,
wrote of “Sibirisches Fieber” which was first looked upon as malaria owing to the
apparently complete absence of the complicating lesions habitually associated in our
minds with influenza.
The same difficulty in early identification was experienced in this country in 1918. At
the end of March of that year the author who was stationed at Camp Sevier, South
Carolina, was one of a Board of Officers appointed to investigate a disease which had
broken out among troops stationed at that camp. At that time the line troops consisted
of three infantry regiments and three machine gun battalions. On the day following a
parade in the city of Greenville a considerable number of men in three out of the six
organizations suddenly took ill. There were a few isolated cases in other organizations,
but in the one infantry regiment and two machine gun battalions the regimental
infirmaries were filled, and some cases were sent to the base hospital. Nearly all were
very mildly ill and exhibited the symptoms of pure uncomplicated influenza as described
above. The onset was sudden, there were the usual pains and aches, the bowels were
regular, there was a feeling of discomfort in the pit of the stomach in many instances,
and there were no sore throats and very little cough. Recovery was as a rule very rapid,
although about a dozen of the entire number developed pneumonia and some of these
died. Physical examination of those only mildly ill and who remained in the regimental
infirmary showed as a rule nothing, but in some instances scattered fine moist rales near
the hilus of the lungs. In some of the organizations the disease was definitely spread
down rows of company tents. Careful bacteriologic examination was made at the time
and the predominating organisms were found to be a gram-negative coccus resembling
micrococcus catarrhalis, and a non-hemolytic streptococcus. This was in uncomplicated
cases.
The Board decided that the disease should be called influenza, but our only basis for
such decision were the clinical symptoms and the contagious character. At that time
none of us dreamed of any possible connection with a severe epidemic to occur later,
and laboratory search for influenza bacilli which was carefully made in view of the
clinical diagnosis showed none of these organisms to be present.
At about the same time a similar epidemic was being experienced at Fort Oglethorpe,
Ga. V. C. Vaughan, in describing this epidemic, remarks: “A disease strongly resembling
influenza became prevalent in the Oglethorpe Camp about March 18, 1918. It soon
assumed pandemic proportions. Within two weeks every organization in Camp Forrest
and the Reserve Officers Training Camp was affected.
“The symptoms were as follows: Headache, pain in the bones and muscles, especially
the muscles of the back, marked prostration, fever, sometimes as high as 104 degrees.
Sometimes there was conjunctivitis, coryza, a rash and possibly nausea, recovery taking
place in a few days.
“In all organizations the epidemic was first located in companies before it became
general.
“The incubation period was short, not over one or two days.
“Some organizations suffered more than others for no apparent reason.
“It is probable that the epidemic disease was recently brought to these camps. If it is
genuine influenza, and the epidemiological features no less than the leading symptoms
seem to point to that disease, there is here offered the most reasonable explanation of
the outbreak which is now possible. No other disease spreads so fast or is so prostrating,
considering its symptoms.”
We will quote at some length from the report of Zinsser of the Chaumont epidemic in
France in 1918, because of the excellence of the description, and particularly because
Zinsser has followed three successive epidemics with successive increases in the
complications and corresponding transformations in the clinical picture. It is worthy of
special note that he has remarked that the influenza, as first seen at Chaumont, showed
nothing in the symptoms that would suggest a predominant respiratory tract infection.
“It will be useful to discuss briefly the early cases as we saw them during the
Chaumont epidemic, not because the observations made there add much that is new
from a clinical point of view, but because they will remove any possible ambiguity
concerning our conception of influenza in its pure uncomplicated form.
“As far as we can judge the little outbreak at headquarters was typical of the first
advent of epidemic influenza in many places. The population of the town, at the time,
consisted of a large office personnel attached to the military administration, scattered as
to billets and places of work; of military units living in barracks and eating at common
messes; and of the townspeople. The epidemic descended upon individual military units
with the suddenness of a storm, striking a considerable percentage of the men, perhaps
most of the susceptible material, within less than a week, and ending almost as abruptly,
with only a few isolated cases trailing behind. Among the more scattered office workers
and among the townspeople it was disseminated more gradually and trailed along for a
longer period.
“These early cases were clinically so uniform that a diagnosis could be made from the
history alone. The onset was almost uniformly abrupt. Typical cases would become ill
suddenly during the night or at a given hour in the day. A patient who had been perfectly
well on going to bed, would suddenly awake with a severe headache, chilliness, malaise
and fever. Others would arise feeling perfectly well in the morning, and at some time
during the day would become aware of headache and pains in the somatic muscles.
“The typical course of these cases may be exemplified by that of J. T. W., a draftsman
attached to the 29th Engineers. He was perfectly well until May 20th, working regularly,
his bowels and appetite normal, considering himself healthy. On May 21st, at 4:30 A.M.
he awoke with a severe headache. He arose, forced himself to eat breakfast and tried to
go to work. He began to feel feverish and chilly. At the same time his headache became
worse, with pains in the back, and burning in the eye balls. At 2 P.M. he reported sick,
and was taken to the hospital with a temperature of 102.8 degrees. At midnight his
temperature dropped to 101.6 degrees, and came down to normal by noon of the 22d. As
he recovered he developed a slight sore throat, great soreness of the legs and a very
slight cough. He recovered completely within a few days.
“These cases with a few exceptions developed no rashes. One or two of them had
blotchy red eruptions which we felt incompetent to characterize dermatologically. The
leucocyte counts ranged from 5,000 to 9,000. A very few went above this. Sometimes
there was a relative increase of lymphocytes, but this was by no means regular. The few
spinal fluids that were examined were normal. As to enlargement of the spleen, we can
say nothing definitely.
“Soon after this we observed the disease in a Division, the 42d, then holding a part of
the line in front of Baccarat. Here it had already developed a somewhat different nature,
due, we believe, to the fact that the men of this Division were not, as were those at
Chaumont, living in a rest area, but were actively engaged in military operations,
working, sleeping, and eating under conditions that involved greater fatigue, less
protection against weather, and greater crowding in sleeping quarters. The Baccarat
cases were much more frequently catarrhal; sore throats, coughs and more serious
respiratory complications were more common. However, they were usually coupled
unmistakably with an underlying typical influenzal attack, sudden onset, pains and short
lived fever. Moreover, there were a great many of the entirely uncomplicated cases
interspersed with the others.
“Still later, in September, October and November, respiratory complications were so
frequent and severe, came on so early in the disease, and the pneumonia mortality
became so high, that the fundamental identity of these later cases with the early three-
day fever might easily have been lost sight of by observers who had not followed the
gradual transformation.
“In consideration of these facts, it is apparent that etiological or other investigations
can throw no light upon the problems of influenza unless they are carried out with
clearer understanding of the differentiation between the complications and the basic
disease.
“The serious respiratory infections of the bronchi and lungs we can set down with
reasonable certainty as complications due, certainly in the overwhelming majority of
cases, to secondary bacterial invaders. It is a matter of considerable difficulty, however,
to know exactly where the basic disease stops and the complications begin; and whether
we must regard the mild sore throat and conjunctival injection which so often
accompany the simple cases as a part of this basic clinical picture, or as the simplest
variety of complication. This is much more than an academic question, since, as we shall
see, the bacteriological analyses of such lesions have played an important role in
etiological investigations.”
Symptoms in Former Epidemics.
The difficulty in making a decision in the presence of an epidemic is very similar to
that of deciding whether the epidemics of former times were in each case influenza.
Some few have been recorded in which the description has corresponded fairly well to
that of primary uncomplicated influenza. Thus, concerning the epidemic of 1557 in
Spain, Thomas Short wrote as follows: “At Mantua Carpentaria, three miles from
Madrid, the epidemic began in August.... There it began with a roughness of the jaws,
small cough, then a strong fever with a pain of the head, back, and legs. Some felt as
though they were corded over the breast and had a weight at the stomach, all of which
continued to the third day at furthest. Then the fever went off, with a sweat or bleeding
at the nose. In some few, it turned to a pleurisy or fatal peripneumony.”
Most of the descriptions, however, have been of a general character and include
descriptions of the complicated periods of the epidemic. One of the more complete of the
early descriptions was that by Lobineau in 1414, who wrote: “C’était une espèce de
rhume, qui causa un tel enrouement que les chastelets furent obligez d’interrompre leurs
séances; on dormoit peu et l’on souffroit de grandes douleurs à la teste, aux reins et par
tout le reste du corps; mais le mal ne fut mortel que pour les vieilles gens de toute
condition.”
With this exception we possess no very good or complete description of influenza
prior to the epidemic of 1510. After that time they have as a rule been detailed enough to
enable identification. Hirsch bases his conclusions concerning the year 1173 chiefly on
the following quotation: “Sub hisdem diebus universus orbus infectus ex aeris nebulosa
corruptione, stomacho catarrhum causante generalem tussim, ad singulorum perniciem,
ad mortem etiam plurimorum immissam vehementer expavite.” Nearly all that we have
to go on in this description is the widespread incidence of the disease and the presence
of respiratory symptoms, particularly cough. In 1323 the description emphasizes only
the high morbidity. Thus, Pietro Buoninsegni writes: “In questo anno e d’Agosto fu un
vento pestilenzia le per lo quale amalò di freddo e di febbre per alcuni dì quasi tutte le
persone in Firenze e questo madesimo fu quais per tutta Italia.” The same author
describes the epidemic of 1327, emphasizing again the high morbidity and in addition
the low death rate: “In detto anno e mese fu quasi per tutto Italia corruzione di febbre
per freddo; ma pochi ne morirono.” Again in 1387, he emphasizes the same two features.
Pasquier, in writing of the epidemic of 1403 in France, says: “En Registres de
Parlement on trouve que le vingt-sixième jour d’avril 1403 y eut une maladie de teste et
de toux, qui courut universellement si grande, que ce jour-là le Greffier ne pût rien
enrégistrer et fut-on contraint d’abandonner le plaidoyé.” Here the high morbidity and
the symptoms, particularly cough and pain, are emphasized. In 1414, Baliolanus
describes again the high morbidity and symptoms, particularly cough and hoarseness:
“Eoque frigore humanis corporibus concepto ... tussis maxima atque raucitas orta unde
nullus pene ordo, aetas et sexus liber evasit.” In 1411, Pasquier writes the following: “En
1411 y eut une autre sorte de maladie dont une infinité de personnes furent touchez, par
laquelle l’on perdoit le boire, le manger et le dormir ... toujours trembloit et avec le estoit
si las et rompu que l’on ne l’osoit toucher en quelques parts. Sans qu’aucune personne
en mourut.”
Subsequent to 1510 descriptions have been as a rule more definite. There are,
however, exceptions to this statement and these fall in the epidemics concerning which
there is some dispute.
Manner of Spread.
More characteristic and more important from an epidemiologic standpoint than the
symptomatology in general, as we have discussed it, is the mode of development of the
epidemic as a whole.
Human intercourse.—Before the days of bacteriology the contagiousness of the
disease was little discussed. Its infectiveness was in fact not universally established until
the epidemic of 1889–1890. One of the first writers who attempted to see in the
influenza a contagious disease was Ch. Calenus who wrote in 1579: “Contagiosum dico
morbum, quia etsi quidem ab occulta quadam coeli influentia, principaliter eum profisci
haud dubium est ... eo in loco quo jam grassabatur inter homines citius eos invadabat,
qui cum affectis frequenter conversabantur, quam eos, qui a consuetudine affectorum
studiose abstinebant.” This keen observer saw that those who carelessly exposed
themselves to close contact with cases of influenza were more likely to develop the
disease than those who protected themselves in every way possible. The “contagious”
school first developed in England, where Haygarth, Hamilton, Gray, Hull, Duggard,
Bardsley, and others, in 1775–1803 described the disease as being not in the air, but in a
specific contagion. Others who considered influenza a contagious disease were Simonin,
Lombard, Petit de Corbeil (1837), Blanc (1860), and Bertholle (1876).
Watson (1847) quotes Cullen as saying that this species of catarrh proceeds from
contagion. He, himself, is not convinced of this fact. He says the visitation is too sudden
and too widely spread to be capable of explanation in that way. “There are facts in the
history of influenza which furnish a strong presumption that the exciting cause of the
disorder is material, not a mere quality of the atmosphere; and that it is at least
portable. The instances are very numerous, too numerous to be attributed to mere
chance, in which the complaint has first broken out in those particular houses of a town
at which travelers have recently arrived from infected places.... What I wish to point out
now is the fact that the influenza pervades large tracts of country in a manner much too
sudden and simultaneous to be consistent with the notion that its prevalence depends
exclusively upon any contagious properties that it may possess.”
Parkes, writing in Reynolds’ System of Medicine in 1876, views the subject more as we
see it today: “The rapidity of the spread would seem at once to negative any connection
between human intercourse and the propagation of the disease; yet there is some
affirmative evidence. It does not appear to follow the great lines of commerce; but when
it has entered towns and villages in which the investigation can be carried on, it is
curious how frequently the first cases have been introduced, and how often the
townspeople nearest the invalids have been first affected. In this country especially,
Haygarth in 1775 and 1782, and Falconer in 1802, collected so many instances of this
that they became convinced that its propagation was due entirely to human intercourse.
So also, when it passes through a house, it occasionally attacks one person after another.
But if it is introduced in this way it afterwards develops with marvelous rapidity, for we
cannot discredit the accounts of many thousands of persons being attacked within a day
or two, which is quite different from the comparatively slow spread of the contagious
diseases. This sudden invasion of a community makes it, to many persons, appear highly
improbable that any effluvia passing off from the sick should thus so rapidly
contaminate the atmosphere of a whole town.

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