Textbook of Veterinary Parasitology Introduction To Parasitology. Protozoology

Andrei
Daniel MIHALCA
Textbook of
Veterinary
Parasitology
Introduction to parasitology. Protozoology.
AcademicPres
Andrei D. MIHALCA
TEXTBOOK OF VETERINARY
PARASITOLOGY
Introduction to parasitology
Protozoology
AcademicPres
Cluj-Napoca, 2013
© Copyright 2013
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Mihalca Andrei Daniel
Textbook of Veterinary Parasitology:
Introduction to parasitology; Protozoology / Andrei Daniel Mihalca. Cluj-Napoca:
AcademicPres, 2013
Bibliogr.
Index
ISBN 978-973-744-312-0
339.138
Director editură – Prof. dr. Carmen SOCACIU
Referenţi ştiinţifici:
Prof. Dr. Vasile COZMA

Conf. Dr. Călin GHERMAN
Editura AcademicPres
Universitatea de Ştiinţe Agricole şi Medicină Veterinară Cluj-Napoca
Calea Mănăştur, nr. 3-5, 400372 Cluj-Napoca
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E-mail: eap@usamvcluj.ro
Table of contents
1 INTRODUCTION TO PARASITOLOGY ..................................................................................... 1

1.1 DEFINING PARASITOLOGY. DIVERSITY OF PARASITISM IN NATURE. ................................................. 1
1.2 PARASITISM AS AN INTERSPECIFIC INTERACTION ............................................................................... 2
1.3 AN ECOLOGICAL APPROACH TO PARASITOLOGY ................................................................................... 5
1.4 A BRIEF HISTORY OF PARASITOLOGY ..................................................................................................... 6
1.5 TYPES OF PARASITES ..............................................................................................................................10
1.6 TYPES OF HOSTS ......................................................................................................................................14
1.7 LIFE CYCLE OF PARASITES .....................................................................................................................16
1.7.1 Types of parasitic life cycles ...............................................................................................16
1.7.2 Stages in the external environment ................................................................................19
1.7.3 Getting in/on the host ...........................................................................................................22
1.7.4 Migration and development in the host ........................................................................24
1.7.5 Biological background for host specificity ...................................................................26
1.8 HOST-PARASITE INTERACTIONS ...........................................................................................................27
1.8.1 Pathogenicity of parasites ...................................................................................................28
1.8.2 Immunity of host to parasites ............................................................................................31
1.9 CLASSIFICATION OF PARASITES ............................................................................................................33
1.9.1 Principles of zoological taxonomy ...................................................................................33
1.9.2 Major parasitic taxa ................................................................................................................35
SELECTED REFERENCES AND FURTHER READING.............................................................................................35
2 PROTOZOA ................................................................................................................................... 37
2.1 GENERAL CONSIDERATIONS ..................................................................................................................37
2.2 DIVERSITY OF PARASITIC PROTOZOA ..................................................................................................38
2.3 THE FLAGELLATED PROTOZOA .............................................................................................................38
2.3.1 Kinetoplastids ...........................................................................................................................40
2.3.1.1 Equine dourine ....................................................................................................................42
2.3.1.2 Vector-borne trypanosomoses in domestic animals ..........................................47
2.3.1.3 Canine leishmaniosis ........................................................................................................60
2.3.1.4 Feline leishmaniosis ..........................................................................................................69
2.3.2 Trichomonads ...........................................................................................................................69
2.3.2.1 Genital trichomonosis in cattle.....................................................................................70
2.3.2.2 Buccal trichomonosis in dogs and cats .....................................................................75
2.3.2.3 Anterior digestive trichomonosis in birds ..............................................................76
2.3.2.4 Intestinal trichomonosis in birds ................................................................................81
2.3.2.5 Intestinal trichomonosis in mammals .......................................................................83
2.3.2.6 Histomonosis of poultry ..................................................................................................84
2.3.3 Diplomonadids .........................................................................................................................88
2.3.3.1 Giardiosis ...............................................................................................................................88
2.4 APICOMPLEXA .........................................................................................................................................93
2.4.1 Eimeriidae ..................................................................................................................................96
2.4.1.1 Intestinal coccidiosis in mammals ..............................................................................98
2.4.1.2 Intestinal eimeriosis in birds ..................................................................................... 110
2.4.1.3 Hepatic eimeriosis in rabbits ..................................................................................... 119
2.4.1.4 Renal eimeriosis in geese ............................................................................................. 121
2.4.2 Cryptosporidiidae ................................................................................................................ 123
2.4.2.1 Cryptosporidiosis ............................................................................................................ 123
2.4.3 Sarcocystidae ......................................................................................................................... 130
2.4.3.1 Sarcocystoses .................................................................................................................... 131
2.4.3.2 Toxoplasmosis .................................................................................................................. 141
2.4.3.3 Neosporosis........................................................................................................................ 155
2.4.3.4 Other heteroxenous coccidia parasitic in domestic animals ........................ 166
2.4.4 Hepatozoidae.......................................................................................................................... 167
2.4.4.1 Canine hepatozoonosis ................................................................................................. 168
2.4.4.2 Feline hepatozoonosis ................................................................................................... 173
2.4.5 Babesiidae................................................................................................................................ 173
2.4.5.1 Babesioses .......................................................................................................................... 174
2.4.6 Theileriidae ............................................................................................................................. 184
2.4.6.1 Theilerioses ........................................................................................................................ 184
2.5 CILIOPHORA .......................................................................................................................................... 189
2.5.1 Ciliates of domestic animals ............................................................................................ 190
2.5.1.1 Balantidiosis ...................................................................................................................... 190
2.5.1.2 Buxtonellosis ..................................................................................................................... 193
SELECTED REFERENCES AND FURTHER READING.......................................................................................... 193
MIHALCA | Te xtboo k o f Ve teri nary Par asi to lo gy |
1 INTRODUCTION TO PARASITOLOGY
para (beside) and sitos (grain, food). If we

1.1 Defining parasitology. Diversity
summarize different definitions given to
of parasitism in nature.
parasites, there are many similarities but
The amount of information in the field of also notable differences (table 1.1).
parasitology is huge, and more than 20
international peer-reviewed scientific
Table 1.1 Different definitions given to the
journals are currently being published in parasite
this biomedical field. Parasitology is,
An animal that lives completely at the expense of
arguably, one of the most intriguing and plants, animals, or humans1
fascinating biological sciences and A plant or animal that lives upon or within
another living organism at whose expense it
certainly one of the most complex ones, obtains some advantage2
involving a broad interdisciplinary An organism which lives in or on another
organism and benefits at the other’s expense3
approach. Knowledge from fields like An organism that lives in or on and takes its
taxonomy, phylogeny, ecology, nourishment from another organism4
biochemistry, genetics, molecular
1 - Mehlhorn (2008); 2 - Gosling (2005); 3 - Soanes
biology, immunology, epidemiology, (2008); 4 - Webster's New World Medical
Dictionary (2008)
pharmacology, pathology, etc. is required
for this complex approach. We will try to
limit this chapter to the essentials.
When attempting to define parasitology Based on most of these definitions, many

you get a snowball effect. To make it organisms could be considered parasitic.
simple, parasitology represents the study Even if all viruses, many bacteria, many
of parasitism. Parasitism is a very fungi, but even some plants or
complex interaction between two species, vertebrates are ecologically parasitic
one called parasite and the other called organisms, customarily, parasitology
host. However, to give a more complex comprises the study of parasitic protists
definition is trickier than expected, as and invertebrate animals (mostly
suggestively emphasized by Bush et al. helminthes and arthropods, but also
(2001): “if you assemble 10 scientists and some other small groups of metazoans).
ask them to define parasitism, you would Parasitism is a relatively common way of
obtain 10 different answers”. life, and practically every major phylum
of Kingdom Animalia includes parasitic
Etymologically, the word parasite derives
species, some of them exclusively, at least
from the association of two Greek words:
in one stage of their life cycle (table 1.2).
1|I n t r o d u c t i o n t o P a r a s i t o l o g y
Table 1.2 Animal phyla with parasitic 1.2 Parasitism as an interspecific

representatives*
interaction
Percent of parasitic
Phylum1
species2 Any interaction in which a species of
Porifera <1
Placozoa 0 organism spends a part of or its entire life
Myxozoa 100 in association with another species is
Cnidaria <1 called symbiosis. The word symbiosis
Ctenophora ~1
Priapula 0 (Greek: syn = along with, together; bios =
Nematomorpha 100 life), as originally used by Heinrich Anton
Nematoda ~50
de Bary (1831-1888) refers to organisms
Loricifera 0
Kinorhyncha 0 living together. Some suggestions to use
Onychophora 0 this term only for the bilateral positive
Arthropoda3 ~3
interspecific relationships (equal to
Tardigrada4 0
Platyhelminthes ~80 mutualism) are confusing and will not be
Mollusca ~1 considered herein.
Annelida ~6
Sipuncula 0 Partner species that are involved in a
Rotifera ~1
symbiosis may benefit from, be harmed
Acanthocephala5 100
Nemertea <1 by, or not be affected by the association.
Phoronida 0 Despite some expected overlaps, there
Bryozoa 0
Brachiopoda 0
are five main types of symbiotic relations:
Gastrotricha 0 phoresis, inquilinism, mutualism,
Entoprocta 0 commensalism and parasitism. Phoresis
Chaetognatha 0
Gnathostomulida 0
and inquilinism do not imply trophic
Echinodermata <1 interactions.
Hemichordata 0
Chordata <1 Phoresis (also called phoresy) (Greek:
Cycliophora ? pherein = to bear) refers to interactions
Rhombozoa 100
Orthonectida 100
where one partner (the host)
mechanically carries one or more
* Adapted from Bush et al. (2001)
individuals from another species (the
1 Several classifications are available in the phoretic organism) (figure 1.1).
literature. The phyla name used in this book are
Nevertheless, some phoretic species can
those listed on Animal Diversity Web (ADW):
http://animaldiversity.ummz.umich.edu eventually cause harm to their host
2 At least in one stage of their life-cycle
mainly because of overburdens. In the
3 Herbivorous insects are not included
4 Including pentastomes (according to ADW) pictured case, the interaction can
5 According to ADW, Acanthocephala is part of
arguably be called parasitism, as the
phylum Rotifera
damage is purely mechanical and no
physiological or trophic mechanisms are
Some estimates state that about half of
involved.
the known species on Earth are parasitic
at least in one of their life stage. Inquilinism (also called inquilism) is
another type of pure mechanical
interaction where two or more organisms
of different species share a dwelling used in this work refers to the broader
place. concept, where commensalism includes
all types of associations when one
In a mutualistic symbiosis, both partners
partner (the commensal) benefits and the
benefit from the relationship (figure
other (the host) is not harmed. Moreover,
1.2). The extent to which each partner
some others consider phoresis and
benefits, is difficult to assess, but it is
inquilinism particular types of
generally accepted that for any benefit
commensalism.
there is a certain biological cost.
Figure 1.2 One of the most common

Figure 1.1 Phoretic mites on insects are
mutualistic interactions, the lichen.
extremely frequent in nature. (Photo
(Photo Andrei D. Mihalca)
Andrei D. Mihalca)
With the view of all above, parasitism

The term commensal (literally meaning
can be defined as a symbiosis (certainly
“together at the same table”) was first
the most common one) in which one of
used by the Belgian parasitologist P.J. van
the symbionts (the parasite) benefits at
Beneden (1809-1894) to explain the
the expense of the other (the host). All
associations in which one animal shares
the main aspects of parasite-host
food obtained by another animal. There is
interactions as well as the types of hosts
some controversy on how broad this
and parasites will be detailed in the
meaning should be. Some authors
following chapters. An interesting type of
consider that commensalism do not
parasitic-like interaction is known to
involve any physiological interaction nor
occur in echiurans, a small group of
dependency between the partners, and
vermiform, bottom-dwelling marine
only the spatial proximity allows the
organisms. In this case, males (1-3 mm in
commensal to feed on nutrients captured
length) are parasitic in the kidneys of
or ingested by the host. Yet, the meaning
females (80 mm in length). It is highly With high probability, most mutualistic

arguable if this particular association symbioses probably began as parasitic
could be considered parasitism, as it is an ones, with one organism attempting to
intraspecific interaction not an exploit another one. As brilliantly
interspecific one. perceived by Paracer and Ahmadjian
(2000) in their monograph on symbiosis,
To include a certain symbiotic interaction
if one considers parasitism as an
(figure 1.3) in one of the types defined
antagonistic relationship then mutualism
above is more or less conventional. Many
can be regarded as a standoff or a draw
relationships are dynamic, and there may
between the two antagonists. The widely
be frequent transitions from one type to
accepted theories of the origins of some
another. Symbiotic associations may
cell organelles like mitochondria or
change because of external factors
chloroplast consider that these are
(environmental or host-dependent) or
transformed bacteria that may have
due to internal influences (symbionts-
begun as parasitic symbionts in larger
dependent).
prokaryotic cells. On the contrary, a
The evolutionary approach to symbiotic mutualistic or commensalistic association
interactions is the most interesting one. may degenerate into a parasitic one if the
For instance, a parasitic association can defense mechanisms of the host are
evolve into mutualism or commensalism. decreased.
Figure 1.3 Main features of symbiotic associations which involve trophic interactions
(phoresis and inquilinism are excluded).
The first exhaustive attempt to classify of the parasite however, differs. During
symbiotic interactions was made by M.P. the parasitic phase, as shown above, the
Star in 1975. He used several criteria for environment of the parasite is the host’s
his classification like location of symbiont body. However, the vast majority of
within the host, persistence, dependence parasites have at least one stage in the
and specificity of symbiosis. Parasitism external environment during their life
basically fits to this system with some cycle, also very important in the
peculiarities detailed in Chapter 1.5. understanding of this complex
interaction.
Ecology of the host itself greatly

1.3 An ecological approach to influences the adaptations of the parasite
parasitology in order that it could easily infect the
host. The best examples with this view
We can regard parasites from many refer to parasites with heteroxenous life-
points of view, but certainly the medical cycles (see Chapter 1.7).
aspects of parasitism, especially in
humans and domestic animals are the An important question of an ecological
most considered worldwide. However, approach to parasitology is what the role
especially in wild animals, parasites do of parasites within the ecosystem is.
not cause apparent disease, and the There are well-defined theories stating
relative balance between parasites and that parasitism plays a major role in the
hosts is the result of a complex and long evolution of species diversity and
coevolution. regulation of host populations.
If we consider parasitology a branch of Another question is if and how parasites

ecology, the habitat and environment of are able to regulate biodiversity in
the parasite is provided by another general and host populations in
organism, the host. Many ecological particular. Some consider parasites as a
principles which apply to free-living threat to biodiversity, mainly in the case
organisms can be applied to parasites. of endangered hosts. Nevertheless,
The only particular situation is that the parasites are part of our biodiversity as
environment of the parasite is alive and are their hosts. Parasites of endangered
actively fights against it. Therefore, the species can sometimes play a significant
main issues for such an approach to role in the conservation efforts. At least
parasitology include adaptations of one documented case of parasite-
parasites to their environment and life mediated extinction was described in the
style, adaptations of hosts to antagonize snail Partula turgida, where the last-
parasites and mainly the nature of host- known individual was killed in captivity
parasite relationship. To put it simply, by a microsporidian parasite. However, in
ecological parasitology studies the the case of highly host-specific parasites,
complex relationships between parasites, the extinction of the host equals with the
hosts and environment. The environment extinction of the parasite itself (host-
parasite co-extinction). It might be the
case of the rhino ticks (i.e. Dermacentor helminthes of dogs, pigs and fish. Galen of
rhinocerontis) from Africa. Pergamum (131-199), the Roman
physician and philosopher of Greek origin
One thing is for sure. A world without
(figure 1.4), recognized three
parasites would look completely different
macroparasites of humans: Ascaris,
than the world we know today, not
Taenia and Enterobius. Human
necessarily in a good way.
hydatidosis was already known by
Aretaeus of Cappadocia (81-138).
1.4 A brief history of parasitology
History of medical sciences is a

fascinating topic and basic knowledge is
required for a proper understanding of
progress dynamics in certain fields. There
are several reviews on history of
parasitology, most of them focusing on
human parasites. Some of these works
focus also on general parasitology, and a
great resource is the review of Cook GC
(in Gillespie SH, Pearson RD. 2001.
Principles and Practice of Clinical
Parasitology. Wiley. 752 pp.).
Early records. Since humans became Figure 1.4 Galen of Pergamum.

aware of their social and ecological (reproduced from a lithograph by Pierre
identity, they were also probably aware Roche Vigneron)
of some macroparasites like larger
helminthes or cutaneous arthropods
living associated with Homo sapiens or Spontaneous generation. All these early
animals nearby (domesticated or records and many other observations did
hunted). However, the first written not have a real biological background.
documentation on a parasitic organism is The general belief until the mid-
found in the Papyrus Ebers (~1550 BC). nineteenth century was that parasites,
In ancient Egypt, several other writers like all other living organisms, appear
were aware of some major helminthic through spontaneous generation. This
infections of humans, like theory, synthesized by Aristotle, was
schistosomiasis, dracunculiasis or firstly doubted on by the Dutch biologist
ascariasis. Dead female Dracunculus Jan Swammerdam (1637-1680) and by
worms have been found in Egyptian the Italian physician Franceso Redi
mummies older than 3000 years. In (1626-1697). The later did not agree that
ancient Greece, Aristotle (384-322 BC) flies arouse spontaneously from rotting
mentioned in his writings parasitic meat. Despite his morphological proof on
the sexual reproduction of A. monograph on parasitic organisms

lumbricoides, the British anatomist “Osservazioni intorno agli animali viventi
Edward Tyson (1650-1708) was also an che si trovano negli animali viventi“ [Notes
adept of spontaneous generation. A on living animals found in living animals]
particular application of this theory was (figure 1.6). Five years later, Nicolas
extrapolated to parasitology by Marcus Andry (1658-1742) was the first to
Bloch (1723-1799) and Johan Göze illustrate the scolex of a human
(1731-1793). The two famous European tapeworm, Taenia saginata in his “De la
parasitologists embraced the opinion that génération des vers dans le corps de
parasites were “inborn in their host”. The l’homme” [On the generations of worms
concept of spontaneous generation was inside the human body] (figure 1.7).
finally abandoned after strong
experimental proofs brought by Luis
Pasteur (1822-1895).
Emergence of parasitology as a science

(17th and 18th centuries). Although
most historical records of parasites are
related to humans, the birth of
parasitology as a science is linked to
veterinary medicine.
Figure 1.6 Original drawing from Redi’s

“Osservazioni intorno agli animali viventi
che si trovano negli animali viventi”
depicting: “a big worm found in the kidney
of a marten” (in the middle); “a worm
found under the skin of a lion” (right); “a
worm very frequently found under the skin
of martens and skunks”. (left)
Figure 1.5 Francesco Redi. (reproduced

Eighteenth century brought three major
from an engraving by Lodovico Pelli)
contributions in parasitology. In 1760,
Pierre Pallas (1741-1811) wrote a
dissertation called “De infestis viventibus
Francesco Redi (figure 1.5) is considered
itraviventia”. Göze, who discovered the
the father of parasitology, after he
scolex of Echinococcus in hydatid cysts,
published in 1694 the first scientific
published in 1787 his "Versuch einer parasitologists arose in the scientific

Naturgeschichte der Eingeweidewürmer circles of the century. Probably the most
tiericher Körper" [Natural history of prominent of them was Carl Rudolphi
intestinal worms from the body of (1771-1832). The Swedish scientist
animals]. Last but not least, Bloch, who wrote two monumental works
was the first to note the hooklets on the “Entozoorum sive vermium intestinalium
scolex of tapeworms, wrote in 1782 historia naturalis” from 1808 and
“Abhandlung von der Erzeugung der “Entozoorum synopsis cui accedunt
Eingeweidewürmer und den Mitteln wider mantissa duplex et indices locupletissima”
dieselben“ [Treatise on the Generation of from 1819 which substantially increased
Intestinal Worms and the means of their the number of known species of
extermination], winning the gold medal parasites.
for best essay at the Copenhagen
The French parasitologist Félix Dujardin
Academy of Sciences (figures 1.8 and
(1801-1860) was the first to understand
1.9).
that the life cycle of trematodes and
cestodes involve an intermediate host. In
1845 he published his most important
work: “Histoire naturelle des helminthes
ou vers intestinaux” [Natural history of
helminthes or intestinal worms] (figure
1.10).
As mentioned above, basically all

published parasitological works of the
time originated from mainland Europe.
First English texts appeared as
translations from German, French or
Latin. The first book of parasitology
written by a British scientist was
“Entozoa, an Introduction to the Study of
Helminthology” in 1864 by Thomas S.
Cobbold (1828-1886).
The end of the nineteenth century

marked a shift in the concepts of
parasitology. Step by step, scientists
Figure 1.7 Cover of Andry’s “De la
understood the medical importance of
génération des vers dans le corps de
parasites in humans and animals. Thus,
l’homme”, re-published in 1750.
from a branch of zoology, parasitology
was more and more viewed as a medical
Parasitology in the nineteenth science.
century. Several outstanding
Figure 1.8 Cover of the first edition of

Bloch’s gold medal essay.
Figure 1.10 Cover of the first edition of

Dujardin’s major work.
The first journal entirely devoted to

parasitology, “Archives de Parasitologie”
had its first volume published in 1898
(figure 1.11) by Émil Raphaël Blanchard
(1819-1900). However, after 16 volumes
and a break during the WW1, the
publication was suspended in 1919.
Overseas, the father of American
parasitology was a paleontologist, Joseph
Leidy (1823-1891).
Modern parasitology. Definitely, the

most dramatic shift in modern
Figure 1.9 One of the ten plates of parasitology as in many other natural
Bloch’s book. sciences was the discovery of nucleic
acids and of molecular biology
techniques. In the last decades, molecular interactions with the host. Moreover, the
tools became almost ubiquitous in categories frequently overlap. Like in
biological or medical parasitological many other areas of science,
research. classifications are used mainly for
scholastic purposes. The main criteria
But there is still a long way to go. Many
used for categorizing parasites are:
parasitic diseases are becoming
emergent. Some, otherwise harmless (1) Location of parasites within the
parasites are killing immune host
compromised hosts (i.e. HIV positive).
 Ectoparasites are organisms living
Despite enormous amount of research
parasitically on the outside of their
and money, there is still no vaccine for
host. Although this broad definition
malaria, the deadliest parasitic disease on
seems clear enough, some comments
Earth. And the list can continue….
are required. Certain parasites are
normally living on the skin
(integument), hair, feathers or scales
of their hosts. These are the typical
ectoparasites (i.e. ticks, some mites,
fleas, lice, biting insects etc.). Other
arthropods are living within the
structures of the skin (i.e. Demodex in
the hair follicles; mange-causing
mites in the dermis etc.) but are
customary considered ectoparasites.
Larval forms of Hypoderma species
migrate through various parts of the
hosts’ body and finally they stop
subcutaneously (figure 1.12), hardly
being considered ectoparasites.
Parasites also inhabit various
external mucosae of their hosts (i.e.
Thelazia in the conjunctiva; Oestrus
Figure 1.11 First volume of Archives de the nasal cavities; monogeneans or
Parasitologie. ciliates on the gills of fish (figure
1.13); some trichomonadids within
the buccal or genital mucosa;
Otodectes mites in the ear canal etc.)
1.5 Types of parasites
Their classification as ectoparasites
is debatable.
Except the taxonomic approach, there are
several other criteria to classify parasites,  Endoparasites are those which
all of them conventional, as they do not inhabit the internal organs of their
always properly reflect the complex hosts.
10 | I n t r o d u c t i o n t o P a r a s i t o l o g y
brain, muscles, tendons, heart, blood

vessels, serosae etc. Moreover, some
unicellular organisms (i.e. protists) are
intracellular parasites
(intracytoplasmatic or intranuclear). As
shown in the previous paragraph, some
ectoparasites could be arguably
considered endoparasites.
(2) Size of parasites
 Microparasites are those not visible

by humans with naked eye. We
include here protists, larval stages of
most helminthes, most of the
Figure 1.12 Larvae of Hypoderma diana
monogeneans, mange causing mites
are commonly found in the subcutaneous
etc.
tissue of roe deer. (Photo Andrei D.
Mihalca)  Macroparasites are visible to the
human eye without the aid of the
microscope. Although some parasites
like Dermanyssus mites of birds
(figure 1.14) or Strongyloides
nematodes from the intestine of
various vertebrates are hardly visible
macroscopically, they are considered
macroparasites. On the other hand,
there are enormous-sized parasites.
For instance, many cestodes
frequently reach lengths of several
meters (i.e. Diphyllobothrium latum, a
tapeworm of fish-eating mammals,
including dogs and humans can reach
up to 12 meters in length). The
Figure 1.13 Ciliated protozoa largest known trematode,
(Ichthyophthirius multifiliis) parasitic on Nematobibothrioides histoidii from
the gills of common carp. These parasites the muscles of the sun fish can reach
also infect the integument. (Photo Andrei a length of 12 meters. The largest
D. Mihalca) known parasitic nematode is
Placentonema gigantissima from the
placenta of female sperm whales,
Also called internal parasites, they can which can reach up to 8.5 meters in
inhabit all organ systems: digestive tube, length.
liver, respiratory tube, urinary system,
(4) Number of hosts required for the

completion of life cycle
 Homoxenous (Greek: homos =

identical; xenos = host) parasites
include those species which require a
single host category for the
completion of their life cycle.
Homoxeny defines parasite
transmission through hosts of same
ontogenetic category. These hosts
should not necessarily be one and the
same species. A homoxenous
parasite, therefore, can be
Figure 1.14 The red poultry mite, monoxenous, oligoxenous or
Dermanyssus gallinae, parasitic on polyxenous. Homoxeny is also called
chicken are visible with the naked eye, direct life cycle. Some examples of
but a careful examination should be homoxenous parasites include:
performed. (Photo Cristian Magdaș) apicomplexans from genera
Cryptosporidium and Eimeria;
monogeneans; certain nematodes of
domestic animals or humans (Ascaris,
(3) Host specificity Strongylus, Oxyuris, Strongyloides,
etc.). The vast majority of parasitic
 Monoxenous parasites are limited to
arthropods also have homoxenous
a single host species in certain life
life cycles (mange causing mites,
stages of their development. Many
fleas, lice etc). A particular type of
Eimeria species are strictly host-
homoxenous development was
specific and could be included here.
described in Sarcocystis gallotiae
 Oligoxenous parasites have a small parasitizing lizards. For this species
host range (2-5 species). Adults of of apicomplexan parasite,
Echinococcus granulosus are typical transmission occurs by cannibalism,
examples. However, larval forms of so both the definitive and
the same parasite have a broad range intermediate host are different
of hosts (polyxenous). individuals from the same species
(dihomoxenous life cycle). In some
 Polyxenous parasites have a broad
parasites with typical homoxenous
range of hosts (low or no host
life cycle, occasionally, in order to
specificity). For instance, Toxoplasma
cross some trophic boundaries, they
gondii is a polyxenous parasitic
use an additional non-obligate host.
apicomplexan.
They are called facultative
heteroxenous parasites and
examples include Toxocara (an
ascarid nematode of dogs and cats), cycle takes place as free-living stages;
Syngamus (a respiratory strongyle of in other cases, adult females become
galliforme birds) and many others. parasitic. Another example of
facultative parasites is the case of
 Heteroxenous (Greek: heteros =
larval stages of Calliphoridae flies.
different; xenos = host) parasites
They are opportunistic and have the
require transmission via alternation
ability to exploit living tissue,
of hosts of different ontogenetic
although characteristically they are
categories. This type of development
carrion feeders.
is also called indirect life cycle.
According to the number of hosts,
these parasites are called
(6) Duration of parasitism
diheteroxenous (i.e. Fasciola
hepatica), triheteroxenous (i.e.  Temporary parasites are in contact
Dicrocoelium dendriticum) or with their host for short periods
tetraheteroxenous (i.e. Alaria alata). during a certain stage of their life
The term polyheteroxenous is also cycle. Mosquitoes or leeches are
used to refer to parasites requiring typical examples. If a temporary
more than two hosts. parasite visits its host several times
during a particular life stage it is
called a periodic parasite.
(5) Obligativity of parasitic life
 Permanent parasites infect their
 Obligate parasites are those which host for longer times. All adult stages
need a host for survival, development of trematodes and cestodes are
and/or reproduction during at least associated with their definitive host
one of their life stages. In some during their entire adulthood.
species of parasites, all
developmental stages are found
associated with only one host (i.e. (7) Parasitic life stage
Trichinella, lice etc.). In some others,  Pre-imaginal parasites are parasitic
only certain stages are obligatory only during their immature life
parasitic. For instance, in many stages, while adults are free-living.
nematodes, the first larval stages are All myiasis causing flies are pre-
free-living, while the later stages and imaginal parasites. In these species,
adults are obligatorily parasitic (i.e. usually the adult stage is short living
Strongylus nematodes of horses). and many times it doesn’t even feed.
 Facultative parasites are generally In the representatives of phylum
free-living species, which may Nematomorpha, the larval stages are
accidentally become parasitic. The always obligatory parasites while the
nematodes of genus Strongyloides adults are free-living.
can undergo two types of
development. In certain cases, all life
 Imaginal parasites infect their hosts particular. Basically, a host is any living
only during their adult stage, while organism which harbors another one,
immature stages are free-living. Fleas parasitic. The following terminology used
of genus Ctenocephalides (figure for host classification is not based on
1.15) parasitic on dogs and cats are single criteria.
imaginal parasites.
Definitive host (or final host) is
traditionally defined as the host where
the parasite reaches sexual maturity or as
the host which harbors the adult
parasites. Even if this definition looks
clear and simple, due to the complexity
and diversity of parasites and parasitic
interactions, some comments are
required. Most homoxenous metazoan
parasites reach sexual maturity in the
host, thus this should be called definitive
host. However, as this host is singular,
and no other organism is required in the
development of homoxenous parasites
(i.e. intermediate host), it is easier to use
just the term “host”. Moreover, in some
Figure 1.15 Heavy infestation with the homoxenous parasites, only the
flea, Ctenocephalides canis on a dog. Only immature stages are parasitic, while the
the adults are parasitic; larvae and adults are free-living, thus, the term
nymphs are found in the dog’s “definitive host” would not fit to the
environment. (Photo Andrei D. Mihalca) generally accepted definition. On the
other hand, there are parasites with
facultative heteroxenous life cycles. In
 Note: in many parasites, immature this case, it would be useful to use the
and adult stages are both parasitic in term “definitive host” to differentiate
the same or in different hosts. The them from the eventual facultative
term to include these cases is not intermediate or paratenic hosts.
well-defined, but permanent parasite Moreover, in parasitic protozoa there is
can be a feasible option, although it no such stage as “adult” or concept of
overlaps with the previous criteria. “sexual maturity”. Conventionally a
definitive host for heteroxenous parasitic
protozoa is the host in which sexual
1.6 Types of hosts reproduction occurs. However, in some
parasitic heteroxenous protozoans the
The ecological concept of “host” would life cycle does not include any sexual
not exist without the concepts of reproduction; hence the definition of
symbiosis in general and parasitism in definitive host in this case is arguable.
Asexual reproduction is also known in ecological or trophic. For examples,

adult females of homoxenous nematodes humans are dead-end host for many
of genus Strongyloides, so the traditional parasites (i.e. Echinococcus, Trichinella,
definition should be reconsidered. etc) as it is unlikely that definitive
carnivore hosts will prey on humans.
Intermediate host is any host involved in
heteroxenous life cycles which is not Notes: (1) In some cases, a single
definitive and in which the parasites individual can be definitive and
undergo some developmental and intermediate host for the same parasite.
morphological change. In For example, a cat which harbors the
polyheteroxenous life cycles, gametogonic (sexual) stages of
intermediate hosts are customarily Toxoplasma gondii in its intestines is a
numbered according to their definitive host. However, cats can also
consecutiveness in the ontogeny of the develop systemic infection with
parasite (i.e. intermediate host 1, merogonic stages of T. gondii making
intermediate host 2, etc.). them intermediate hosts. Often, the same
cat can harbor both stages, being in the
Paratenic host (or transport host) is
same time intermediate and definitive
used by some parasites to bridge a
host, but in different life cycles. (2)
trophic gap. Ontogenetically, they are not
Another unusual situation is encountered
obligatory in the life cycle of parasites,
in the life cycle of the nematodes of genus
but ecologically they are very important.
Trichinella (figure 1.16). The same
The most accepted definition considers
individual acts first as definitive and later
the paratenic host as an organism which
on as intermediate host in a particular
serves to transfer a larval stage or stages
heteroxenous life cycle.
from one host to another but in which
little or no development takes place. The
term is rather appropriate in
helminthology than in protozoology.
Reservoir hosts are those organisms

which are responsible to maintain the
parasite populations in certain
ecosystems.
Vector hosts are defined as organisms

which transmit certain pathogens from
one host to another. However, definitions
widely vary according to the vectored
pathogen.
Dead-end hosts are usually intermediate

or paratenic hosts which are not able to Figure 1.16 Larva of Trichinella britovi
transmit the parasites to further hosts. parasitic in the skeletal muscles of red
Limitations are most commonly fox. (Photo Călin M. Gherman)
1.7 Life cycle of parasites In homoxenous life cycles parasites

require a single host to complete their
Every living organism has a life cycle development. This way of development is
(also known as developmental cycle or encountered in some parasitic
life history). Life cycle is a series of protozoans, in all monogeneans and in
developmental stages through which an various nematode species. There are
organism goes through. Always, the last three different possible situations:
stage from a life cycle must be able to
 In most homoxenous parasites, there
produce the initial stage from the
is an alternation of stages in the
subsequent cycle. In parasitic organisms,
environment with parasitic stages
the life cycle is extremely complex and it
(figure 1.17). The host acquires the
is the results of coevolution with their
parasite from the environment via
hosts. Regardless of the taxonomic group,
various routes, most commonly by
development of parasitic species most
ingestion. Typical examples for this
often comprises an alternation of free-
case are apicomplexan protozoans of
living and parasitic stages.
genus Eimeria. In some other cases,
In order to complete their life cycle, infective stages from the
parasites have to overcome three critical environment actively enter the host,
steps: by penetration of skin or mucosae
 the immune system of the host(s); (i.e. Ancylostoma, Bunostomum, etc.).
 the adverse environmental factors;
 the ecological requirements for host-

to-host transmission.
Despite all odds, an impressive number of

parasitic species succeeded through the
caudine forks of evolution.
1.7.1 Types of parasitic life cycles
As shown above (Chapter 1.5), there are

Figure 1.17 Typical homoxenous life-
two main types of parasitic life cycles:
cycle (E = external environment; H =
homoxenous and heteroxenous. Each
host).
species has a characteristic life cycle
which will be detailed in the
corresponding section of this textbook,
 Although not common, in certain
but some general aspects should be
homoxenous parasites the life cycle
discussed further on.
can be completed without stages in
the external environment. This is
possible due to autoinfection of the

single host (figure 1.18). For
instance, the parasitic females of the
nematodes of genus Strongyloides
typically lay embryonated eggs which
pass through the host’s feces to the
external environment where they
hatch. Subsequently, infective larvae
will penetrate through the skin of a
new host. However, in some cases,
eggs are able to hatch while still Figure 1.18 Homoxenous life-cycle in
inside the host’s intestine, so larvae autoinfective parasites (E = external
will be autoinfective to the same environment; H = host).
host. Another possibility herein,
involving two different individuals is
the sexual transmission of some
protozoans (Trypanosoma
equiperdum, Tritrichomonas foetus).
 The third possibility for homoxenous

life cycle was described for certain
species of genus Sarcocystis parasitic
in lizards. These parasites are
transmitted from host to host by
cannibalistic behavior during which,
lizards from the very same species
eat each other’s tails. This particular Figure 1.19 Dihomoxenous life-cycle (H
life cycle (figure 1.19) was = host)
denominated as dihomoxenous and
sometime even the same individual
lizard can act as both definitive and Heteroxenous development comprises of
intermediate host. a definitive hosts and one or more
intermediate hosts. Although the
Heteroxenous life cycles are very
possibilities and variations in the
complex and ecologically challenging
alternation of hosts and stages in the
pathways in the development and host-
external environment are multiple, the
to-host transmission of parasites. Several
following situations will be considered:
groups of parasitic organisms have
exclusively heteroxenous development.  Most of the so called vector-borne
All trematodes, all cestodes and all parasites (i.e. Babesia, Theileria,
acanthocephalans are included here. Trypanosoma, Leishmania, Dirofilaria,
Many protozoans and nematodes also etc.) have a typical diheteroxenous
embrace heteroxeny. life cycle with direct host-to-host
transmission and with no stages in

the external environment (figure
1.20). Transmission occurs both
ways through hematophagy. Another
interesting diheteroxenous life cycle
with no external stages has been
described in hemoparasites of genus
Hemolivia. The definitive hosts are
ticks which acquire the infection by
hematophagy from tortoise
intermediate hosts. Remarkably, the
tortoises get the infection by
ingesting infected ticks. Figure 1.21 Diheteroxenous life-cycle
with single indirect transmission (E =
external environment; DH = definitive
host; IH = intermediate host)
 In other groups of diheteroxenous

parasites there is no direct
interaction between the definitive
and the intermediate host, and
transmission from one host to
another always occurs through some
external stages (figure 1.22). For
instance, in the trematode Fasciola
Figure 1.20 Diheteroxenous life-cycle
hepatica, definitive hosts shed
with no external stages (DH = definitive
parasitic eggs to the pasture where
the larval stage (miracidium) hatches
and penetrates a snail intermediate
 Many diheteroxenous parasites - like host. After several asexual
most of the cestodes and reproductions, cercariae actively
acanthocephalans, but also some leave the snail and encyst as
apicomplexan protozoans (i.e. metacercariae on vegetation. A new
Sarcocystis, Toxoplasma, Neospora, definitive host will ingest them and a
etc.) - are characterized by indirect new life cycle begins.
transmission through the external Most trematodes have a typical
environment from the definitive host triheteroxenous development,
to the intermediate host and direct involving very diverse possibilities.
transmission through predatorism Considering a single situation (figure
from the intermediate host to the 1.23), we will illustrate the life cycle
definitive host (figure 1.21). of Dicrocoelium dendriticum.
Ruminant definitive hosts are known to occur in the cestode

shedding the eggs of this parasitic Diphyllobothrium latum infecting humans
liver trematode, through their feces and other piscivorous mammals.
to the external environment.
Figure 1.23 Triheteroxenous life-cycle (E

Figure 1.22 Diheteroxenous life-cycle = external environment; DH = definitive
with double indirect transmission (E = host; IH = intermediate host)
external environment; DH = definitive
1.7.2 Stages in the external
environment
The first intermediate host (IH1), in this
case a terrestrial snail will ingest these In the very previous chapter we showed
eggs and inside its body the miracidium that in many parasitic life cycles,
will hatch and multiply by asexual transmission from a host to another
reproduction. When reaching to the requires passage through the external
cercarial stage, they actively emerge from environment. For an organism which is
the snail’s body and are ingested by a primarily adapted to a parasitic lifestyle,
second intermediate host (IH2) which is the contact with environmental factors
an ant. Inside the ant’s body, the can seriously affect its survival. On the
cercariae will encyst into a other hand, parasitism as a way of life
metacercariae. Further transmission to a probably evolved in previously free living
new definitive host implies accidental organisms as an adaptation to avoid
ingestion by ruminants of infected ants. these factors.
The chances for this apparently
An interesting situation of organism
hazardous event are increased by the
which is able to opt for a free-living or a
pathogenic effect of the metacercarial
parasitic lifestyle is known for nematodes
stage on ants, causing them impaired
of genus Strongyloides. In these
motility. Another similar example of life
nematodes, only females are parasitic in
cycle but involving different hosts is
various parts of the digestive tube of their
host. By parthenogenesis, parasitic complex developmental changes,

females of Strongyloides produce eggs essential for their further transmission.
which embryonate and first-stage larvae For instance, in coccidia, the cysts are
hatch. In the external environment larvae called oocysts, which in most cases when
either develop into female infective shed through the feces of the host are not
larvae or grow and molt four times to sporulated, hence non-infective to a new
produce a single free-living generation host. During its environmental life, if the
consisting of both males and females. physical conditions are proper, oocysts
What factors determine whether larvae sporulate and become infective. However,
will develop into free-living stages or into in other protozoans (i.e. Giardia) the cyst
infective forms is still not fully known, is mainly important as a resistance stage,
but it is believed they may depend on and excystation usually occurs when they
environmental conditions such as pH, reach in their typical parasitic habitat in a
pO2, pCO3, consistency of substrate, new host. More complex situations are
temperature and level of nutrients. known for parasites with a certain degree
of host-specificity, when only the contact
Parasites use various strategies to
with a suitable host triggers excystation.
survive or to avoid environmental
Mechanisms for excystation include
conditions while being in their journey
rehydration and action of host digestive
from a host to another.
enzymes on the cyst wall.
Many protozoans are able to secrete a
Encystment as a survival strategy is also
resistant covering and enter a latent
known for trematodes (flukes). Typically,
stage called cyst. Encystment is very
trematodes have a three-host life cycle.
common among free-living protozoa
The definitive host is always a vertebrate,
during harsh environmental conditions
the first intermediate host is always a
but also in most parasitic protozoa when
mollusk and second intermediate hosts
they are outside their host, in the
are various metazoans. In few cases, the
environment. The encystment provides
life cycle comprises only two hosts: the
protection against unfavorable
vertebrate and the mollusk. Nevertheless,
environmental conditions but also
regardless of the number of hosts,
provides a biological background for
trematodes always have two stages in the
nuclear division. The triggers for
environment. The definitive vertebrate
encystment include lack of nutrients,
host passes through the feces the eggs of
water loss, decreased oxygen
the fluke. If the life cycle involves aquatic
concentration or changes in the
mollusks, the first larval stage of the
temperature or pH. During encystment in
trematode (called miracidium) hatches
protozoans, a cyst wall is produced,
from the egg and it actively swims
movement organelles (cilia or flagella)
foraging for its mollusk host. As a survival
are lost and food reserves (i.e. starch,
strategy in terrestrial cycles, miracidia do
glycogen) are stored within the cell. In
not hatch but remain inside the egg. The
certain types of parasitic protozoans, the
next free living stages of trematodes in
environmental cystic stages suffer
ontogenetic order are cercariae. They
actively leave the mollusk’s body and larvae stay inside the eggs to avoid
either forage for the second intermediate environmental factors (i.e. in ascarids or
host or become encysted on vegetation. pinworms). In other cases, larvae hatch
and are infective for the definitive host.
In tapeworms (cestodes) the usually
For instance, third stage larvae (L3) of
complex life cycle requires at least one
Strongylidae parasitic in horses are
stage in the external environment. The
swallowed together with the grass. They
definitive host (always a vertebrate)
hatch as L1 and remain in the
which hosts the adult stages in its
environment where they undergo two
intestines sheds the eggs through the
molts before turning into infective L3.
feces. In certain groups of cestodes (i.e.
During this time, they avoid drying out by
Pseudophyllidea) the life cycle is related
being active during cooler periods of the
to aquatic environment; hence the eggs
day (morning, dusk, dawn) and hiding in
are adapted to float to enhance their
shade over sunny days. In certain groups
chance to be swallowed by a suitable
of nematodes, after L1 hatch, they must
intermediate host. In other species of
immediately get into an intermediate
“aquatic” tapeworms, larval stages called
host to avoid the improper
coracidia (singular, coracidium) hatch
environmental factors (i.e.
from the eggs and swim waiting to be
Protostrongylus).
ingested by a crustacean. These aquatic
stages are usually not very resistant (i.e. Most arthropods are external parasites so
coracidia can survive only 24-36 hours) they are exposed to environmental
and normally do not feed. On the other factors all the times. Additionally, many
hand, in other groups of cestodes (i.e. arthropods are temporary parasites,
Cyclophyllidea), eggs containing embryos hence most of the time they spend away
(oncospheres) are very resistant in the from the host. Biting insects like
environment. They can easily survive mosquitoes or sandflies are parasitic only
several months before being ingested by for very short time, when they are
a suitable vertebrate host. feeding. Ticks spend a great part of their
life in the search of a suitable host,
In nematodes, environmental stages are
dwelling in the vegetation of burrows. In
known for most of the groups. Notable
other species, only larvae are parasitic
exceptions are species of genus
and adults are typically free-living
Trichinella which are transmitted from a
creatures (i.e. myiasis-causing insects).
host to another by predatorism or vector-
Other insects (fleas for instance) are
borne nematodes (i.e. Dirofilaria).
parasitic only as adults while imago
However, typical nematodes pass from a
stages are free-living and relying on
host to another through the external
environmental food sources. In
environment. The diversity of life cycles
mosquitoes, larval stages develop in the
in nematodes makes it very hard to
water. This is why successful campaigns
outline some general developmental
against mosquito-borne diseases are
patterns. Nevertheless, in most of the
focused on desiccations. Other parasitic
cases, the infective stage is a larva. Some
arthropods however, lack environmental Transmission strategies are extremely

stages (lice). diverse in the world of parasites. Some of
them are remarkable examples of
(co)evolution and natural selection of
1.7.3 Getting in/on the host successful traits.
One of the most crucial milestones in the

life cycle of a parasitic organism is the
successful detection of a suitable host.
Parasites have evolved many different
strategies to increase the chance of
successfully finding a host. One of the
most common strategies used by
parasites is the production of an
enormous number of offspring. Most of
the offspring will be unsuccessful and
only a limited number will encounter a
suitable host.
Parasites can use passive dispersion

(random chance to contact a host) or
Figure 1.24 Many important tick species
active host finding (when mobile parasite
spend the majority of their lifetime in the
stages are actively searching for the host
wait of their host, on vegetation. This
using various sensorial features). In
host-finding behavior is called questing.
active strategies host detection is
essential. To detect the proximity of a
potential host, parasites use complex
sensory organs. The first larval stages of
In homoxenous life cycles, transmission
digenetic trematodes are called
of parasites from a host to another is
miracidia. They are able to swim at a rate
direct. The host usually sheds stages to
of about 2 mm per second and use their
the environment. In most of the cases
chemoreceptors to find a suitable snail
these stages are not yet infective for a
host. After locating it, the miracidium
new host, but they spend some time and
attaches to the snails integument and
undergo some biological changes
using cytolytic enzymes it embeds deeper
becoming infective. They will enter the
and deeper into the snail’s body. In
new host passively (i.e. ingestion of
questing ticks (figure 1.24), the
infective eggs, cysts, oocysts, larvae) or
detection of the host is based on complex
actively (i.e. skin penetration by larval
sensorial organs called Haller organs,
hookworms or schistosome cercariae).
which are able to perceive CO2 from the
breath of hosts but also on temperature Particular situations of direct
and movement detection. transmission with no stages in the
external environment are known. Some
situations include direct transmission and complex. Many parasites are

through sexual contact. Trichomonas transmitted from a host to another by
vaginalis in humans or Trypanosoma predation. One of the typical models is
equiperdum in equines are examples of the life cycle of cestodes in Taeniidae
sexually transmitted parasitic diseases. family. Typical definitive hosts for these
Skin contact between an infected and a tapeworms are carnivorous mammals
healthy individual is the way how scabies which acquire the infection after preying
mites (Sarcoptes) get to a new host on infected intermediate hosts. Larval
(figure 1.25). taeniids which infect these intermediate
hosts usually induce severe lesions to
Transmission strategies for parasites
make them more susceptible to be
with heteroxenous life cycles are more
predated. This adaptation enhances their
complex. Transmission from a host to
chance to get to the definitive host.
another can be via the environment,
Similar examples (figure 1.26) are
where there is no direct contact between
known for various nematodes
definitive and intermediate hosts.
(Eustrongylides in fish intermediate
hosts) or trematodes (Dicrocoelium in
ants).
Figure 1.25 Sarcoptic mange in a camel.

Parasite transmission occurs by direct
host-to-host contact. (Photo Andrei D.
Figure 1.26 Fish infected with the
Mihalca)
nematode parasite Eustrongylides excisus
are easier preys to dice snakes, Natrix
In this case, detection of hosts follows the tessellata. (Photo Andrei D. Mihalca)
same principles as for homoxenous There is a significant number of parasites
parasites. When the transmission from which infect their host through
the definitive host to the intermediate hematophagy by other parasites. These
host requires direct contact between the are the so called vector-borne parasitic
hosts, strategies are sometimes intriguing
infections. The vectors are usually blood 1.7.4 Migration and development in
eating arthropods (ticks, mites or insects) the host
and they play the major role for
inoculating various parasites to the Parasites are adapted to a multitude of
vertebrate host. Probably the most well- habitats within the host. However, the
known examples are among protozoans. site where parasites gain access to the
Plasmodium species causing malaria are host is different than the target
vectored by certain mosquitoes. organ/tissue. So the parasites have to
move from the site of infection to the site
Another tropical disease, the sleeping
of predilection within the host’s
sickness is caused by various species of
organism. In some other cases, the site of
Trypanosoma. Their transmission is done
infection is the same as the typical site for
by tsetse flies. Blood sucking insects are
the final stage in that particular host, but
also responsible for vectoring metazoan
parasites need to undergo some
parasites. Many filarial nematodes are
development in order to survive there.
injected as larvae to their vertebrate host
For this development they might migrate
by mosquitoes or flies (i.e. Dirofilaria,
through various tissues before returning
Loa, Onchocerca, Wuchereria)
to the initial site.
Except the aforementioned possibilities
Most parasites enter the host via the
of host infection, there are also some
digestive tube after being ingested (see
particular situations. A form of
Chapter 1.7.3 for details). Some of these
autoinfection known as retrofection has
parasitic species will need to get to their
been described for pinworms
typical habitat within the host. As
(Oxyuridae). The eggs of these nematodes
situations are quite diverse, we will use
hatch on the anal skin and mucosa and
some examples instead of drawing a
the larvae migrate up the bowel to the
general picture.
cecum. Another type of autoinfection is
known in the hydatid disease where the Herbivores acquire the infection with the
protoscolices of Echinococcus are able to liver fluke Fasciola hepatica after eating
infect other tissues in the same host grass with encysted cercariae. In the
individual by metastasis. intestine of the herbivores, cercariae
excyst and start their journey towards
Last but not least, vertical transmission of
the bile ducts from the liver. Their
parasites from the mother to the
migration can follow three pathways: (1)
offspring is another strategy used by
some travel directly through the intestine
some parasites. The zoonotic protozoan
wall, penetrating the peritoneum, the
Toxoplasma is one prominent model.
liver capsule and hepatic tissue; (2)
Roundworms of genus Toxocara are also
others will use the common bile duct or
known to transplacentally pass from
(3) after penetrating the intestinal wall
mothers to fetuses during pregnancy.
they will enter the blood stream and
through the hepatic portal venous system
will reach the liver.
If in Fasciola hepatica there are multiple dogs, the larvae use the same migration
possible routes, most helminthes which route until they reach the lungs, but
enter the host’s body through the instead of leaving the blood they continue
digestive system use the blood or their journey back to the heart via the
lymphatic stream for migration. The main pulmonary veins. After they reach the
gate for parasites to enter the circulatory right atrium they pass into the right
system from the intestine is the hepatic ventricle and from there, through the
portal system. This remarkable venous aorta the get to various tissues (muscles,
system drains the blood with nutrients brain, etc.). This migration pattern is
absorbed by the intestinal mucosa and called entero-pneumo-somatic.
transports it to the liver. Together with
Another nematode, Trichinella spiralis
these molecules, microscopic parasites
enters its carnivorous host after this
make their way to the liver and further
feeds on the infected meat of another
on, through the posterior vena cava to the
host. After completing its life cycle in the
right atrium of the heart. From the right
intestine, newborn larvae use several
atrium they pass to the right ventricle
pathways to get to the skeletal muscles.
and continue their travel via the
These include direct invasion of
pulmonary arteries to the lungs. In the
capillaries and lymphatic vessels in the
lungs they either leave the blood stream
intestine as well as migration through the
entering the respiratory ducts or they
intestinal serosa to the peritoneal cavity
continue their blood adventure and
or via the hepatic portal vein blood to the
return to the heart through the
general circulation.
pulmonary vein to the left atrium and left
ventricle. Among tapeworms (Cestoda) we take
into discussion again the family
The best group to illustrate the diversity
Taeniidae. Their eggs, if ingested by a
of migrations is represented by ascarid
suitable intermediate host will hatch in
nematodes. Ascarids of horses, pigs or
its intestine. The newborn embryo will
humans (genera Ascaris and Parascaris)
migrate via the circulatory system to
are within the first type, leaving the
various organs, depending on the
vascular system in the lungs.
tapeworm species. Eggs of Taenia solium
Subsequently they migrate through the
from human feces, if ingested by a pig,
bronchi and trachea until the pharynx
will hatch in its intestine. The embryos
from where they are swallowed and
will migrate via the blood and will spread
reach again the digestive tube. During
systemically to skeletal muscles of pigs.
this migration they undergo several
Similar migration route is known for
molts and they grow in size accordingly.
Taenia saginata but intermediate hosts in
This type of migration is called entero-
this case are bovines. For both species,
pneumo-tracheo-enteral. Ascarids of
humans are the definitive hosts and they
genus Toxocara (parasites of carnivores
acquire the infection after eating raw or
and cattle) use even more complex
undercooked meat from the respective
migration pathways. If larvae of Toxocara
intermediate host.
canis (parasitic in canids) infect adult
In unicellular parasites, the mechanism of state that a parasite with a narrow host
spreading in the host’s body is usually range depends on its host in a greater
involving intracellular parasitism in degree than one with a broader host
transport cells. Protozoans like range. Medically, the importance of host
Toxoplasma gondii enter the host by the specificity resides in the possibility of the
digestive route. In the intestine they generalist parasites to jump on to a new
enter macrophage cells and move host species and the possibility of
throughout the body spreading to various development of a new, emerging disease.
tissues and inducing a systemic infection. Moreover, some of these parasites are
transmissible from vertebrate animals to
Other parasites use different entry routes
humans often producing important
to the body. Nematodes from the family
conditions known generically as
Ancylostomatidae penetrate the skin or
zoonoses.
oral mucosa of their host. However, the
migration is hematogenous as well. Several hypotheses try to explain the
mechanism for host specificity. However,
It is beyond the scope of this general
none of them is fully explaining the
chapter to exemplify all the parasites and
complexity of parasite-host interaction in
their migration patterns. Though, one
nature. All of them have limitation and
idea is evident: most parasites infect the
probably the mechanism is a combination
host via the digestive route and use the
of these factors. They were reviewed
circulatory system of the host to get to
recently by Schmid-Hempel in his
the predilection tissue/organ. During this
excellent monograph on Evolutionary
migration, most of them undergo
Parasitology. Below is a synthetic account
complex changes, some of them aimed to
of these theories.
evade the host’s immune system.
(1) Host range is limited by
Development in the host is extremely
phylogenetic constrains: some
varied according to the taxonomic group
parasites tend to have more host species
and will be discussed in more detail in
when the hosts belong to a species-rich
the respective chapters.
taxonomic group (many similar enough
hosts to be infected); for instance,
microsporidia are typical parasites of
1.7.5 Biological background for host invertebrates and rarely of worm-
specificity blooded vertebrates; one reason is that
microsporidia do not tolerate high
Parasites can infect variable numbers of
temperatures.
host species. Specialized parasites infect
a narrow spectrum of host species while (2) Host range depends on the
generalist parasites infect a wide range of phylogenetic age of the parasite group:
host species. Medically and ecologically, during the evolutionary history of a
the degree of host specificity is one of the parasite group, the host range expands as
most important characteristics of a the parasites evolve. For example in some
parasite. An ecologic approach might genera of fleas parasitic in small
mammals, host specificity is low as (7) Host range depends on immune

compared to other flea taxa. defenses: Although still not fully
understood, the immune mediated host
(3) Host range depends on
specificity can be synthesized in the
transmission mode: some parasites
following sentence: the host range is
with active transmission (i.e. with mobile,
given by the parasite’s capacities to evade
free-living stages) can be more selective
the host’s immune system.
regarding the host than parasites with
passive transmission (i.e. transmitted by
direct contact between hosts or by
unspecific vectors). 1.8 Host-parasite interactions
(4) Host range depends on the stages Life-cycle of parasites is usually an

of the parasitic life cycle: in many alternation of free living and parasitic
heteroxenous parasites the larval stages developmental stages. During this
have low specificity for the intermediate parasitic phase, stages of the parasites
host while the adult parasites are more are located within various tissues of their
specialized to a narrow range of host. The interactions between parasites
definitive hosts. When the parasitic stage and their hosts are complex and not
is a encysted form (hypobiotic) the always fully understood. As for all living
selection is probably weaker on cysts beings, natural selection shapes the
than on the active adult forms. A good evolution of both, the parasite and the
example to support this theory is the host (independently or together),
tapeworm Echinococcus granulosus. through the same general mechanisms.
Larval stages (known as hydatids) infect
virtually almost all mammal species Usually, parasite-host interactions are
while adults infect only canids. long term relationships, resulting in a
non-lethal coexistence of both partners.
(5) Host range depends on the However, in certain cases, parasites can
virulence of the parasites: if a parasite seriously impair the homeostasis of their
is more virulent the host specificity hosts, sometimes resulting in the death of
should be broader; if the host range of a the later. In other cases, the immune
virulent parasite is narrow, the number system of the host is able to keep parasite
of susceptible individuals in the receptive development under control and even
population might be decreased by the eliminate it completely.
parasite, leading to co-extinction.
The parasite-host interaction has been
(6) Host range depends on parasite commonly described as an antagonistic
geographic distribution: parasites with relation, where both organisms are in a
a wider geographical distribution tend to permanent struggle for survival. This
encounter a larger range of likely hosts antagonistic state might be easily
than parasites with a more territorially questionable from evolutionary point of
restricted distribution. view, but medically, it eases the
understanding of parasitism as such.
In this short chapter we will summarize parasites on their host but rather to be
the host-parasite interactions focused on its medical and veterinary
independently. First approach will side. Hence, in the next paragraphs, we
include the actions and effects of will approach the pathogenic effect of
parasites on their host, mainly from parasites on their host, or, to put it in
medical point of view (i.e. how parasites other words, how parasites are able to
produce disease). In the second part, the produce diseases.
reaction of host will be discussed, with
Certainly there are many factors
emphasis on its immunologic strategies.
influencing the pathogenicity of parasites.
Some of them are related to the host,
some others to the parasite. The factors
1.8.1 Pathogenicity of parasites related to the host include: species,
breed, age, sex and individual immunity.
To the inexperienced reader, it seems The species is very important when
strange to find out that most of the wild considering pathogenicity. Some species
animals (invertebrates or vertebrates) are very prone to develop clinical signs
harbor parasites. We can say with almost when infected by certain parasites, while
no chance to be wrong, that each single others are infected but evident symptoms
animal burdens at least one parasite at a are absent. For instance, humans are very
certain time. The situation in domestic sensitive to the infection with the
animals is not very much different. nematode Trichinella spiralis and develop
However, the clinical effects are not a severe disease, often lethal if not
present all the time; on the contrary, the treated. On the other hand, infected pigs
onset of the disease is the exception for or carnivores can harbor immense
most parasite-host associations. number of larvae in their muscles
By bearing in mind the definition of without any sign of disease. Even within
parasitism we can easily conclude that the same host species, there might be
parasites are supposed to induce some variations between different breeds.
pathology to their host. And this is true. Usually, highly specialized breeds are
Nevertheless, these lesions are in most more sensitive to parasitic infections
situations minor and not reflected in the than local breeds. Probably the most
general health status of the infected host. prominent example is the existence of the
In wild animals (maybe even in so called trypanotolerant breeds of cattle,
domestic), the “non-clinical” parasitism is sheep and goat, very resistant to the
likely to influence in a bigger or smaller infection with the otherwise deadly
extent the overall fitness of the host. agents of Nagana in Africa (figure 1.27).
Although “fitness” is hard to be evaluated, When colonists introduced highly
there are multitudes of examples in this productive European cattle breeds in
direction. Africa with the hope of huge profits, their
efforts were soon vanished by massive
The aim of this section is not to discuss
die-offs due to the tsetse fly transmitted
the ecological effect and influence of
trypanosomoses. Another significant
host-related factor which influences mostly related to immunity is a key factor

pathogenicity is the age. Parasites are when considering parasite pathogenicity.
usually able to infect all age groups of For causes not so evident, in certain host
their host. However, in many situations, groups with similar populational features
only the young ones develop (severe) (same species, breed, age or sex), some
clinical diseases. Coccidia of genus individuals develop a more severe
Eimeria are able to produce epidemic parasitic diseases than others.
mortality in chicken or young domestic
The second group of factors influencing
rabbits, but adults are usually infected
the pathogenicity comprises those
without showing clinical signs. This is
related to the parasite. Maybe the most
particularly important mainly from
important in this category is the intensity
epidemiologic point of view, when adults
of the infection. Usually the higher the
with undetected infections are the main
number of parasites within a host
source of infections for the young
individual is, the more severe the clinical
offspring.
signs are. The ascarid nematodes infect a
wide variety of hosts. When only few
nematodes are present in the intestine,
the clinical effect is usually absent.
However, when the infection intensity is
of tens or hundreds of individual
parasites, severe symptoms or death due
to intestinal obstruction may occur.
Another important factor is the strain
within the parasitic species. Some strains
may be more pathogenic than others or
may have different host affinities.
The mechanism by which parasites are

pathogenic can be grouped in five main
categories: physical damage, spoliation,
Figure 1.27 Some local African cattle toxin production, inoculation effect and
breeds are resistant to trypanosome interactions with the host’s defense
infections. (Photo Andrei D. Mihalca) mechanism. Most parasites fit into
several of these categories, if not in all
together.
Sex of the host is also able to influence Physical damage can take various forms,
the clinical course of the disease. The depending on the organ affected or the
human genital parasitic protozoan parasite species or stage involved. Some
Trichomonas vaginalis is commonly parasites, due their large size or high
producing clinical infection in females but number in the host’s tissues and organs
males are often asymptomatic carriers. can induce severe mechanical trauma.
Last but not least, individual resistance, Bladder worms (vesicular structures of
larval cestodes) located in retarded growth. With effects similar to

parenchymatous organs are compressing spoliation, the malabsorption caused by
the surrounding tissues inducing intensive intestinal mucosal damage is
atrophy. This is highly evident in case of also a common pathogenic feature of
the “coenurus” type larvae of Taenia parasitic infections.
multiceps located in the brain of small
ruminants. For large parasites or large
parasite groupings in luminal organs (i.e.
intestine, bronchi etc.) one of the most
common extreme effects is obstruction.
The most common parasites responsible
for intestinal obstruction in dogs, horses
and humans are ascarid nematodes
(figure 1.28). Parasites are also
responsible for direct tissue destruction.
Parasites can destroy the tissues by
several ways. Migrating parasites (see
Chapter 1.7.4) are responsible for
important traumatic lesions in various
organs. Other situations include direct
tissue damage during feeding or Figure 1.28 Ascarid nematodes like
attachment. Most parasites possess Toxocara canis in dogs are often
various adherence structures to avoid obstructing the host’s intestine. (Photo
being eliminated by the host. These Andrei D. Mihalca)
structures (i.e. hooks, spines, suckers
etc.) are highly irritating to the host’s
tissues, causing local destruction at the Toxin production by parasites can have
site of parasite fixation. local or systemic effect. The toxins can
result either as parasite waste products
Spoliation (the act of plundering) or
or due to massive destruction of
nutritional robbing is common among
parasites. The agents of human malaria
intestinal parasites. The parasites utilize
(apicomplexans of genus Plasmodium)
the same food resources as their hosts do.
are producing a toxin called hemozoin,
Large parasites or large parasite
responsible of an overall reduced
groupings are able to use huge amounts
phagocytic performance by host’s white
of certain nutrients ingested by the host.
blood cells. The saliva of ticks contain
The fish-borne tapeworm
various products, which, when injected
Diphyllobothrium latum absorbs large
into the host may induce general
amounts of vitamin B12 from the host’s
paralysis. Following the death of large
intestine inducing systemic deficit which
numbers of individuals of Toxocara canis,
results in anemia. Other parasites are
the post-mortem release of toxins
responsible for unspecific spoliation,
resulting in general malnutrition and
induces nervous signs similar to epilepsy This section can hardly be more detailed
in puppies. than this, but pathogenesis will be
discussed individually for each parasite
The inoculation effect refers to
in the chapters to follow.
situations when parasites facilitate the
invasion of other microorganisms inside
1.8.2 Immunity of host to parasites
the hosts body, tissues or organs. Several
bacteria are commonly found in the Usually, the immune system of the host is
intestine where they are harmless. able to eliminate or to stop the parasitic
However, if they are carried by parasites invasion. Most hosts are hence resistant
in other organs or tissues (liver, brain, to the majority of parasitic infections.
peritoneum, etc.) they are able to Some parasites which are host specific
produce severe infections. In other cases, are able to infect individuals from a single
parasites induce lesions to the mucosa of host species, while all the other host
the intestine or respiratory ducts, organisms are able to stop the parasite
allowing pathogenic bacteria or viruses invasion. This gives the so called host
to produce the infection which is susceptibility or resistance to certain
otherwise unlikely through unharmed parasites. However, resistance is not
epithelium. One of the most well-known synonym to immunity. Immunity refers
inoculation effects of parasites is the case to those mechanisms by which
of vector-borne infections, when specialized cells or tissues of an organism
hematophagous arthropods are are able to recognize foreign (non-self)
transmitting various pathogens to their structures and eventually protect against
hosts (i.e. ticks, tsetse flies, mosquitoes, potential invasions. The immune system
sand flies, biting midges etc.). is present in various degrees of
The most severe and complex complexity in all animal organisms,
pathogeneses in parasitic infections are invertebrate or vertebrate.
caused by the altered immune response Most vertebrate animals possess in
of the host. The host responds to the general two types of immunity: the innate
presence of parasites by inflammation. immunity and the acquired immunity.
Severe granulomatous lesions or strong
inflammatory reactions are produced by The innate immunity (also known as
migrating nematode larvae in various non-specific immunity) includes various
tissues. Parasites are also able to induce inborn defense mechanisms known in all
changes on the surface of various cells, plants and animals. There are certain
cheating the host’s immune system and physical or chemical barriers which
producing autoimmune responses. The prevent invasion by pathogens. In
red blood cells infected with Babesia are vertebrates, the skin together with
recognized as non-self and destroyed by mucosal layers lining the inner lumen of
the host’s own immune system resulting respiratory ducts and digestive tube are
in severe hemolytic anemia. the first obstacle for most pathogens,
including parasites. Except these
anatomical barriers, the innate immune hypereosinophilia, increased

system includes important components: immunoglobulin E (IgE) production,
the cytokines, the complement system or mastocytosis and goblet cell hyperplasia.
a range of specialized cells like mast cells, Immunity against biting arthropod saliva
phagocytes (macrophages, neutrophils, has been also described in detail.
dendritic cells), basophils, eosinophils,
Despite the complex immune system
natural killer cells or gamma-delta T cells.
involved in the protection of host,
The acquired immunity (also known as parasites are often able to evade all these
adaptive or specific immunity) is known mechanisms and to produce infection or
only in vertebrates. Nevertheless, the even severe disease or death. The
specific immune response is activated by avoidance strategies are both complex
the innate components. The adaptive and interesting. One common mechanism
immunity is responsible for protecting is antigenic variation when the parasite
the organism specifically against is one step ahead the immune system of
pathogens and to “remember” specific the host. By the time the antibody is
antigens (immune memory). The main produced, the surface of the parasite has
factors of the acquired immunity are a completely new antigenic structure so
antibodies, produced by B lymphocytes. T the initial antibodies are useless. This
lymphocytes are also part of the acquired strategy is used by many important
immunity. There are several types of T protozoan parasites (i.e. Plasmodium
cells know, each of them with specific falciparum, Trypanosoma brucei) or
functions: helper, cytotoxic, memory, molting nematode larvae. Another
regulatory, natural killer, gamma-delta interesting avoidance mechanism is
etc. Acquired immunity can be active molecular mimicry, when the parasite is
(post-infection or post vaccination) or able to pass undetected (i.e. Plasmodium
passive (maternal transfer or after falciparum). Some parasites are able to
immunoglobulin administration). produce immunoglobulin cleaving
proteases (i.e. Dirofilaria immitis,
Compared to prokaryotic pathogens
Fasciola hepatica) which are destroying
(viruses and bacteria), traditional
all adherent antibodies. Others are
parasites (protists, helminthes,
producing prostaglandin E2 (i.e. Brugia
arthropods) are much larger in size and
malayi, Taenia taeniaeformis) which has a
have a much more complex antigenic
strong anti-inflammatory effect. Many
surface. Moreover, some of the parasitic
helminth or protozoan parasites are able
antigens are excretory antigens, not
to interfere with the complement
surface antigens, and are produced
cascade, blocking certain steps in its
intermittently. There are several
activation (Echinococcus granulosus,
components of the immune system which
Taenia solium, T. taeniaeformis,
act in the defense against parasitic
Trypanosoma brucei, T. cruzi, Entamoeba
protozoa, mostly antibodies and T cells.
histolytica, Leishmania spp.). These are
In the case of helminthes, the infections
only few of the extremely various known
are usually associated with
molecular mechanisms.
Except these intimate mechanisms, there taxonomic position of each parasite. So

are also some general strategies which the most important objective of this small
allow parasites to avoid host’s immune section is to make scholars understand
system. Most parasites are located in the the practical importance of taxonomy in
intestinal lumen. This can be the process of teaching and learning.
evolutionarily explained by the low
All parasite species are grouped in
amounts of immune effectors present at
systematic assemblages called taxa based
the surface of the intestinal mucosa. The
on certain morphological and biological
only immunoglobulin normally present in
features. For instance, genera like
the intestinal lumen is IgA, but this has
Sarcocystis, Toxoplasma, Neospora,
almost no effect against helminthes.
Hammondia and Besnoitia are all
Other parasites simply hide from the
included in the family Sarcocystidae. It
immune effectors. Larval cestodes
means that all members of these genera
(bladder worms) are isolated within a
share common characteristics, the ones
cystic membrane and some unicellular
of the family grouping all of them. One of
parasites develop inside various cells of
these characteristics is that all species in
the host organisms (i.e. Toxoplasma,
the family Sarcocystidae are
Babesia).
heteroxenous. So if one knows that any of
Detailed studies of immunology are the genera above is part of Sarcocystidae,
available for many parasites. A practical it also knows that its life cycle is
use of this knowledge is the possibility of heteroxenous.
immunodiagnostic of parasitic infections
by detection of circulating antibodies or
antigens using various laboratory or 1.9.1 Principles of zoological
clinical tests: intradermal allergy test taxonomy
(IDR), indirect hemagglutination (IHA),
indirect fluorescent antibody (IFA), Zoological nomenclature is the system of
complement fixation (CF), enzyme-linked scientific names applied to taxonomic
immunosorbent assay (ELISA), western units of extant or extinct animals. These
blot (WB) etc. units are called taxa (singular: taxon).
Parasites, as all animal taxa, are classified
1.9 Classification of parasites according to the rules of the International
Code of Zoological Nomenclature. The
Definitely, taxonomy is not the most
species is the basic unit and taxonomical
important part of medical parasitology.
rank in biological classification. Except
Most veterinary students consider
species, there are seven main taxonomic
taxonomy boring and very difficult to
ranks: Domain, Kingdom, Phylum, Class,
learn and remember. Moreover, they do
Order, Family and Genus.
not understand why it is important to
know basic taxonomy of parasites. On the The taxa are hierarchically arranged so
contrary, others tend to overestimate its that always a higher taxon includes
importance and learn by heart the usually several lower ones (i.e. one
kingdom includes several classes, one occurrences are abbreviated (i.e. H.

family includes several genera, one genus sapiens, C. lupus). As a rule, the names of
includes several species). To face the genus and species are written with italics.
increasing diversity of described life There are also typical terminations for
forms, taxonomists introduced various supraspecific taxonomical ranks
intermediary ranks for further divisions. (table 1.3), although exceptions are
For instance a class might contain several known. Biological taxonomy is probably
subclasses, a subclass could include the most dynamic science. Entire taxa are
several superorders or more families permanently reordered (reclassified)
could be all included in the same according to molecular phylogenetic
superfamily. studies. Hence, it is very difficult to put
down on paper a kind of “officially”
Each taxon above the rank of species gets
recognized taxonomical hierarchy.
a scientific name in one word
Moreover, different authorities have
(uninominal name), always spelled with
different opinions.
capital letter. A species always has a
binomial name (composed of two words).
The first word is always spelled with Table 1.3 Scientific names of metazoan
capital letter and represents the name of parasites
the genus. The second word is called the
Rank Termination
specific epithet and is spelled with lower Order -ida
case (i.e. Homo sapiens, Canis lupus). Superfamily -oidea
Family -idae
Sometimes, especially when in a text the Subfamily -inae
species name was written in full, the next
Table 1.4 Main taxa of parasites
Phylum Class* Common name

Euglenozoa Kinetoplastea
Parabasalia Tritrichomonadea
Trichomonadea
Flagellates
Hypotrichomonadea
Fornicata Retortamonadea
Trepomonadea
Apicomplexa Coccidia Coccidia
Cryptosporidea Cryptosporidia
Haematozoea Piroplasms
Ciliophora Litostomatea Ciliates
Platyhelminthes Trematoda Flukes
Cestoda Tapeworms
Nematoda Secernentea Roundworms
Adenophorea
Acanthocephala Archiacanthocephala Thorny-headed worms
Arthropoda Pentastomida Tongue-worms
Insecta Insects
Arachnida (Subclass Acari - order Ixodida) Ticks
Arachnida (Subclass Acari - except Ixodida) Mites
*Only classes of veterinary significance are included
Parasitology. Caister Academic

1.9.2 Major parasitic taxa Press. 232 pp.
All species of parasites are included in 5. Gillespie S, Pearson RD (2001)

domain Eukaryota. The unicellular Principles and Practice of Clinical
heterotrophic mobile species are Parasitology. Wiley. 752 pp.
included in a paraphyletic group referred 6. Gosling PJ (2005) Dictionary of
to as Protista. Protista includes the Parasitology. Taylor & Francis
heterotrophic Protozoa, which groups Group. 394 pp.
animal-like unicellular organisms. They
7. Grove DA (1990) A History of
include the following phyla with
Human Helminthology. CAB
representatives parasitic in domestic
International. 856 pp.
animals: Euglenozoa, Parabasalia,
Fornicata, Apicomplexa and Ciliophora. A 8. Mehlhorn H (2008) Encyclopedia of
group formerly regarded as protists are Parasitology, 3rd Edition. Springer-
Microsporidia which now are classified Verlag. 1573 pp.
within Fungi. All the other parasites are
9. Odening K (1976) Conception and
members of Kingdom Animalia. Table
Terminology of Hosts in
1.4 lists the major phyla and classes of
Parasitology. Advances in
parasites. The right column from the
Parasitology 14:1-93.
table lists the most widely used terms in
English. 10. Paracer S, Ahmadjian V (2000)
Symbiosis: An Introduction to
Biological Associations. Oxford
University Press. 304 pp.
Selected references and further
reading 11. Roberts L, Janovy J (2008)
Foundations of Parasitology, 8th
1. Bowman DD (2008) Georgis' Edition. McGraw-Hill. 728 pp.
Parasitology for Veterinarians, 9th
12. Schmid-Hempel P (2011)
Edition. Saunders. 464 pp.
Evolutionary Parasitology: The
2. Bush AO, Fernández JC, Esch GW, Integrated Study of Infections,
Seed JR (2001) Parasitism: The Immunology, Ecology, and
Diversity and Ecology of Animal Genetics. Oxford University Press.
Parasites. Cambridge University 496 pp.
Press. 576 pp.
13. Soanes C (2008) Compact Oxford
3. Cox FEG (2002) History of Human English Dictionary of Current
Parasitology. Clinical Microbiology English. Oxford University Press.
Reviews 15:595-612. 1210 pp.
4. Elsheikha HM, Khan NA (2011) 14. Taylor MA, Coop RL, Wall RL (2007)
Essentials of Veterinary Veterinary Parasitology, 3rd
Edition. Wiley-Blackwell. 600 pp.
15. Thomas F, Renaud F, Guégan JF Parasitism. Oxford University Press.

(2005) Parasitism and Ecosystems. 240 pp.
Oxford University Press. 232 pp.
17. Webster's New World Medical
16. Thomas F, Guégan JF, Renaud F Dictionary (2008) 3rd Edition.
(2009) Ecology and Evolution of Wiley. 480 pp.
2 PROTOZOA
2.1 General considerations apparatus, lysosomes, ribosomes, rough

and smooth endoplasmatic reticulum and
Recent phylogenetic studies brought a nucleus with the genetic material
apparent chaos to traditional systematics organized in chromosomes. The nucleus
of living organisms. Through time, is separated by the rest of the cytoplasm
unicellular eukaryotic organisms were by a nuclear membrane, hence the name
included in various taxonomic groups. eukaryote (Greek: eu = true; karyon =
Currently, they are all referred to with nucleus). The number, structure and
the name Protista. However, this term position of these organelles within each
has no taxonomic ranking. Within cell are highly dependent on the
protists we include autotrophic, taxonomic group.
heterotrophic and phototrophic
Parasitic protozoa can inhabit virtually all
organisms. Traditionally, all
organ systems and tissues of their host,
heterotrophic protists are included in the
with both intracellular (i.e.
group known as Protozoa.
apicomplexans) or extracellular (i.e.
Protozoa are found in all possible flagellates, ciliates) locations. Some of the
habitats and include free-living or parasitic protozoa cannot survive in the
symbiotic forms. Among the later, environment (i.e. flagellates) and
parasitic protozoa can be associated with therefore are transmitted from host to
all types of hosts, from plants to animals. host by direct contact or using living
Protozoans are a group of very old and vectors (i.e. arthropods). In some other
divers unicellular organisms, groups (i.e. apicomplexans) when
hypothetically originating from the long eliminated by the hosts to the
coevolution of two or more symbiotic environment, they transform into
prokaryotic cells. With this view, the resistant stages, like cysts or oocysts.
mitochondria and the chloroplasts from Parasitic protozoans obtain their food
the eukaryotic cells were originally from their hosts. Mechanisms used for
prokaryotic endosymbionts of larger uptake of nutrients include phagocytosis,
cells. All protozoans have a typical pinocytosis, osmosis or active ingestion
eukaryotic structure of the cell. The cell via a cell “mouth” called cytostome.
membrane may be naked or covered with Maybe the most heterogenic process in
locomotion structures like cilia or protozoa is reproduction. Some groups
flagella. Within the cytoplasm, the use only asexual reproduction (binary
organelles include mitochondria, Golgi fission or cell division). All flagellates use
37 | P r o t o z o a
this multiplication mechanism. Some within the metazoans while

other groups employ also sexual Microsporidia is within Fungi.
reproduction. In apicomplexans, the
fecundation of micro- and macrogametes
is a typical phase of the life cycle. Ciliates 2.3 The flagellated protozoa
use conjugation to exchange genetic
information during multiplication. Flagellates are motile protozoans, many
Protozoans are extremely important from of them free-living, but some pathogenic
medical point of view. In humans, to humans and animals. The locomotory
diseases like malaria, sleeping sickness or structures are known as kinetids. The
Chagas’ disease are responsible for genera of medical importance are
millions of fatalities every year. In currently included into three phyla (table
domestic animals protozoans cause 2.1).
massive economic losses especially in They infect almost all animal phyla
tropical areas (i.e. Nagana of livestock) occupying various habitats within their
but also worldwide (i.e. eimeriosis of host, with either extra- or intracellular
poultry). Last but not least, several location. Most of the species feed by
parasitic protozoans are transmissible osmosis and reproduce by binary fission.
from animals to humans. These zoonotic
Phylum Euglenozoa includes a single
conditions include toxoplasmosis,
class of medical importance, Class
sarcocystoses or leishmaniosis. All major
Kinetoplastea (table 2.1). The class
groups will be detailed in the following
comprises of organisms with a
sections.
kinetoplast, a cell organelle containing a
particular type of mitochondrial DNA.
The kinetoplast is located close to the
2.2 Diversity of parasitic Protozoa basal body of the flagellum, and is easily
visible at Giemsa staining as a deep
Several classifications of protozoans are
purple dot. Several genera are included
available in the literature, and apparently
here, but only two will be considered in
none is generally accepted. Several
this book, as the others are parasitic
complex phylogenetic approaches gave
mostly in invertebrates. All diseases
birth to new clades, but these will not be
produced by members of this phylum are
considered here. Herein, we chose an
treated under Chapter 2.3.1 and the
adaptation of the revised classification of
members will be generically called
eukaryotes by Adl et al 2012.
kinetoplastids.
The protozoans of veterinary importance
Phylum Parabasalia includes organisms
are grouped in five phyla (see text
which have a parabasal apparatus. The
below). Other higher ranked taxonomic
kinetid consists of four kinetosomes.
groups, previously included within
Three classes of veterinary significance
Protozoa were shown to be distinct
are included here (table 2.1). Most
groups. Myxozoa are currently included
genera of medical importance in this
phylum were formerly known as trichomonoses and will be discussed in

trichomonads. In general, they possess a Chapter 2.3.2.
variable number of flagella, according to
Phylum Fornicata includes species with
genus. In most of the cases, they have a
single or one pair each of kinetids and
group of flagella at their apical pole and
nuclei. They usually possess a feeding
an additional recurrent flagellum which
groove or a cytopharyngeal tube
runs backward, along an undulating
associated with each kinetid. The phylum
membrane. Each flagellum originates in a
includes two classes of medical
basal body. Another common feature of
importance (table 2.1). Although genus
species from this group is the presence of
Chilomastix is currently included here
an axostyle. This structure plays the role
and not considered to be related to
of a cytoskeleton. Generally, this group
trichomonads, it will be listed under the
lacks mitochondria. All the species in this
chapter referring to them (2.3.2). Genus
group will be referred to as
Giardia and giardiosis will be discussed
trichomonads. They are responsible for a
separately in chapter 2.3.3.
group of diseases medically known as
Table 2.1 Current classification of flagellates parasitic in domestic animals (adapted after Adl et al. 2012)
Phylum Class Genera Disease (Chapter)

Euglenozoa Kinetoplastea Trypanosoma Equine dourine (2.3.1.1)
Vector-borne trypanosomoses in
domestic animals (2.3.1.2)
Leishmania Canine leishmaniosis (2.3.1.3)
Feline leishmaniosis (2.3.1.4)
Parabasalia Tritrichomonadea Tritrichomonas Genital trichomonosis in cattle
(2.3.2.1)
Intestinal trichomonosis in birds and
mammals (2.3.2.4, 2.3.2.5)
Histomonas Histomonosis of poultry (2.3.2.6)
Trichomonadea Trichomonas Anterior digestive trichomonosis in
birds (2.3.2.3)
Tetratrichomonas Buccal trichomonosis in dogs and cats
(2.3.2.2)
Intestinal trichomonosis in birds and
mammals (2.3.2.4, 2.3.2.5)
Pentatrichomonas Intestinal trichomonosis in domestic
mammals (2.3.2.5)
Hypotrichomonadea Trichomitus Intestinal trichomonosis in domestic
mammals (2.3.2.5)
Fornicata Retortamonadea Chilomastix Intestinal trichomonosis in birds
(2.3.2.4)
Trepomonadea Giardia Giardiosis in domestic animals

(2.3.3.1)
body and running forward along an

2.3.1 Kinetoplastids
undulating membrane).
Introduction. Kinetoplastids include The trypomastigote (figure 2.2) is the
several genera parasitic in invertebrates, most important stage from diagnostic
vertebrates and plants. Only two genera point of view, as it is the most frequently
(Trypanosoma and Leishmania) are of encountered in the blood of the
veterinary importance. The main feature vertebrate host. Its trepan (= drill) shape
of Trypanosomatidae is the presence of a gave the name to the genus. The
single flagellum and a kinetoplast. Based trypomastigotes are usually lanceolate in
on their life cycles, members of this shape, like a flat elongated blade, oval or
family are either homoxenous or elliptic in transverse section and with
heteroxenous. All species parasitic in tapering ends. Conventionally, the
domestic animals are heteroxenous, with anterior end is considered the one
stages alternating between the directed forwards during locomotion.
invertebrate and the vertebrate host. The body surface of trypanosomes is
However, a single species, namely covered with a periplast. The main cell
Trypanosoma equiperdum is transmitted organelles are the nucleus, the
directly by coitus and does not require an kinetoplast and the locomotion system
additional host. (figure 2.1).
General morphology. The morphology The kinetoplast, defining structure of all
of trypanosomatids is heterogenic during members of order Kinetoplastida (hence
different stages of the life cycle. The main the name), is always located in the close
feature distinguishing the morphological vicinity of the basal body. The locomotion
stages of Trypanosomatidae is the system (also known as the mastigont
position of the flagellum. The most system) is represented by the flagellum
common morphological types (figure and the basal body. The single flagellum
2.1) are: amastigote (rounded or originates from the posterior end, then
elongated forms lacking flagellum); runs forward along an undulating
sphaeromastigote (rounded forms with membrane, and freely terminates at the
a free flagellum); promastigote anterior end of the cell. At the starting
(elongated forms with antenuclear point of the flagellum stays the basal
kinetoplast and flagellum arising near it body (also called blepharoplast). Most
but emerging from the cell at the anterior stages are mobile, but mobility is seldom
end); epimastigote (elongated forms observed, as most morphological
with juxtanuclear kinetoplast and examinations require fixation and
flagellum arising near it but emerging staining.
from the side of the body);
Ecology and transmission. With the
trypomastigote (elongated forms with
exception of T. equiperdum, all species of
postnuclear kinetoplast; flagellum arising
Trypanosomatidae parasitic in
near it, emerging from the side of the
vertebrates have heteroxenous
development. Vertebrates are considered
definitive hosts and invertebrates are the invertebrate host. This cyclic (indirect)
intermediate hosts, also referred to as transmission is the typical one for
vectors. For all species parasitic in heteroxenous trypanosomes. In some
mammals, the intermediate hosts are cases, direct transmission from mammal
insects from orders Hemiptera (true to mammal was reported, when blood
bugs), Diptera (true flies) and stages are mechanically passed by
Siphonaptera (fleas). The insects take up hematophagous insects or by syringe
the bloodstream forms of the parasites inoculation of infected blood. However,
when feeding on infected mammals. In the ability of vectors to mechanically
the insect intermediate hosts, they transmit the disease is measured in
undergo a cycle of development with the minutes, while the typical cyclic
final production of special infective forms transmission equals sometimes the
called metacyclic (Greek: meta = after) whole life duration of the insect.
trypanosomes. These are transmitted to a
Medical importance. Diseases caused by
new definitive vertebrate host by various
members of genus Trypanosoma have the
ways, according to the location of the
generic name of trypanosomoses
final developmental stage within the
(singular: trypanosomosis). Most of the
vector. Transmission from vector to the
infections occur in tropical areas of the
mammal occurs only after the
world where they cause severe, often
trypanosomes have completed their
lethal conditions in humans and animals
entire cycle of development in the
as well.
Figure 2.1 Main stages of trypanosomes: a - amastigote; b - sphaeromastigote; c -

promastigote; d - epimastigote; e - trypomastigote.
Figure 2.2 General structure of a trypomastigote, the blood stage of trypanosomes.
The only pathogenic species occurring in signs to what we know today as dourine.
temperate areas seems to be T. Apparently, the first description belongs
equiperdum, the agent of equine dourine. to the Byzantine veterinarian Chiron in
Many other trypanosomes are not his book on the diseases of horse,
pathogenic, although infections are “Mulomedicina Chironis” (~ 400 AD).
common worldwide. Genus Leishmania is Dourine is mentioned also in a treatise of
responsible for several infectious veterinary medicine published in the 12th
conditions in humans and animals century by the Arabian, Ibn-al-Awan in
worldwide. Among domestic species, Seville. The first description of the
dogs and cats are the only common hosts disease in Europe was done in a Prussian
to these parasites. horse by Ammon and Dirkhausen in
1796. The causative agent was seen for
the first time by Rouget in 1894, who
2.3.1.1 Equine dourine demonstrated its presence in the blood of
an Algerian horse. In 1900, Buffard and
Dourine (Arabic: darina = mangy, dirty), Schneider reproduced dourine in a horse
also known as the covering disease, is a after they subcutaneously injected the
chronic protozoal disease, with venereal parasite isolated from a naturally
transmission, naturally occurring in infected horse. One year later, in 1901,
equids. It is eradicated in most of the Doflein described and named the
countries but is still present in parts of causative agent Trypanosoma
Africa and Asia. Main clinical signs equiperdum.
include edematous lesions of the Etiology. In classical parasitology
genitalia, typical skin plaques and textbooks, the agent of equine dourine is
paralytic nervous signs, usually followed considered to be Trypanosoma
by death. equiperdum. Recent molecular analysis of
Historical notes. Ancient Arab texts different laboratory strains originating
mention a disease in horses with similar from endemic areas, brought controversy
on the validity of this species. medial position. The length of T.

Trypanosoma equiperdum is very closely equiperdum ranges from 15.6 to 31.3 m
related to several subspecies of in Asian strains and from 22.3 to 29.0 m
Trypanosoma brucei: T. brucei brucei, T. in Russian strains.
brucei gambiense and T. brucei
Life cycle. T. equiperdum is the only
rhodesiense, all agents of African
trypanosome not transmitted by an
trypanosomoses in a variety of hosts, but
invertebrate vector. Transmission occurs
also to Trypanosoma evansi, which causes
mainly during mating from stallions to
a disease called Surra. Some authors
mares and vice versa. There are some
suggest considering the agent of dourine
reports stating that foals from infected
as a subspecies of T. brucei (T. brucei
mothers can get the infection through
equiperdum). Until the status of the
their conjunctival mucosa during birth or
species will be clarified, the conventional
even through milk contaminated from
name T. equiperdum will be used herein.
lesions of the udder. Transmission by the
Several natural strains were described means of unsterilized instruments used
over time, varying mainly in for artificial insemination has also been
pathogenicity. Even if in the last decades cited.
no single strain was isolated from natural
Unlike other species of the genus, T.
infections, at least 12 laboratory strains
equiperdum is primarily a tissue parasite
are available worldwide (table 2.2).
which rarely invades blood. They are
extracellular parasites, typically
Table 2.2 Available laboratory strains of T. inhabiting the surface of the mucosa or
equiperdum* between the epithelial cells. In stallions,
they are found also in the seminal fluid.
Code Origin Host
BoTat 1.1 Morocco, Horse Later in the course of infection they
1924 invade also surrounding tissues or even
STIB 818 China, 1979 Horse
OVI South Africa, Horse blood.
1977
ATCC 30019 France, 1903 Horse Nutrition takes place by osmotic
ATCC 30023 France, 1903 Horse absorption of dissolved substances from
American America (?) Horse
stabilate the host’s tissues, through the body
Canadian Canada (?) Horse pellicle.
stabilate
Alfort (?), 1949 Horse Experimental infection of laboratory
AnTat 4.1. (?) (?)
Hamburg (?) (?) animals is possible, but difficult. In order
SVP (?) (?) to establish the infection in murine
TREU 2259 (?) (?)
rodents, first inoculation using a natural
* - modified from Claes et al. (2005)
strain should be done in splenectomized
animals. Once the strain becomes
Morphology. T. equiperdum is a
adapted, it can be subsequently passed
monomorphic species of trypanosome,
virtually for unlimited times. Wild strains
morphologically indistinguishable from T.
can be adapted after several passages to
evansi. The nucleus is usually located in
laboratory animals (mice, guinea pigs, Pathogenesis. All the lesions and
rabbits, dogs), but they change their symptoms of dourine are related to the
pathogenic properties. However, first histotropism of T. equiperdum for the
inoculation form naturally infected epithelial tissues of the genital mucosae
horses typically fails. Attempts to infect or skin. After the onset of the infection,
domestic ruminants or pigs resulted in the flagellates invade also surrounding
inapparent disease and low or no tissues. It is questionable if they are able
detectable parasitemia. to penetrate intact mucosae or they
priory need some degree of abrasion.
Epidemiology. Since the 19th century,
However, it seems they invade local
dourine has occurred sporadically in
capillaries.
Europe. Around 1918, the disease was
reported only in Russia, Turkey, Hungary The local effect is considered to be
and Spain. During World War II, the induced by a toxin secreted by the
disease was spread by army into Western parasite which causes vasomotor
Europe. After the war, dourine was disturbances with exudation of the
eradicated from Western Europe by plasma and inflammatory reaction in the
systematic screening and control, invaded tissues. The nervous damages
including stamping out. are considered to be also the result of the
toxin, carried systemically by the blood
Currently, natural infections occur only in
stream. If all the motor and sensory
horses, donkeys and their hybrids in
alteration can be attributed to nerve
Africa, Asia and parts of Russia.
damage, the emaciation is due to the
Occasional outbreaks are known
secondary atrophy of the muscles.
sporadically from Europe, following
However, the toxin was never isolated,
international trade with horses. Official
but other proof which sustains the toxin
OIE reports state that the only countries
hypothesis is the sudden death of
where dourine occurred in the last years
laboratory rodents infected with a high
are: Botswana, Mongolia, Ethiopia,
number of parasites.
Kyrgyzstan, Namibia, Pakistan, Russia
and South Africa. This officially reported Not all strains of T. equiperdum invade
distribution of the disease may not be the blood stream of horses. Parasitemia is
accurate because testing of horses in more common in laboratory rodents
many countries is not being done where trypanosomes invade the blood 2-
routinely. 3 days after the inoculation.
All equines are theoretically susceptible Immunology. As some species of equids

to the infection with T. equiperdum. or some breeds of horses are naturally
However, the donkeys and mules are resistant to infections, there is certainly
more tolerant than horses. Even among an inborn immunity acquired through a
horses, there is an evident difference in long parasite-host coevolution. The
sensibility, with thoroughbred breeds immune factors responsible for the
more susceptible than native ones. defense against the agent of dourine
include both humoral and cellular types,
with an important role of phagocytosis. The chronic disease is conventionally

There are some evidences that passive divided into three phases. During the
immunity can be transmitted from first phase of the infection, the common
immune mares to foals during pregnancy. lesions are localized within external
genitalia. In mares, the first usual sign of
Despite many other similarities, there is
infection is a small amount of vaginal
no cross immune protection between T.
discharge. Swelling and edema of the
equiperdum and T. evansi. Moreover, T.
vulva develop later and extend along the
equiperdum is able to periodically shift its
perineum to the mammary glands and
surface glycoprotein antigens, allowing
ventral abdomen, accompanied by
chronic, persistent infections.
vulvitis, vaginitis, polyuria and elevated
Clinical signs. Symptoms vary tail. These last signs mimic heats, and
considerably, depending mostly on the usually mares are receptive to males. If
infecting strain. Those originating in pregnant, abortion may take place when
northern Africa, Europe and Asia seem to the infection is with more virulent strain.
be more virulent than those from In stallions, the initial signs are edema of
southern Africa and from the former the prepuce and glans penis, of variable
American strains. The nutritional status degree which may spread to the scrotum,
of the animal and other stress factors can perineum, ventral abdomen and thorax.
influence the severity of symptoms. Paraphimosis may is not uncommon. In
The incubation period is variable. Clinical both sexes, the swelling may resolve and
signs usually appear within a few weeks reappear periodically. Following edema,
of infection but may not be evident until vesicles and ulcers usually appear on the
after several years. Although acute, genitalia. They may heal and leave
asymptomatic or latent infections are permanent white scars, called
known, the most common character of leukodermic patches. In some outbreaks,
the dourine in horses is chronic. The conjunctivitis and keratitis are common
duration of the disease in mild chronic ocular signs in infected animals. The
cases may persist for 1-2 years, and second stage of chronic dourine is more
occasionally up to 4-5 years. or less pathognomonic. Typical cutaneous
Experimentally, horses infected with plaques or skin thicknesses can occur,
laboratory have survived for up to 10 with sizes ranging from extremely small
years after infection with these strains. In to several centimeters. Interestingly,
more severe chronic cases, animals die these plaques have also been observed
after several months. In acute forms, sporadically in animals infected with T.
disease lasts for 1-2 months, or, evansi. To complicate the understanding
exceptionally one week. As a rule, of the taxonomic status of the causative
dourine is a fatal disease and the average agent, in the case of certain strains of T.
mortality is about 50%. Recovery can equiperdum these typical skin lesions do
occur spontaneously, especially in not occur. The third phase usually onsets
stallions. after several month from the infection
and is characterized by progressive
anemia and disorders of the nervous in North America and Europe. Also
system. Initially these signs consist of xenodiagnosis is considered feasible.
restlessness and the tendency to shift
Direct parasitological diagnosis by
weight from one leg to another followed
observing the flagellates in samples is
by progressive weakness and
achievable in the first 4-5 days of the
incoordination. Paralysis of the hind legs
infection. Scrapings of the vaginal mucosa
and paraplegia and ultimately
in mares or urethral washings in stallions
recumbency and death are the final
are recommended in this case. In the later
stages of infection.
stages of the infection the parasites may
All these symptoms are characterized by be found in aspiration of fluids from
periods of exacerbation and relapse that edema and cutaneous plaques, especially
may vary in duration and occur several shortly after eruption.
times before death. Recovery is also
possible, especially in infection with less
virulent strains. The disease caused by
more virulent strains is often acute and
the mortality rate is higher. In other
equids (i.e. zebras) animals can be
positive and show no clinical signs.
Pathology. If the outcome of the disease

is death, anemia and cachexia are the
most evident lesions of gross necropsy.
Signs of early disease like edema can be
found as indurated areas on the genitalia
or ventral parts of abdomen and thorax.
Internal lymph nodes are hypertrophied.
If nervous signs occurred before the
death of the animal, perineural Figure 2.3 Trypanosoma equiperdum in a
connective tissue is infiltrated with blood smear from an artificially infected
edematous fluid and a serous infiltrate rodent. (Photo Andrei D. Mihalca)
may surround the spinal cord, especially
in the lumbar or sacral regions.
Detection in blood smears from naturally
Diagnosis. Most commonly, the diagnosis infected horse is exceptional, but possible
is based almost exclusively on clinical in laboratory rodents (figure 2.3). In
signs. As the isolation of the parasite from countries where other trypanosomoses
infected tissues or blood is rather than dourine occur in horses, the
difficult, other laboratory methods were morphological differentiation of T.
used through time for etiological equiperdum from other species (i.e. T.
diagnosis. The use of complement evansi and T. brucei) is impossible.
fixation test (CFT) was widely spread in
implementation of eradication programs
Xenodiagnosis (inoculation of suspicious solution injected im with a

samples to laboratory animals) was second injection after 24 h at half
successfully achieved in splenectomized dose;
animals or after intratesticular injections
 suramin: 10 mg/kg bw, given iv
in rabbits.
for two or three treatments at a
Serology has been used in combination weekly interval;
with clinical diagnosis. The complement
 quinapyramine dimethylsulfate:
fixation test (CFT) is the recommended
3-5 mg/kg bw in divided doses
test for international trade. Uninfected
injected sc.
equids, mainly donkeys and mules, often
show false positive results due to Control. As no immune prophylaxis
anticomplementary effects in horse measures are available, the most effective
serum. Indirect fluorescent may help to way for preventing and controlling the
resolve these cases. Other serologic tests disease are systematic surveys for
include ELISA, radioimmunoassay, identifying positive animals by serology.
counter immunoelectrophoresis, agar CFT has been used successfully for
gel immunodiffusion (AGID) and card eradication programs in North America
agglutination. However, cross-reactions and Europe. Infected animals should be
can occur, especially with T. brucei and T. euthanized or castrated to prevent
evansi, but correlations with clinical signs further transmission. All equids in areas
might be helpful. A test that can where dourine is diagnosed should be
distinguish equine piroplasmosis, quarantined and breeding should be
dourine and glanders by immunoblotting stopped for until no new positive cases
has been developed in USA but it is not are found. To avoid accidental
commercially available. transmissions in endemic areas, during
artificial breeding, all instruments should
Differential diagnosis is done against
be sterilized properly. In dourine free
coital exanthema, contagious equine
countries, importation of horses from
metritis, Surra, Nagana, anthrax, equine
endemic countries should be prohibited.
viral arteritis, equine infectious anemia,
purpura hemorrhagica, malnutrition,
helminth infestations etc.
2.3.1.2 Vector-borne
Treatment. Although reported in some
trypanosomoses in domestic animals
endemic areas, treatment is not
recommended as asymptomatic infected Vector-borne trypanosomoses include
carriers may result. If attempted, mainly tropical infections of humans and
treatment should be done with animals caused by several species of
trypanocidal drugs. Suggested treatments genus Trypanosoma (table 2.3). Two
include: severe diseases affect humans: the
 diminazene aceturate (i.e. sleeping sickness in Africa and the Chagas
Berenil): 7 mg/kg bw, as a 5% disease in South America.
Table 2.3 Main vector-borne trypanosomoses of animals and men*
Main vertebrate
(Sub)Species Disease Vector Transmission Distribution
host
T. theileri cattle, antelopes Nonpathogenic Tabanidae Feces Worldwide
T. rangeli humans, wide Nonpathogenic Reduviidae Bite South
range of domestic America
and wild
mammals
T. lewisi rats, humans (?) Nonpathogenic Rat fleas Feces Worldwide
(?)
T. cruzi humans, virtually Chagas’ Disease Reduviidae Feces South
all mammals America
T. evansi camels, equines, Surra Tabanidae Mechanical Asia, Africa,
bovines, goats, Stomoxys Australia,
dogs and wild spp. South and
animals Central
America
T. vivax ruminants, Nagana Glossina Bite Africa, South
equines, camels (Souma) spp. Mechanical America
Tabanidae
T. congolense bovines, equines, Nagana Glossina Bite Africa
sheep, goats, spp.
camels, pigs, dogs
T. simiae pigs, camels, Nagana Glossina Bite/Mechanical Africa
horses, cattle spp.
T. suis pigs Nagana Glossina Bite Africa
spp.
T. brucei brucei domestic animals, Nagana Glossina Bite Africa
camels, antelopes, spp.
carnivores
T. brucei humans, pigs, Sleeping Glossina Bite Africa
gambiense sheep sickness spp.
T. brucei humans, cattle, Sleeping Glossina Bite Africa
rhodesiense pigs, goats, dogs, sickness spp.
primates, various
wild animals,
including
antelopes
* Compiled from Maudlin et al. (2004)
Trypanosomoses bear different names in in 1680. However, the first accurate

animals, according to their geographical description of a blood stage was done in
distribution and etiologic agent. 1841 by Gabriel Valentin (1810-1883) in
However, some vector-borne blood smears from trouts. The genus
trypanosomoses are also present in Trypanosoma was erected in 1843 by
temperate areas (i.e. the T. theileri David Gruby (1810-1898) for
asymptomatic infections of cattle hemoflagellates found in the blood of
worldwide). frogs.
Historical notes. Probably the stages of The first major discovery from medical
the first seen trypanosome were those of point of view came only in 1880, from
T. theileri from the gut of horse flies, by Griffith Evans (1835-1935). While
Antonie van Leeuwenhoek (1632-1723) working as a veterinarian in India, he
discovered the agent of Surra, a disease of importance, T. theileri, T. rangeli, T. lewisi

local horses and camels. Later, the and T. cruzi are included in this group.
species was named in his honor, T. evansi. They always possess a free flagellum. The
Another major milestone in the history of kinetoplast is large and it is never located
trypanosome research was represented terminally. The posterior end of the body
by the works of David Bruce (1855- is pointed. Reproduction in the
1931). Between 1894 and 1897 when he mammalian host is discontinuous,
was working in southern Africa, he typically taking place in the amastigote or
proved that the disease of livestock epimastigote stages. With the exception
known as Nagana was also caused by a of T. cruzi, the other species are not
trypanosome. As a tribute for him, this pathogenic.
species was later named T. brucei. Bruce
The salivarian trypanosomes include
was the first scientist to prove the vector-
those species in which the metacyclic
borne nature of trypanosomoses. He
trypomastigotes develop in the “anterior
demonstrated that Nagana is transmitted
station” (proboscis and salivary glands)
from wild to domestic animals by the bite
and the transmission is inoculative.
of tsetse flies. Interestingly, the same
Species from this group include: T. vivax,
hypothesis, though not proved, was
T. congolense, T. simiae, T. brucei, T. evansi
suspected 40 years before Bruce’s
and T. suis. The free flagellum may be
demonstration by the famous British
present or absent and the kinetoplast is
explorer of equatorial Africa, David
always located subterminally or
Livingstone (1813-1873). Joseph Dutton
terminally. The posterior end of the body
(1879-1905) was the first to describe the
is usually blunt. Reproduction in the
agent of sleeping sickness in humans, T.
mammalian host is continuous and takes
gambiense. He died three years later by
place in the trypomastigote stage. Most of
the disease he had been studying.
the species are pathogenic to mammals.
Etiology. There are several species of
Morphology. Specific morphological
genus Trypanosoma involved in the
details for the stages in the blood of
etiology of vector-borne trypanosomoses
vertebrates of each species were given
of domestic and wild mammals (table
above. Nevertheless, morphologic
2.3). Traditionally, members of genus
identification to species level is not
Trypanosoma parasitic in domestic
generally feasible, and new molecular
animals are divided into “Stercoraria”
techniques tend to replace the traditional
and “Salivaria”.
microscopy for this goal. All
The stercorarian trypanosomes (Latin: morphological characters given below
stercoralis = living in feces) comprise refer to the stage from the blood of the
species in which the development of the vertebrate host. T. theileri (figure 2.4) is
metacyclic stages in the vector takes a common, non-pathogenic parasite
place in the fecal medium of the hind gut inhabiting the blood of various domestic
(“posterior station”) and transmission is and wild ruminants worldwide. It is one
contaminative. Among species of medical of the largest mammalian trypanosome
(60-70 m in length). The posterior end report from Malaysia, where the species
of the body is pointed. The kinetoplast is has been isolated from a human clinical
located near the nucleus, the later being case.
positioned centrally in the cell. The
T. cruzi has a wide host range. More than
undulating membrane is well developed
150 species of mammals were reported
and the free part of flagellum relatively
to be infected with this species, and
long.
virtually all mammals are considered to
be susceptible. It causes the Chagas
Disease, a severe condition of humans
from several South American countries.
The species is a small, “C” shaped
trypanosome, measuring 16.3-21.8 m in
length. The large kinetoplast is located
near the posterior end of the cell.
T. evansi is probably the widest

distributed pathogenic trypanosome,
causing a disease called Surra. Infection
occurs in many hosts, but the most
important include dromedaries, equines
and dogs. The trypomastigotes (16.8-24.9
m) are usually slender, with a long free
Figure 2.4 Trypanosoma theileri in a flagellum and a rounded posterior end.
blood smear from a naturally infected However, the species is quite
cow. This species does not seem to be polymorphic, and stumpy or intermediate
pathogenic for their bovine or wild hosts forms have been described.
(Photo Viorica Mircean) There are several species of the genus
Trypanosoma listed as the agents of a
group of diseases of livestock from Africa,
T. rangeli is a non-pathogenic species collectively called Nagana: T. vivax, T.
infecting humans and a multitude of wild congolense, T. simiae, T. suis and T. brucei.
and domestic mammals. The
trypomastigotes are slender and large T. vivax causes a disease called Souma in
west, central, east and South Africa. Its
(26-34 m). The kinetoplast is
hosts are various ungulates (cattle, sheep,
subterminal and relatively small.
goats, horses, camels, antelopes). It was
T. lewisi is parasitic in rats worldwide. also introduced to West Indies, Central
The body is curved and pointed at the and South America together with cattle
posterior end, with a mean length of 21- imported from Africa.
37 m. The well-developed free flagellum
In the New World, the disease got the
delimitates a more or less developed
various names (Secadera, Huequera,
undulating membrane. There is a single
Cacho Hueco) and interestingly, became
transmitted mechanically by non-tsetse

vectors (horse flies and stable flies).
Mean length is between 21.0 and 25.4
m. There are two recognized
subspecies: T. vivax vivax (in Africa) and
T. vivax viennei (in the New World).
T. congolense infects a broad spectrum of

domestic hosts. It is a small species, with
a mean length between 11.5 and 14.0 m.
There are several strains with no
taxonomic status which differ in certain
morphological feature but also virulence.
T. simiae is primary a parasite of pigs,

Figure 2.5 Trypanosoma brucei from
with high pathogenic importance, though
laboratory culture. (Photo Andrei D.
the name is misleading, meaning “of
Mihalca)
monkeys”. Morphologically, the species
resembles T. congolense but it is more
motile. The average length is 14.9-19.0 Life cycle. General aspects regarding
m, with the kinetoplast typically development and biology of
occupying a marginal position near the trypanosomatids were given above. Yet,
posterior end of the body. each species has its own peculiarities.
T. suis parasitize suids in several regions The metacyclic trypanosomes of the
of Africa, being relatively pathogenic. It stercorarian species (T. theileri, T.
exhibits slow movements. The body is rangeli, T. lewisi, T. cruzi) develop in the
short and stumpy (14.0-16.0 m), with a posterior part of the vector’s gut and are
small kinetoplast in subterminal position. discharged through the feces of the
T. brucei (figure 2.5) includes several insect. The metacyclic stages then invade
strains, some of them assigned to the vertebrate host through the wound
subspecies. T. brucei gambiense and T. caused by the insect bite, through skin
brucei rhodesiense are responsible for abrasions or other wounds. If infected
human sleeping sickness. insects are swallowed by vertebrates,
trypanosomes may enter the
Another subspecies, T. brucei brucei bloodstream through various contact
completes the list of etiologic agents of mucosae. Inside the mammalian body,
Nagana of livestock in Africa. The development of trypanosomes varies
trypomastigotes of the later subspecies according to species.
are polymorphic, with slender,
intermediate and stumpy forms with In T. theileri, T. lewisi multiplication is by
wide variation of the cell’s average binary or multiple fission of
length, between 11.0 and 42.0 m. epimastigotes in the plasma of blood. In
T. cruzi binary fission of amastigotes
takes place inside the reticuloendothelial Glossina (figure 2.6). Transmission from
cells (i.e. macrophages) from the liver, the vector to the vertebrate host is
spleen or bone marrow but also in inoculative, through the saliva.
myocardial tissue.
In T. vivax, trypomastigotes from the
Various intermediate hosts were blood of the vertebrate host multiply by
reported for stercorarian trypanosomes: binary fission. When ingested by tsetse
flies, they become epimastigotes in the
 For T. theileri the vectors are
esophagus, than multiply and migrate to
tabanids (horse flies). Several species
the pharyngeal region where they
were proven to transmit the
transform to metacyclic trypanosomes.
parasites to cattle: Tabanus
These are the infective stages and are
glaucopis, T. striatus and
inoculated to a new vertebrate host.
Haematopota pluvialis. Some authors
There are several species of Glossina
suggested that also hippoboscids are
reported as vectors for T. vivax: G.
feasible vectors for T. theileri.
morsitans, G. pallidipes, G. longipalpis, G.
 For T. rangeli the intermediate hosts swynnertoni, G. austeni, G. palpalis, G.
are bugs of subfamily Triatominae fuscipes, G. tachinoides, G. vanhoofi, etc. In
(family Reduviidae). The main geographical areas where tsetse flies are
vectors are Rhodnius prolixus, R. not present (parts of Africa, South
pallescens, Triatoma infestans, T. America), tabanids are able to transmit
dimidiata and many other the disease mechanically, by bite.
experimental insect hosts.
 T. lewisi is transmitted by rat fleas. In

temperate areas, the main vector is
Nosopsyllus fasciatus while in tropical
and sub-tropical regions the natural
vector is Xenopsylla cheopis. Many
other flea species were infected
experimentally and were able to
transmit the trypanosomes.
 T. cruzi is using as vectors bugs of

Triatominae subfamily. Many species
were reported as insect hosts, the
most important genera being
Triatoma, Rhodnius, Panstrongylus
and Eratyrus.
In the other group, Salivaria, the

Figure 2.6 Glossina sp. feeding on human
metacyclic trypanosomes develop in the
host. (Photo Andrei D. Mihalca)
salivary structures of insects. The main
vectors are tsetse flies from genus
In T. congolense the aflagellated parts of Africa free or cleared of tsetse,

trypomastigotes multiply in the blood and parts of Central and South America.
continuously and are transmitted to According to OIE, Nagana is spread over
tsetse flies. After ingestion, they arrive to the territory of 37 countries (mostly sub-
the midgut of the flies, change shape to Saharan African) on 10 million square
longer and slender trypomastigote forms kilometers. It is the most important
which migrate to the pharynx where they disease of cattle in Africa. At least 30
become epimastigotes. Finally the species of wild mammals are known as
epimastigotes transform to aflagellate natural reservoirs for Nagana-causing
infective metacyclic trypomastigotes. The trypanosomes, although they do not
main vectors for T. congolense are: G. show clinical signs of infections. Nagana
morsitans, G. palpalis, G. pallidipes, G. is widespread also because of the high
longipalpis and G. austeni. number of competent biological vectors.
About 23 species of tsetse flies (genus
T. simiae has at least ten species of
Glossina) are competent vectors for
competent vectors in genus Glossina.
trypanosomes. Moreover, an infected fly
However, mechanical transmission by
remains infective for all its life.
other blood-sucking dipterans was
reported commonly. Experimental work,
showed that the complete cyclic
development of T. simiae in G. brevipalpis
takes 20 days.
Only two vector species are known for T.

suis: G. brevipalpis and G. vanhoofi. The
cycle in the tsetse fly takes about 28 days.
All subspecies of T. brucei develop in the

midgut, proboscis and salivary glands of
various Glossina species. In the case of T.
b. brucei, mechanical transmission by
tabanids (horse-flies) or Stomoxys has
also been described.
Epidemiology. The geographical

distribution of animal vector-borne Figure 2.7 Distribution of genus Glossina
trypanosomoses is closely related to the is shown with red shading (redrawn,
distribution of their vectors. African from Leak, 1999)
animal trypanosomoses occur where the
tsetse fly vector exists in Africa, between
Virtually all domestic mammals are
latitude 15°N and 29°S (figure 2.7). As
susceptible to clinical infection with
some species of Trypanosoma can also be
African trypanosomoses. However, there
transmitted mechanically by biting flies,
are several livestock breeds considered
the distribution range of Nagana is also in
to be resistant (known as trypanotolerant
breeds). These include West African infection with the first peak at 14-21 days
indigenous cattle breeds (N’Dama, of infection. This first peak corresponds
Baoule, Muturu, Laguna, Somba and to the first presence of specific
Dahomey), East African zebu breeds antibodies.
(Orma Boran and Maasai zebu) and
Lymphocyte sequestration and increased
African indigenous breeds of small
macrophage population are responsible
ruminants (West African dwarf sheep
for the splenomegaly. The same applies
and goats, and East African goats).
to the liver, which might be increased and
The infection sources are blood, lymph congested due to increased phagocytic
and other fluids of infected animals. activity by Kupffer cells. Trypanosome
infection is also responsible for a more or
Pathogenesis. After the transmission by
less severe pancytopenia. The resulting
tsetse flies, trypanosomes undergo a
anemia is responsible for further pathology
period of multiplication in the dermis and
in the myocardium and blood vessels
subdermis where they enter the afferent
irrigating the heart, finally inducing cardiac
lymphatic vessels.
decompensation. In female cows, chronic
At the inoculation site, a lesion called infection leads to infertility, endometritis
chancre will develop 4-10 days after the and abortion.
tsetse bite. This cutaneous lesion
Blood biochemistry changes in infected
precedes the detection of trypanosomes
animals consist of: decreased cholesterol
in the blood by 4-6 days. The
and lipid concentration, reduced total
development of the chancre is depended
serum lipids, decreased serum albumins
on the infective dose and the rhythm of
and increased globulin. There is no
parasite multiplication but generally its
change in the level of total proteins,
cellular population consists of
calcium, iron or fibrinogen. During
neutrophils, lymphocytes, macrophages
parasitemic phases, the animals are
and mast cells, associated with edema
hypoglycemic. Hematology is
and congestion.
characterized by leucopenia, anemia, and
After a period of multiplication in the thrombocytopenia.
skin, trypanosomes appear in very high
Immunology. The primary immune
numbers in the afferent lymph that
response is targeted mainly on the
drains from the site of vector inoculation.
variable surface glycoproteins (VSG),
Subsequently, the draining lymph nodes
which cover the surface of the parasites.
become significantly enlarged because of
Based on the type of VSG, trypanosomes
B-cell proliferation and local migration of
are grouped in (sero)demes. Reinfection
other leucocytes. Through the lymphatic
of the animals with trypanosomes from
system, the trypanosomes finally gain
the same deme is usually associated with
access to the main blood stream and to
a reduced chancre development. The
the all the internal organs. Detection of
antigenic variability in T. congolense and
trypanosomes in the blood is possible
T. b. brucei is huge; hence development of
usually during the second week after the
immunity against all demes is virtually
impossible. On the other hand, the painful swelling of the skin, of variable
number of VSG types in T. evansi and T. size. The symptoms in the acute phase
vivax is more limited. include high fever, which subsequently is
correlated with the fluctuating
Clinical signs. Despite the diversity of
parasitemia, anemia of variable severity
agents involved in the etiology of
(depending on the breed and age of the
Nagana, many clinical features are
infected animal), enlarged lymph nodes,
common to all domestic animals,
enlarged spleen, weakness and lethargy.
regardless the host or trypanosome
Abortion or birth of weak offspring and
species. However, there are particular
high neonatal mortalities are also
pathogenic characteristics, listed in table
common. In 1-4 weeks after the infection,
2.4.
the animals are unable to rise and death
may occur. If infected animals survive,
Table 2.4 Pathogenicity of Trypanosoma they usually go into the chronic phase.
species causing Nagana in different hosts* This is characterized by a persistent
anemia, stunted growth, decrease of
Degree of severity
productions (i.e. milk) and infertility.
Sheep, goats
However, there is no loss of appetite. The

Donkeys
Camels
Horses
Cattle
(Sub)Species
Dogs
Pigs
chronic phase might last even for years,

before the death of the animals.
T. vivax 3 2 2 1 2 0 0 There are various clinical differences of
T. congolense 3 2 2 2 3 1 2
T. simiae 0 1 0 0 0 3 0 Nagana which are dependent on the host
T. suis 0 0 0 0 0 3 0 species. In local cattle from Africa,
T. brucei brucei 1 2 3 3 3 1 3
0 - nonpathogenic; 1 - mild; 2 - moderate; 3 - severe. Nagana is usually chronic, although
* - from Maudlin et al. (2004) hyperacute forms are also known. The
severe drop in the packed cell volume is
As shown in table 2.3, Nagana is a group correlated with decrease in milk
of diseases caused by various species of production. The anemia in this stage
Trypanosoma, which affects a wide range must be differentiated from other types
of domestic animals in Africa and South of infectious or parasitic anemia (i.e.
America: large and small ruminants, babesiosis, anaplasmosis, strongyles or
camels, horses, donkeys, pigs and heavy tick-infestations). Small
carnivores. ruminants usually display fewer and less
severe symptoms than bovines. However,
There are many descriptions on the
in both sheep and goats, the milk
clinical course of the disease originating
production is significantly decreased and
in observation on natural or
the infection is associated with low
experimental infections. The prepatent
reproductive performance and neonatal
period is 1-3 weeks. In some (but not all)
mortality. In camels, the disease is
animals, at the site of the tsetse fly bite an
usually chronic, rarely lethal. Horses and
inflammatory reaction called chancre
donkeys are very sensitive to T. b. brucei
may develop. This might appear as
Nagana and they usually develop an acute
or hyperacute disease, with subcutaneous Pathology. Four types of lesions are

edema, keratoconjunctivitis, ataxia and associated with trypanosomoses in
paralysis. If affected by T. vivax or T. animals: inflammatory, congestive,
congolense, equids are more resistant, hemorrhagic and degenerative affective
and they develop chronic or various organs: skin, lymph nodes,
asymptomatic infections. In pigs, spleen, liver, heart, central nervous
infections are rare, and clinical, severe, system, eyes, testes, ovaries etc.
acute forms are likely to be caused by T.
The characteristic skin lesion is called
simiae. The other Nagana-causing species
chancre, and if it is visible
are responsible for reproductive
macroscopically it appears as a 2-5 cm
disorders in pigs. In dogs, the infection
swelling at the site of vector bite.
with T. b. brucei produces and acute
Histological sections show edema and
disease, with high fever, generalized
mast cell degranulation at the site of
edema, keratitis and rabies-like
trypanosome initial development in the
symptoms, followed by death.
skin.
The other animal trypanosomosis, Surra,
The gross appearance of lymph nodes is a
is more widely distributed (Africa, Asia,
marked increase in size. This
South America) than Nagana and its
enlargement is evident mainly in the
specific pathogenicity is different. The
nodes draining the lymph from the site of
agent, T. evansi is producing severe
the infected tsetse bite. Histologically,
syndromes in camels, horses and dogs,
this enlargement corresponds to a
with significant mortalities. In camels,
proliferation of B cells, with expansion of
Surra is usually acute in young camels
lymphoid follicles in the cortical and
and pregnant females and it evolves with
medullar areas and reduced paracortex.
high fever, anemia, extreme weight loss,
subcutaneous edema, kerato- The spleen is increased in size during the
conjunctivitis, hypertrophy of lymph acute phase. The associated
nodes, neurological signs, abortions and histopathology consists of development
death. In horses from Africa and Asia, the of secondary lymphoid follicles and
disease is similar to Nagana. In South expansion of the red pulp. The
American horses and donkeys, Surra is hepatomegaly and hepatic congestion are
rather chronic, with less severe clinical also common lesions in the acute
signs. Dogs in Asia and South America are trypanosomoses.
sensitive and develop the acute disease In histological sections, the main lesions
with signs similar to Nagana. Cattle are consist in hyperplasia of the Kupffer cells,
more resistant to Surra. periportal mononuclear cell infiltration
The cause of death in animal and centrolobular necrosis. Severe
trypanosomoses is usually congestive lesions are found in the heart. The blood
heart failure, caused by the persistent vessels irrigating the heart congested,
anemia, myocardial damage and with swollen and vacuolated walls and
alteration of vascular permeability.
perivascular edema. The most severe Direct methods include:

cardiac lesion consists in myocardosis.
 The simplest methods to confirm the
Other lesions observed in animals diagnosis are parasitological
suffering of trypanosomoses are: methods by which parasites can be
pituitary necrosis, orchitis or testicular seen under a microscope. The most
degeneration, cystic ovaries, useful sample to detect the parasites
endometritis, meningoencephalitis, is blood. This can be examined
directly (fresh or stained smears) or
Diagnosis. Although laboratory diagnosis
using concentration methods. Direct
is more or less essential, in the field
detection in smears is not
conditions where vector-borne
considered being sensitive enough,
trypanosomoses occur are hardly
mainly because of the low numbers
available or quasi-absent. So
of trypanosomes in the blood. This
veterinarians and animal health officers
can be partly overcome by collecting
should rely to a great extent on
blood early in the morning and from
symptoms. Although clinical signs are not
peripheral capillaries (i.e. tail or ear).
considered to be characteristic, they
Smear can be examined fresh (wet
should not be disregarded. Cattle with
blood films) enabling the detection of
anemia, fever, weight loss, enlarged
live, motile trypanosomes. Stained
lymph nodes, lacrimation, abortion and
smears (thick or thin) are also useful
rough hair coat should be at least
but with limited value, mainly in the
suspected as acute Nagana. In hyperacute
chronic phase. However, if no
cases animals are found dead and
centrifuge is available, this can be a
systemic hemorrhage is dominating the
simple option.
pathological picture. If symptoms
progressively remit following  Two blood concentration methods
administration of trypanocidal drugs, the are available: the microhematocrit
diagnosis is confirmed. centrifugation technique (Woo
If animals die and necropsy is performed method) and dark-field/phase-
the atrophy of fat, enlarged lymph nodes, contrast buffy-coat technique
spleen and liver, subcutaneous edema (Murray method) (OIE, 2012).
and hemorrhagic lesions can be also  The Woo method is based on the
indicative of trypanosomoses. separation of the blood components
However, laboratory techniques are the depending on their specific gravity.
only ones which can confirm the After the blood is collected into a
etiological diagnosis. They can be divided heparinised capillary tube and one
in direct methods (identification of the end is sealed, the tubes are
parasites, parasitic antigens or parasite centrifuged in a microhematocrit
DNA) and indirect methods (serology). centrifuge at 9000 g for 5 minutes.
After centrifugation, the tube is
examined under the microscope at
the separation level of the plasma-
cell interface (buffy coat) using the molecular techniques to identify the
40 objective. The Woo method is parasite’s DNA. These include PCR,
more sensitive than direct Real-Time PCR and Restriction
examinations techniques. According Fragment Length Polymorphism
to OIE (2012), in the case of T. vivax, (RFLP).
the sensitivity of this method is
Indirect methods (serological methods)
100% when the parasitemia is >700
include:
trypanosomes/ml blood and it
decreases to 50% when parasitemia  Indirect Fluorescent Antibody Test
is between 60 and 300 (IFAT)
trypanosomes/ml blood. When  Enzyme-Linked Immunosorbent
parasitemia is lower than 60
Assay (ELISA), targeted on detection
trypanosomes/ml blood the Woo
of anti-Trypanosoma antibodies.
method usually fails to detect the
infection.  Card Agglutination Test (available for
T. evansi).
 The Murray method is similar to
Woo method, but the buffy coat is  Immune Trypanolysis Test (available
extracted from the tube on a only for T. evansi).
microscope slide (after the tube is The main problem with highly specific
cut) and examined under a dark-field and highly sensitive laboratory tests
or contrast-phase microscope. (molecular methods or serology) is their
 Other concentration techniques price and the need for sophisticated
(used mostly in the diagnosis of equipment which is rarely available in
human trypanosomoses) include the the countries which really need them.
anion exchange method (using the Acute Nagana differential diagnosis in
miniature anion-exchange cattle includes in the acute phase
chromatography technique) or in babesiosis, anaplasmosis, theileriosis,
vitro cultivation. anthrax and acute pasteurellosis. In the
 Identification of the parasite can be chronic stage, various helminthosis and
achieved also using animal malnutrition must be considered. In
inoculation (using mice and rats) horses infected with T. evansi the
followed by examination of their differential diagnosis is made with
blood. African horse sickness (a vector-borne
viral infection), equine viral arthritis,
 Another direct method which is equine infectious anemia or dourine. In
aiming this time parasitic antigens camels, the T. evansi infection shows
but used with inconsistent results is similar signs anthrax and in dogs rabies
ELISA. should be also considered, mainly
 The most sensitive methods which because both diseases are endemic in
are more and more routinely used in many tropical countries.
laboratories worldwide are
Treatment. The number of drugs used in treatments (with prophylactic drugs like
the treatment of animal trypanosomoses isometamidium chloride), treatment of
is limited and most of them are available infected animals (diminazene aceturate) or
for almost 50 years (table 2.5). The treatment of clinical cases (any other
treatment is carried out based on certain trypanocide drug).
plans: routine or strategic block
Table 2.5 Drugs used in the treatment of animal trypanosomoses*
Dose Target
Drug Trade name(s) Route Species
(mg/kg) parasites
Diminazene aceturate Berenil, many others 3.5-7 i.m T. congolense Cattle
T. vivax Sheep
T. brucei Goats
T. evansi Dogs
Horses
Donkeys
Homidium chloride Novidium 1 i.m. T. congolense Cattle
Homidium bromide Ethidium T. vivax Sheep
Goats
Pigs
Horses
Donkeys
Isometamidium chloride Samorin, 0.25-0.5 i.m. T. congolense Cattle
Trypamidium, T. vivax Sheep
Veridium T. brucei Goats
T. evansi Horses
Donkeys
Camels
Quinapyramine Trypacide sulphate 3-5 s.c. T. congolense Camels
dimethylsulphate T. vivax
Quinapyramine Trypacide Pro-salt 3-5 s.c. T. vivax Camels
dimethylsulphate:chloride T. brucei Horses
T. simiae Donkeys
T. evansi Pigs
Dogs
Suramin Naganol 7-10 i.v. T. evansi Camels
g/animal Horses
Donkeys
Melarsomine Cymelarsan 0.25 s.c./i.m. T. evansi Camels
* compiled from Maudlin et al. (2004)
Usually only animals with severe acute prophylaxis are known to work. For the
forms are treated. Otherwise they are left control of tsetse fly populations various
to develop immune response which methods have been used over time but
eventually protects them during most of them were aborted (i.e. spraying
subsequent infections. of land with insecticides, clearing of
bush). Nowadays, the commonly used
Control. No vaccines are available.
methods include application of synthetic
However, general prevention measures
insecticides on the animals or biological
(i.e. control of the vector populations,
control using sterile male flies (as
animal husbandry practices, selection of
females tsetse flies reproduce only once
trypanotolerant breeds) and chemical
in their life) or fly traps baited with Donovan are credited with the discovery
pheromones. A proper farming and description of the parasite. The
management should reduce the contact vectors were identified to be the sandflies
of animals with the vectors. Selection of in 1921 by two brothers, Edouard and
trypanotolerant crossbreeds is an Etienne Sergent.
important strategy. These include West
The New World leishmaniosis is known
African indigenous cattle breeds
from, pre-Incan pottery as early as 1st
(N’Dama, Baoule, Muturu, Laguna, Somba,
century AD in Peru and Ecuador and from
Dahomey), East African zebu breeds:
record of Spanish missionaries from the
(Orma Boran, Maasai zebu) and
16th century. The agents, which initially
indigenous breeds of small ruminants:
were considered to be similar to the Old
(West African dwarf sheep and goats, and
World, were accurately described as new
East African goats) (OIE, 2012).
species in 1911 by Gaspar Vianna and the
Chemical prophylaxis is achieved using vectors were recognized as flies from
mainly Isometamidium. genus Lutzomyia in 1922. The first case of
canine leishmaniosis was described in
1903. In 1940, it is estimated that 40% of
2.3.1.3 Canine leishmaniosis the dogs in Rome were infected with
Leishmania.
Canine leishmaniosis is a severe zoonotic Etiology. More than 30 species are
disease, affecting primarily dogs, but also currently recognized in genus
humans and other mammals, transmitted Leishmania, all parasitic in mammals. The
by hematophagous vectors (sandflies). genus is divided in two subgenera
Historical notes. All early notes and the Leishmania and Viannia, based on the site
discovery of Leishmania are related to of development in the sandfly host.
human diseases. The first written Subgenus Leishmania develops in the
documents on the Old World cutaneous anterior alimentary tract of sandflies
leishmaniosis (oriental sore) are known while Viannia develops in the midgut and
from the tablets from the library of King hindgut. Subgenus Leishmania is
Ashurbanipal from the 7th century BC. distributed in the Old World (L.
Avicenna and other Arab physicians also aethiopica, L. donovani, L. infantum, L.
mention the disease as early as the 10th major, L. tropica) and the New World (L.
century by the name of Balkh. The Old amazonensis, L. infantum, L. mexicana, L.
World visceral leishmaniosis (kala azar pifanoi, L. venezuelensis). Subgenus
was first mentioned in India in 1824. Viannia is restricted the New World
However, the first observation of the (Central and South America) and includes
parasite came in 1885 when a Russian several medically significant species: L.
military surgeon, Borovsky saw unknown braziliensis, L. guyanensis, L. panamensis
forms in the blood. A Scottish army and L. peruviana. All of the species listed
physician, William Leishman and a above cause infections in humans, often
physiology professor from India, Charles
with severe syndromes, life-long Life cycle. The life cycle is heteroxenous
disabilities or death. without free living stages. As there is no
direct evidence of sexual reproduction in
The most important species responsible
Leishmania, defining the intermediate
for canine leishmaniosis is L. infantum.
and definitive host is rather arbitrary.
However, several other species of
Hence, as most parasitology resources
Leishmania were reported to infect dogs
consider the sandfly vectors are the
in various geographical regions: L.
intermediate hosts and vertebrates are
donovani, L. tropica, L. braziliensis, L.
the definitive hosts, we will also follow
peruviana, L. panamensis, L. amazonensis.
this concept.
Morphology. Leishmania has two
developmental forms: the motile
extracellular promastigotes (in the
sandfly) and the amastigotes (in the
vertebrate host).
The promastigotes (15 µm in length) are

elongated and have a conspicuous free
flagellum (figure 2.8). The amastigotes
(figure 2.9) are usually found in vacuoles
within the infected macrophages of the
dogs. They are round or oval, lack a free
flagellum and they measure 2.5-5 x 1.5-2
µm. They typically have one large
basophilic nucleus.
Figure 2.9 Amastigotes of Leishmania in

the macrophages of an infected dog.
In the Old World (Europe, Asia, Africa)

the vectors are represented by sandflies
in genus Phlebotomus (figure 2.10) while
in the New World (the Americas) by
genus Lutzomyia. Sandflies are small (cca.
3 mm) blood sucking insects, with
crepuscular and nocturnal activities.
From more than 500 known species of
sandflies (Phlebotominae), around 30
have proven vectorial capacity and other
Figure 2.8 Promastigotes of Leishmania
more than 40 are suspected as probable
from laboratory culture. (Photo Andrei D.
vectors. Other hematophagous
Mihalca)
arthropods (ticks, fleas) have been When the infected female sandfly feeds
suspected to act as competent vectors for again, the promastigotes are injected into
Leishmania, but experimental results are the vertebrate host. Here, the
scarce and hence inconclusive. promastigotes are phagocytized by the
macrophages, they lose their flagellum
and become amastigotes.
Amastigotes multiply intracellularly by

binary fission and increase in number
until they rupture the macrophage.
Subsequently, they invade other cells,
and are disseminated systemically.
Epidemiology. Canine leishmaniosis is

endemic to several areas of the world,
usually in Mediterranean, subtropical and
tropical climates. The disease in endemic
in the countries bordering the
Mediterranean Sea (Southern Europe and
Northern Africa), Asia Minor, parts of
Figure 2.10 Phlebotomus papatasi, a Central Asia and Western China, South
vector for Leishmania infantum. (Photo America (mainly Brazil), Eastern North
David Modrý) America and parts of Sub-Saharan Africa.
However, sporadic cases of canine
leishmaniosis are diagnosed also in non-
In the sandflies, Leishmania develops in endemic countries, mainly because of
the extracellular environment while in intensive travelling and importation of
mammals, development is intracellular. dogs.
When uninfected female sandflies feed on It is estimated that millions of dogs are
the blood of an infected host, they acquire infected in the endemic areas. Dogs are
the amastigotes. The amastigotes are important reservoirs for the human
released from the host macrophage in the infection, mainly in the Old World. The
insect’s gut and they undergo a series of main diagnosis puzzle in these areas, are
transformations and become flagellated. dogs with subclinical infections which are
This initial stage in the sandfly is called a natural source of infection for sandflies
procyclic promastigote. They start to (and indirectly to humans). They remain
replicate and ultimately they detach from undiagnosed, unless serological surveys
the intestinal surface and migrate to are carried out.
foregut and mouthparts of the vector. There are several factors associated with
They are known as metacyclic a higher risk of clinical disease. Age has
promastigotes and they are infective for been shown to be among the most
the vertebrate host. important. Young (2-4 years) and old
(more than 7 years) dogs seem to be the skin and lymph nodes. Otherwise, the
more commonly with symptomatic disease becomes systemic (lymph nodes,
infections. The breed has also been bone marrow, spleen, liver, etc).
incriminated as a risk factor. Certain dog
The incubation period is between 3
breeds are more susceptible to disease
months and 7 years. The main
(German shepherd, Rottweiler, boxer,
pathogenetic mechanism is related to the
cocker spaniel) while others are resistant
immune response. Generally, L. infantum
because of co-evolution with the
is responsible for the depletion of T
pathogen (Ibizan hound).
lymphocytes and a proliferation of B cell
Even in the endemic areas, the higher risk regions in the lymphoid organs. This,
of infection is present in rural areas. This together with the proliferation of other
is caused by various factors, including cellular populations (plasma cells,
more suitable sandfly habitats and histiocytes, macrophages) results in a
availability of other reservoir hosts that significant and systemic
dogs. Various domestic or wild animals lymphadenomegaly, splenomegaly and
are known to harbor the infection, hyperglobulinaemia. However, the
clinically or not: cats, horses, pigs, wild increased immunoglobulin response does
canids, rodents, bats, seals etc. However, not offer protection. Adversely, they are
only few of these are able to transmit the associated with supplementary
infection to sandfly vectors feeding on detrimental effects like immune-mediate
them. thrombocytopenia and
glomerulonephritis. In addition, the large
Although the main route of infection is
amount of circulating immune complexes
via the bite of the vector sandfly, other
(CIC) is responsible for vasculitis, uveitis
mechanisms have been suspected or
and glomerulonephritis. Hence, usually
incriminated: transplacental, venereal
the cause of death in dogs with clinical
and blood transfusion.
leishmaniosis is renal failure. The
Pathogenesis. Not all infected dogs immune-mediated vasculitis is
develop clinical signs. The clinical responsible for tissue necrosis in the skin,
outcome is dependent on various factors. internal organs and in the eye. Another
Some of them are related to the vector interesting pathogenic mechanism
(sandfly species, number and duration of involves the formation of cryoglobulins
the infective bites), some others to the which precipitate when exposed to cold
pathogen (strain-dependent) and others and result in ischemic necroses of
to the host (genetic, age, breed, immune extremities exposed to low temperatures.
status).
The genetic basis for susceptibility or
After the infectious bite by the sandfly, resistance to canine leishmaniosis has
when metacyclic promastigotes invade been shown to be related to certain
the dog’s body, they typically start to mutations and polymorphisms in the
multiply in the macrophages. If the dog is Slc11c1 gene. This gene is responsible for
resistant, it is able to limit the infection to encoding an iron transporter protein,
involved in the macrophage activation but non-protective IgG response against

and development of parasites inside the Leishmania. Overall, there are strong
phagolysosomes. proofs towards a cell-mediated anti-
Leishmania immunity in the so called
Immunology. Both components of the
resistant dogs and a rather humoral
immune system are involved in the
immune response in dogs with clinical
defense against Leishmania in dogs.
signs. For instance, resistant dogs
However, in dogs susceptible for clinical
develop a strong delayed-type
infections, Leishmania is able to evade
hypersensitivity response (indicative of
them, or use it in its own favor.
cell-mediated immunity) when
There are several mechanisms by which inoculated intradermally with Leishmania
Leishmania escapes the innate, non- antigens.
specific immunity. The most important is
Clinical signs. Infected dogs may display
the ability of amastigotes to survive and
a great variety of clinical signs, from
even replicate inside the macrophages.
asymptomatic infection to severe clinical
This is possible due to
syndrome. When the infection is clinical,
lipophosphoglycans produced by the
the diversity of symptoms might be high
parasite which inhibit the maturation of
(table 2.6).
the phagolysosomes.
The role of the specific (acquired)

immune system in leishmaniosis has Table 2.6 Frequency of symptoms in dogs with
clinical leishmaniosis*
been intensively studied mostly on
experimental models in laboratory Symptom Percentage
rodents. How and if the results could be Lymphadenopathy 93.5
Onychogryphosis 75.0
extrapolated to dogs remains uncertain. Cutaneous lesions 58.7
The protective immunity in canine Weight loss 26.1
Cachexia 23.9
leishmaniosis is based on the T Locomotory 22.8
lymphocytes and macrophages. Activated abnormalities
Somnolence 21.7
T cells produce IFN-γ, IL-2 and TNF-α
Conjunctivitis 18.5
which induce the anti-leishmanial activity Anorexia 16.3
of macrophages. The macrophages Polydipsia 13.0
Polyphagia 13.0
produce nitric oxide which is ultimately Onychorrhexis 10.9
responsible for the intracellular killing of Epistaxis 8.7
Diarrhea 6.5
the amastigotes. Another line of specific Sickness 2.2
immune defense are CD8+ and CD4+ Cough 1.1
* - from Semiao-Santos (1995)
cytotoxic T cells which are responsible
for the destruction of macrophages
infected with L. infantum.
Incubation period is considered to be
All these cellular processes are inhibited between 2-8 months, but sporadic
in dogs which develop clinical signs. records extend this period to 15 months
Alternatively, they develop an increased, or even several years. There are several
classifications of canine leishmaniosis. alopecic patches covered by abundant

Some authors divide the disease in squamous debris (figure 2.11),
phases: acute, subacute, chronic and seborrhea and ulcers (figure 2.12). The
latent. In other texts, three types of onset of the cutaneous signs is usually
leishmaniosis are recognized: around the orifices of the head and
asymptomatic, oligosymptomatic and subsequently spread all over the body.
polysymptomatic. However, the most The most severe skin lesions are at the
useful classification is the one based on level of prominent bones. The apparent
the chronology of the clinical signs (early similarity with human cutaneous
symptoms, patent period and final period), leishmaniosis is restricted to the location
accurately described based on of lesions. In humans the pathological
experimental infection trials. changes of the skin are localized, while in
dogs, the cutaneous phase is also
Early symptoms consist of significant
accompanied by visceral pathology. Loss
weight loss, asthenia and apathy. Three
of hair on the tail (“rat tail”) (figure 2.13)
month after the infection, cutaneous
or nasal hyperkeratosis (figure 2.14)
signs may be visible (periorbital and
have also been reported in infected dogs.
auricular alopecia), accompanied by
conjunctivitis, and renal pain on Ocular involvement is frequent in
palpation. Hemorrhagic signs may also be infected dogs with mucous or
present in this early stage. mucopurulent conjunctivitis, keratitis,
corneal ulceration and subsequent
Patent period may vary according to
blindness. Other symptoms include: nasal
dog’s immune status and pathogen strain
discharge, uni- or bilateral epistaxis,
involved, but also to other factors.
progressive muscular atrophy,
Combinations of non-specific symptoms
perionyxis, onychogryphosis (figure
(39-40C hyperthermia, apathy, asthenia,
2.15), onychorhexis, tremor, paralysis of
loss of appetite, polydipsia, loss of
the hind limbs, arthritis etc. Prior to
weight) may appear. One of the most
death, dogs show severe cachexia (figure
present signs is lymphadenopathy, easily
2.16).
detectable by superficial palpation of
popliteal, prescapular and submaxillar Pathology. As explained in the previous
lymph nodes. Ultrasound may reveal in section, the lesions characteristic for
this phase marked hepatomegaly and leishmaniosis are caused primarily by the
splenomegaly. altered immune response. These include
mainly necrotic lesions in the skin, eye
In general, the principal symptoms of
and internal organs.
clinically ill dogs include: skin lesions,
enlarged lymph nodes, weight loss, The skin lesions are usually generalized,
lethargy, ocular lesions, digestive signs and microscopically they involve the
(vomiting, diarrhea) or lameness. decrease of collagen type I and the
decrease of collagen type III fibers.
Skin lesions are also common in infected
dogs. They can appear as non-prurigenic,
Figure 2.11 Exfoliative dermatitis in a Figure 2.13 “Rat tail” lesion in a dog
dog infected with L. infantum. (Photo infected with L. infantum. (Photo George
George Popa) Popa)
Figure 2.12 Cutaneous ulcers and Figure 2.14 Nasal hyperkeratosis in a

erosions in a dog infected with L. dog infected with L. infantum. (Photo
infantum. (Photo George Popa) George Popa)
The ocular lesions include: conjunctivitis, Other lesions associated with the altered
blepharitis and anterior uveitis. In some immune response and CIC include
cases, because of the retention of lacrimal mononuclear myositis, neutrophilic
secretion due to adjacent inflammation, vasculitis, hemorrhages in internal
dogs exhibit keratoconjunctivitis sicca. organs, granulomatous rhinitis, epistaxis
and anemia.
dermatitis. The histopathologic lesions in

the skin are pyogranulomatous with
hyperkeratosis.
Gross lesions include: generalized

lymphadenopathy, splenomegaly and
hepatomegaly, granulomatous nodules in
various internal organs.
Diagnosis. Clinical signs are not enough

for a positive diagnosis of canine
leishmaniosis. Basically, for a certain
diagnosis, the presence of the parasite
must be demonstrated directly (PCR,
cytology, histology, culture) or indirectly
Figure 2.15 Onychogryphosis in a dog
(antibody detection).
infected with L. infantum. (Photo George
Popa) Direct evidence of the amastigotes should
based on microscopic observation of the
parasitic stages in biopsy from lymph
nodes, spleen, bone marrow or skin.
Although this method is 100% specific, its
sensitivity is maximum 80%, depending
on the experience of the examiner and
examination effort. However, direct
identification of Leishmania amastigotes
is not always achievable, even in dogs
with clinical infection. Amastigotes can be
observed also in tissue sections by
histology or immunohistochemistry.
Although not commonly used as routine
diagnostic methods, cultivation (Novy-
MacNeal-Nicolle medium) and
Figure 2.16 Severe cachexia in a dog experimental infection (hamsters) are
infected with L. infantum. (Photo George also possible.
Popa) Probably the most sensitive methods for
the detection of Leishmania infection are
molecular biology techniques. PCR has
Usually the cutaneous lesions are
been used routinely for the detection of
generalized. Several types are mentioned
Leishmania DNA in various tissues (bone
in the literature: exfoliative dermatitis
marrow, lymph nodes, spleen, skin),
with alopecia, ulcerative dermatitis,
blood (whole blood or buffy coat) or body
nodular dermatitis, mucocutaneous
fluids (urine).
proliferative dermatitis, or popular
The easiest diagnosis methods however nucleoside in the structure of tRNA). This
refer to the detection of anti-Leishmania analogue is incorporated into the
antibodies in the serum of dogs. Various structure of the Leishmania RNA, causing
methods have been developed, some of an altered translation and inhibiting
the using whole parasite extracts (more parasite multiplication. Unlike the
sensitive, less specific), some others previous drug, allopurinol is given orally
recombinant protein antigens (more (10 mg/kg body weight), twice a day, for
specific, less sensitive). Whole parasite month or even years. Despite the fact that
extract can cross-react with other the drug has little adverse effects, the
kinetoplastids. Usually, it is considered discontinuation of treatment often results
that high antibody titers in dogs with in clinical relapses. Hence, dogs may
compatible symptoms are indication of require life-long treatment. One of the
clinical leishmaniosis. If clinical signs are most common side effects is
present but antibody titers are low, hyperxanthinuria, resulting in
additional methods are recommended urolithiasis. However, the most effective
(cytology, histology, PCR). therapeutic protocol is the combination
of meglumine antimoniate with
Treatment. Treatment of leishmaniosis
allopurinol.
does not necessarily eliminate the
parasite form the organism and this is Several other drugs have been used for
one of the causes of the frequent clinical the treatment of canine leishmaniosis:
relapses. There are several drugs used for miltefosine (2 mg/kg body weight, orally,
the treatment of canine leishmaniosis. once per day, for four weeks),
The most commonly used are pentavalent amphotericin B (causes renal toxicity).
antimonials. Their mechanism of action is
Except specific treatment, a symptomatic
by inhibiting the enzymes responsible for
therapy must be conducted.
oxidation of fatty acids and glycolysis.
The most commonly used antimonial is Control. None of the several control
meglumine antimoniate which is given by measures used is fully effective. The
subcutaneous injection, for 4-8 weeks, euthanasia of infected dogs is the most
daily, at 75-100 mg/kg body weight. controversial and its efficacy is doubtful
Besides the side effects (local reactions, because of the persistence of reservoirs
nephrotoxicity), there are several reports in wildlife. Environmental control of
of resistant Leishmania strains in Europe. sandflies (spraying, destruction of
breeding habitats) has been also shown
Another compound used in the treatment
to be little effective. Moreover, there is no
of canine leishmaniosis is allopurinol.
prophylactic drug available. However,
This drug was originally developed for
owners can reduce the sandfly bites on
the treatment of gout (hyperuricemia) in
their dogs by avoiding outdoor access
human patients. Its efficacy against
during maximum activity of the vectors
Leishmania is explained by its capacity of
(overnight, warm season) or by using
being metabolized by the parasite into an
prophylactic insecticides (spot-on,
analogue of inosine (a common
collars, sprays).
Currently, there is a commercial vaccine produce also cutaneous signs, mostly

for dogs, but its availability is variable located on the ear pinna.
from country to country. This commercial
Treatment. Despite the lack of extensive
vaccine contains a glycoprotein from L.
clinical studies, the few reported treated
donovani (GP63).
cases suggest that the same protocols
which is used in dog can be successfully
applied also in cats.
2.3.1.4 Feline leishmaniosis
Unlike canine leishmanioses, the disease

2.3.2 Trichomonads
in cats is reported only sporadically. As
most aspects have been already
Introduction. The trichomonads group
presented in the chapter on canine
several genera of medical and veterinary
leishmaniosis, only specific aspects will
importance (table 2.7).
be given here.
The morphological differences between
Historical notes. The first case of feline
species (and even genera) are not very
leishmaniosis was described in Algeria in
easy to discern, mainly if using regular
1912, in a kitten housed together with an
direct examination. They are unicellular
infected dog and an infected child.
organisms, lacking mitochondria with a
Etiology. Several species have been typical anaerobic metabolism. They
reported from cats: L. infantum (Europe, include mostly symbiotic species, but also
South America), L. mexicana (USA), L. few free-living organisms.
venezuelensis, L. braziliensis and L.
General morphology. Although there
amazonensis (South America).
are slight morphological differences
Epidemiology. The disease in cats is between different genera and species,
sporadic, and all cases were reported generally, all trichomonads have a group
from areas endemic to canine of three (Tritrichomonas), four
leishmaniosis: Mediterranean Europe, (Tetratrichomonas, Trichomonas) or five
North Africa, Middle East, and the (Pentatrichomonas) anterior free flagella,
Americas. an additional recurrent flagellum which
delimitates an undulating membrane. The
Clinical signs. In immunologically
axostyle, a rigid rod-like structure runs
competent cats, the predominant
medially through the cell. The axostyle is
symptoms of L. infantum infection are
usually longer than the cell. Due to these
cutaneous (ulcers, nodular dermatitis,
structures, trichomonads show a very
scaling, alopecia) with the lesions located
characteristic movement, making them
mainly on the head. The visceral
easily recognizable in fresh preparations
involvement seems to be limited to cats
coinfected with FIV (Feline Ecology and transmission. The vast
Immunodeficiency Virus) or FeLV (Feline majority of the Trichomonads are
Leukemia Virus). American species parasitic, mutualistic or commensals.
Table 2.7 Most important species of trichomonads
Genus Species Hosts Location

T. gallinae birds anterior digestive system
Trichomonas
T. vaginalis humans genital
cattle genital
T. foetus
cats large intestine
T. suis (=T. pigs digestive, nasal
foetus)
T. enteritis cattle colon
Tritrichomonas
T. caviae cavies cecum
T. muris rodents large intestine
T. minut rodents large intestine
T. wenyoni rodents large intestine
T. eberthi birds cecum
T. canistomae dogs mouth
T. felistomae cats mouth
T. ovis sheep cecum, rumen
T. buttreyi ungulates large intestine
Tetratrichomonas T. pavlovi cattle cecum
T. microti rodents large intestine
T. gallinarum birds, humans cecum
T. anatis ducks intestine
T. anseris geese cecum
Pentatrichomonas P. hominis primates, dogs, cats, rodents large intestine
Trichomitus T. rotunda pigs large intestine
Chilomastix C. gallinarum birds cecum
They inhabit the digestive or responsible for digestive symptoms in

reproductive tracts of vertebrates or animals, usually young ones. One single
invertebrates. Few species are free-living. species (Tritrichomonas foetus in cattle)
The life-cycle is always homoxenous and is producing genital infection. In humans,
generally, they are considered to be host- several species are known, some of them
specific. producing digestive signs, some others
genital symptoms.
Feeding occurs by phagocytosis of fluids,
leukocytes or bacteria from the in-host
habitats. Reproduction is by longitudinal
binary fission, with the formation of large 2.3.2.1 Genital trichomonosis in
numbers of trophozoites. cattle
As there are no cystic stages known, Introduction. Genital trichomonosis is a

transmission between hosts is always by venereal disease of cattle, with long-term
direct contact. impact on fertility in females and
Medical importance. Certain asymptomatic carrier state in bulls, with
trichomonads are important human and worldwide distribution, caused by
veterinary pathogens. Most of the species Tritrichomonas foetus. The disease is
are located in the digestive tract (mouth, mainly important from its economic
gut), others in the genital system. Most perspective.
veterinary important species are
Historical notes. The disease was infected animals. Transmission by

reported and described for the first time artificial insemination has also been
in 1888 by Kunstler in France and later, reported.
in 1890, by Mazzanti in Italy as isolated
cases of infertility. Later reports from
1924-1929 are from Germany, where
enzootic outbreaks were described. The
first cases of bovine genital
trichomonosis in the United States were
found in 1932.
Etiology. The causative agent,

Tritrichomonas foetus has been subject to
several molecular taxonomy approaches,
and its synonymy with T. suis has long
been debated. Most recent taxonomical
papers list them as synonyms.
Three serotypes have been found using

seroagglutination. The “belfast” strain
(common in Europe, Africa and USA), the
“brisbane” strain (in Australia) and the
“manley” strain (the most rare one).
Morphology. Tritrichomonas foetus Figure 2.17 Tritrichomonas foetus.

(figure 2.17) is a spindle to pear shaped
unicellular organism, 10-25 x 3-15 µm,
Passive transmission has also been
with four flagella. Three anterior flagella
reported. This means that, if a non-
are free and the fourth, called the
infected bull had recent coitus with an
recurrent flagellum, runs backward and
infected female, he is able to transmit
delimitates an undulating membrane,
infect another cow in a subsequent
with 3-5 waves. The axostyle is thick and
intercourse.
it protrudes in the posterior part of the
cell. The gynecological examination of cows
can also induce passive transmission, if
Life cycle. The typical habitat for T.
instruments are not sterilized after being
foetus is at the level of genital mucosae of
used before in an infected cow.
cattle, in both sexes. In bulls, they are
found in the preputial cavity, penis Epidemiology. The disease is distributed
mucosa, distal urethra, epididymis, testes worldwide. Bovines are the only
and seminal vesicles. In cows, they infect important infection reservoirs, with
the vaginal mucosa, the uterus and the asymptomatic bulls being responsible for
fetus. Transmission between hosts is by infection of cows mainly by natural
sexual contact between infected and non mating. Nonetheless, experimental
infection has been established in a great more prone to develop chronic infection
variety of mammalian hosts (rabbits, and to become long-time, asymptomatic
laboratory rodents, dogs, small carriers. This is associated with a
ruminants, pigs), but their morphologic trait of epithelial crypts of
epidemiological importance is practically the penis and prepuce, which become
zero. Since the taxonomic debate on the deeper as bulls are aging. Deeper crypts
identity of T. foetus with T. suis, it is still offer a better microaerophilic
not certain if cross infection could occur, environment. Conversely, young bulls are
and how. Moreover, the identification of only transient carriers.
T. foetus from cats with diarrhea make
In cows, immediately after the infection,
this puzzle even more complicated.
the parasite produces a mild infection of
Both breed and age susceptibility has the vaginal mucosa, with vaginitis. During
been reported in bulls. Bulls of some estrus, the flagellates are able to enter the
breeds (Bragus, Simmental, Charolais, uterus through the cervix. Within 7-14
and Angus) seem to be more predisposed days, T. foetus is able to colonize the
to infection than others (Braford). The entire female reproductive tract. The
origin of the breed is likely to be the endometritis is responsible for the
cause of different susceptibility. It has persistence of the corpus luteum which
been estimated that Bos taurus bulls are induces pyometra.
more prone to infection than B. indicus.
The mechanism of fetal death is not fully
The farm management system is also
understood, but cytotoxic and hemolytic
important. The prevalence in bulls tends
effects have been incriminated. The
to be higher in larger farms. Similarly, a
adhesion of T. foetus to mammalian cells
higher bull-cow ratio is directly
is facilitated by a surface adhesin.
correlated with an increased prevalence
of the disease. After the experimental infection in
heifers, the clearance of the parasite
The resistance of T. foetus outside its host
without medication is between 3 and 28
is very limited. Hence, contamination of
months.
new hosts is only by direct contact.
However, the organism can remain Immunology. There is no evidence
infective in frozen semen. showing that after infection, cows will
develop long-term or life-long immunity.
Pathogenesis. As most venereal diseases
However, a maximum 15 month
of domestic animals, bovine
convalescent immunity has been
trichomonosis is asymptomatic in males
reported. Tritrichomonas foetus produces
and symptomatic in females.
extracellular proteases which are able to
In bulls, the parasites live on the mucosal digest immunoglobulins, impairing even
surface and do no invade the epithelial the local immunity.
tissue. One interesting observation
The antigenic structure of T. foetus
following an experimental infection trial,
includes 55-60 proteins
was that bulls older than 3 years are
The surface antigens of T. foetus are able caused by bovine trichomonosis are
to activate the alternative pathway of significant, with losses estimated to 35%
bovine complement. The bovine of the profit in infected farms.
complement system is able to kill T.
Pathology. Following abortion, the
foetus in the presence of specific
lesions are detectable in the placenta and
antibodies. On the other hand,
in the fetus. In late term abortions, the
neutrophils are not efficient in killing T.
placenta shows focal or diffuse invasion
foetus, even in the presence of specific
of the chorionic stroma by the parasitic
antibodies.
flagellates. The typical morphology of T.
Studies have shown that there is no foetus is easily visible in histological
cross-immunity between the three sections stained with Bodian’s silver
serotypes of T. foetus. technique but is imperceptible at routine
staining methods. Additionally,
Clinical signs. The infection of bulls is
monocytic infiltrate is present in the
usually asymptomatic.
placental layers. The aborted fetuses have
In females, a mild vaginitis is the first sign pyogranulomatous bronchopneumonia,
of infection. If the infective mating results interstitial pneumonia, hepatic and
in gestation, the usual outcome is intestinal necrosis with the presence of
abortion between days 50 and 70. About the parasites in the air ducts but also in
one third of the abortions caused by the esophagus, abomasum and intestine.
trichomonosis occur in the first trimester.
Diagnosis. The clinical signs and features
The death of the embryo or fetus during
of the disease are neither characteristic
this early stage is usually followed by a
nor pathognomonic to trichomonosis.
longer interestrous interval. As the
Similar reproductive problems are
abortion is very early, often it goes
caused by bacterial agents (e.g.
unobserved by farm owners. Usually, all
Campylobacter foetus, Leptospira spp.,
fetal membranes are passed after
Ureaplasma diversum) or by nutritional
abortion and the cows recover quickly.
conditions. Hence, the certain diagnosis
Nevertheless, fetal membrane retention
must be based on the identification of the
leads to chronic endometritis and
parasitic agent by various laboratory
possibly permanent sterility. Most cows
methods.
are however able to bare a normal
gestation and deliver normal calves. As a The following section is based on the
result of abortion about 5% of the cows recommendations by OIE (The World
develop pyometra. Detection of pyometra Organization for Animal Health). The
is usually late, and by that time the samples which are used for the detection
uterine mucosa is severely damaged. of T. foetus are: vaginal mucus, vaginal
washing or scrapings, preputial washing
Persistent infection with T. foetus in cows
or scraping, uterine washing, pyometra
results in temporary or permanent
discharge, placental fluid, stomach
infertility, irregular estrus, persistent
content of the aborted fetus.
abortions etc. The economical losses
A correct technique and timing for the T. foetus. A PCR-based assay which is
collection of samples are essential. It is used has certain advantages: increased
important mainly to avoid fecal sensitivity, possibility to detect non-
contamination, or if so, the examiner viable pathogens. Additionally,
should be very experienced in order to immunohistochemistry on tissues
differentiate intestinal flagellates from T. (placenta, fetal lungs) has been also used.
foetus. Contamination can be avoided by
Treatment. For the treatment of bulls,
mechanically removing the dirty hair
various drugs have been used in the past:
around the preputial orifice or around
dimetridazole, ipronidazole and
the vulva. Chemical disinfectants are nor
metronidazole. As all are nitroimidazoles,
recommended, as may inactivate T. foetus
their use in livestock is banned in most
and reduce diagnosis sensitivity.
countries. Hence, currently there are no
Collection of preputial samples from bulls
therapeutic options for treating bovine
can be done using an artificial
trichomonosis. Treatment of bulls can be
insemination pipette, a brush, by
performed only under certain conditions,
preputial washing or by washing the
mainly in the case of expensive, valuable
artificial vagina after seminal material
breeding animals.
collection. Samples from cows are
collected by vaginal washing or by Control. Prevention and control by herd
scraping the cervix with a brush or management are the only reliable
pipette. methods for reducing the economic
impact of bovine genital trichomonosis.
Samples must be examined as fast as
General measures include: control of the
possible. If they cannot be sent to the
animal movement, avoid grazing on
laboratory in maximum 24 hours, they
common pastures where bulls from other
should be included in a transport
herds may have access, purchase only
medium (thioglycollate broth media with
virgin bulls and heifers for restocking,
antibiotics) and kept at temperatures
purchase the animals from T. foetus-free
between 5 and 38°C, away from direct
farms, ask for the preputial washing
sunlight.
result for any bull purchased, graze
Samples can be examined immediately separately cows and bulls, keep the
under the light microscope, or if the average age of bulls as young as possible
sample is poor in trichomonads, after (maximum 3 years), use of artificial
enrichment on cultivation media insemination with tested semen.
(Diamond’s trichomonad medium or
Commercial vaccines for cows are
other commercial media). Tritrichomonas
available in certain countries. They are
foetus should be motile, with typical
killed vaccines and initial vaccination
movements and morphology (pear-shape,
must be given twice, subcutaneously, at
presence of free flagella and undulating
2-4 weeks apart. In the following years,
membrane, presence of axostyle).
all cows must be revaccinated, 4 weeks
More recently, new, molecular techniques prior to the beginning of the breeding
have been developed for the detection of season. Although the vaccine does not
prevent the infection, it significantly axostyle extends far beyond the posterior
decreases the economic impact of the end of the cell. The size is 7-12 x 3-4 µm.
disease by reducing the rate of abortions
and the duration and severity of the
disease.
2.3.2.2 Buccal trichomonosis in dogs

and cats
Introduction. Buccal trichomonosis in

carnivores are poorly known conditions,
caused by flagellates in genus
Tetratrichomonas and characterized by
gingivitis usually in immunodeficient
patients.
Historical notes. Both conditions (in cats

and dogs) were described by Hegner and
Ratcliffe in 1927 in United States.
Etiology. The species responsible for

buccal trichomonosis in cats is Figure 2.18 Tetratrichomonas
Tetratrichomonas felistomae and in dogs canistomae.
it is T. canistomae. As the original
description is very simple, and records of
these parasites are scarce, the taxonomic Trophozoites of T. felistomae (figure
status of T. felistomae and T. canistomae 2.19) have a similar morphology. Their
is uncertain. Moreover, recent studies size is 6-11 x 3-4 µm. They have a well
revealed the presence of flagellates with a visible axostyle and the undulating
different morphology, puzzling even membrane has 3 waves.
more the situation. Life cycle. Not too many aspects are
Morphology. Species in genus known about the biology of these
Tetratrichomonas have 4 free flagella and parasites. They are located in the mouth
one more trailing free flagellum, running of dogs and cats, along the gums or
backwards. Trophozoites of T. canistomae associated with dental calculus.
(figure 2.18) have four anterior flagella, Transmission between hosts is probably
that rise in pairs from a large by direct contact.
blepharoplast at the anterior end of the Epidemiology. In cats, the parasite have
body. The recurrent flagellum starts from been reported only in USA, Italy and
the blepharoplast, runs backwards along Germany. In dogs, the parasite is known
the edge of the undulating membrane and from United States and various European
ends freely at the posterior end. The
countries. No data about resistance in the Pathology. Gingivitis in cats, dental

environment are available. calculus in dogs.
Diagnosis. Fresh wet mounts from dogs

and cat with buccal lesions might reveal
the presence of flagellates. In dogs,
scraping the dental calculi from the lower
jaw and decayed teeth yielded better
results.
Treatment. Unknown.
Control. Unknown, but a proper oral

hygiene with removal of dental calculi
and treatment of buccal inflammations
might be useful.
2.3.2.3 Anterior digestive

trichomonosis in birds
Introduction. It is a worldwide
Figure 2.19 Tetratrichomonas felistomae. distributed parasitic disease of pigeons,
doves, galliformes and birds of prey, with
possible severe buccal lesions mainly in
Pathogenesis. In a recent study, the young birds. The disease in pigeons is
trichomonads in cats were found only in also known as canker. In poultry, the
individuals infected with name of the disease is “roup” and in birds
immunosuppressive viruses: feline of prey “frounce”.
immunodeficiency virus, feline leukemia
Historical notes. The first description of
virus and feline infectious peritonitis
the disease was in pigeons, together the
virus.
etiological agent, by Rivolta in 1878 in
Immunology. Unknown Italy.
Clinical signs. The presence of the Etiology. Only one species is involved,
parasites in cats was associated with namely Trichomonas gallinae. This
gingivitis, while in dogs with dental species must not be confused with
calculus. Tetratrichomonas felistomae was Tetratrichomonas gallinarum, which
never isolated from cats without lesions, infects the large intestines of birds.
while it seems that in dogs, T. canistomae Different strains are know, some of them
can be found also in healthy patients. more pathogenic than the others and
Hence, some authors consider it to be some considered avirulent, part of the
mostly non-pathogenic. normal buccal fauna. One of the most
virulent strains is Jones’ Barn, which is
able to kill even adult pigeons at 8 days

after the infection.
Morphology. Trophozoites (figure 2.20)

are piriform to rounded, 6-19 x 2-9 µm,
Four free flagella extend forward, and the
fifth runs backward along the margin of
the undulating membrane. Unlike in
genus Tetratrichomonas, there is no free
trailing flagellum.
Life cycle. The parasites inhabit the

mucosal surface of the anterior digestive
system (mouth, pharynx, esophagus,
crop) and head sinuses in pigeons and
doves. Although it seems that only
Columbiformes are the natural host for T.
gallinae, the infection was reported in
many other groups of domestic or wild
birds. Among domestic species, chicken
and turkeys are susceptible to infections. Figure 2.20 Trichomonas gallinae.
The infection was reported in captive
finches and canaries as well as in quails.
Among wild avian species, the most Epidemiology. The parasite is
important clinical disease was described distributed globally, with virtually all
in raptors. Moreover, many experimental domestic and wild pigeon populations
trials succeeded transmitting T. gallinae positive for the infection. In domestic
to many other host species, showing the fowl (chicken, turkey) the infection is
parasites lacks specificity. rather sporadic. In birds of prey, the
infection has been reported with variable
Mammals are not susceptible to natural prevalence in several countries where
infection. They multiply rapidly by binary studies were performed. Nevertheless,
fission. Only a single stage is know, the the source if infection for the other birds
trophozoite. are always pigeons or doves.
Transmission no new host is realized by Young pigeons are particularly
direct contact between infected and non- susceptible for the diseases, while adults
infected birds. In pigeons, the adult birds are usually asymptomatic carriers.
are infecting their nestlings during the Certain breeds (i.e. tumbler) were shown
regurgitation and feeding. Birds of prey to be more sensitive to the infection. The
get the infection when feeding on other severity and clinical outcome of canker is
infected birds. Other birds get the also influenced by certain environmental
infection by drinking contaminated factors: poor ventilation, overcrowding,
water. unbalanced diet, excessive humidity.
Interestingly, the prevalence of infection extremely virulent strains can produce

is usually higher in adults than in young. mortality rates up to 50%.
The outbreaks and the prevalence are
In the acute cases, the duration of the
positively correlated with humid seasons.
disease is 10-14 days. The typical clinical
Stress is also a factor contributing to
picture includes: partial or total loss of
clinical outbreaks.
appetite, weight loss, ruffled aspect and
Although the resistance of T. gallinae in listlessness. Some pigeons which still
the environment is very limited, it present appetite have difficulties in
survives enough time in drinking water swallowing. Other birds may also show
to facilitate transmission in birds which signs of respiratory distress. When
do not feed their newly hatched offspring, examining the mouth, small, whitish or
like chicken or turkey. yellowish adherent masses are seen on
the surface of the buccal and pharyngeal
Pathogenesis. The chronic infection is
mucosa (figure 2.21). Sometimes, these
usually accompanied by a low number of
caseous nodules join and become large
parasites which are not able to produce
enough to completely obstruct the
the disease. When certain factors are met
pharynx (figure 2.22). These small
(see above), the parasite multiplies very
nodules disappear spontaneously within
fast and invades the surface of the upper
few days and the bird becomes healthy.
digestive system, causing severe
In other cases, the infection results in
inflammation followed often by death in
death. Interestingly, the severity of
the acute form. In severe infection, T.
nodular lesions is not correlated with the
gallinae colonizes also the sinuses and
severity of clinical form.
the liver.
The most virulent strains produce the
Immunology. Despite the lack of
first oral lesions after 1 week, as
targeted studies on the immune response
yellowish areas on the mucosa of mouth
of birds to the infection with T. gallinae, it
and the tissue bordering the nasal cleft or
seems that if the original exposure is not
palatal flaps. When nodules become big
followed by death, sufficient immunity is
enough to obstruct the food passage, the
developed to protect the adults against
clinical course becomes rapid, with
clinical disease. Non-exposed adults
extreme and fast weight loss and fluid
introduced to infected colonies develop a
accumulation in the crop which virtually
severe form of trichomonosis and may
can drown the bird. Death occurs in
even die. It is not fully understood if there
about 10-12 days from the first clinical
is cross acquired immunity against the
sign (around 20 days from infection).
different strains of the parasite.
Sometimes also diarrhea is present.
Clinical signs. Infection may vary from
The infection with less virulent strains
asymptomatic cases to severe outbreaks
can be asymptomatic or can cause
with over 90% mortality, mainly in young
maximum excessive salivation and mild
birds. In adults mortality is rare, but
stomatitis.
whitish fluid. The crop may be covered

with a diphteric membrane which lines
the digestive mucosa down to the
glandular stomach.
Histology shows congestion with

mononuclear inflammatory infiltration in
the lamina propria of the larynx and
pharynx, surrounded by area of necrosis.
The liver may show signs of congestion or

areas of yellow necrosis, with peritoneal
adhesions. Microscopically these
correspond to hyperemia, hepatocellular
necrosis, hyperplasia of the bile duct, all
Figure 2.21 Small, disseminated caseous
with heterophils and mononuclear
nodule on the surface of buccal mucosa in
infiltration and presence of
a pigeon naturally infected with T.
multinucleated giant cells.
gallinae. (Photo Andrei D. Mihalca)
The heart may also be affected, with
caseous material deposited on the apex.
In birds of prey and gallinaceous birds, Similar lesions are occasionally reported
buccal trichomonosis is a severe in all organs found in direct contact with
condition and the clinical expression is the liver: small intestine, spleen,
somehow similar with the one described pancreas, air sacs, lungs, kidneys.
in pigeons. Additionally, these hosts show
moderate or severe dyspnea along with
nasal and oral exudation. In exotic birds
(i.e. budgerigars, finches) clinical sings
include also wasting, vomiting and
diarrhea.
Pathology. The lesions are usually

limited to the anterior digestive system,
liver and sometimes to the respiratory
system. The less virulent strains usually
produce only buccal and pharyngeal
lesions while more virulent strains are
able to cause damage to various internal
organs. Yellowish to grayish necrotic
lesions are found on the mucosa lining
the mouth, pharynx, esophagus, crop and Figure 2.22 Large caseous nodule in the
proventriculus. Sometimes, the crop and palatal flaps area in a pigeon naturally
the proventriculus contain a greenish or infected with T. gallinae. (Photo Andrei D.
Mihalca)
Microscopic lesions in the respiratory

organs of pigeons infected with virulent
strains are predominantly congestive and
inflammatory. Severe congestion might
be present in the lungs, with extensive
infiltration of heterophils and
mononuclear cells in the mucosa of the
trachea and hyperplasia of tracheal
mucous cells. If kidneys are involved, the
microscopic lesions consists of mild
tubular necrosis with mononuclear
infiltrate.
Diagnosis. The diagnosis might be done

in healthy birds to estimate the Figure 2.23 Collection of the pharyngeal
asymptomatic carrier status. This swab for the diagnosis of buccal
approach is essential in pigeon housings, trichomonosis in pigeon. (Photo Andrei D.
to detect the infection in adults, before Mihalca)
the reproduction season. The etiological
diagnosis is of course important also in
clinically ill birds. Treatment. Several drugs are available
for the treatment of trichomonosis in
The most reliable diagnosis is by pigeons: metronidazole (60 mg/kg body
demonstrating the presence of weight); dimetridazole (50 mg/kg body
trichomonads by microscopic weight); ronidazole (30 mg/pigeon), all
examination. Wet smears should be orally. As resistance to these drugs was
prepared using cotton-tipped swabs reported in various strains of T. gallinae,
soaked in warm sterile physiological commercial products containing
saline (figure 2.23). The content must be combination of these (i.e. metronidazole
immediately examined under the + ronidazole) have been developed. All
microscope, using medium or large these products are soluble, and are given
magnification in order to observe the in drinking water for 5-6 consecutive
typical morphology. When the intensity days. The recommended concentration is
of the infection is low, the small number 0.05%.
of parasites might go undetected. In these
cases, an initial enrichment by cultivation Control. General measures like a good
is helpful. hygiene, avoiding overcrowding and
stress should reduce the impact of the
A variety of cultivation can be used, but disease. Treatment of the adult pigeons
the most recommended is Diamond’s before the breeding season will certainly
medium. For more sensitive diagnosis, reduce the parasite load and mortality in
various PCR assays have been developed, squabs to come.
but their use as routine examinations
might be costly.
2.3.2.4 Intestinal trichomonosis in gallinarum have been reported as causing

birds caecal infection in chicken and turkeys.
Morphology. All species have the typical

Introduction. Is a worldwide distributed
morphology of trichomonads, but small
parasitic disease of various birds species,
differences in size, shape, number of
with digestive clinical signs mainly in
flagella or internal structure allows more
young birds.
specific identification.
Historical notes. Tetratrichomonas
Tetratrichomonas gallinarum (figure
gallinarum was described in 1911 from
2.24) has a piriform body, 7-15 x 3-9 µm.
chickens.
Like all member of its genus, it has four
Etiology. Several species have to be free anterior flagella, and a recurrent
considered as etiologic agents of flagellum which runs along the edge of
intestinal trichomonosis in domestic the undulating membrane and ending
birds. However, their taxonomic status with a free part. The axostyle is long,
(or even validity) and pathogenic slender and pointed.
potential have been questioned by recent
Tetratrichomonas anatis has an elongated
molecular biology works.
body, 13-27 x 8-18 µm, with four anterior
Although Tetratrichomonas gallinarum is flagella, a long undulating membrane a
still listed by most veterinary the recurrent flagellum with a free
parasitology textbooks, its pathogenic termination. Tetratrichomonas anseris
potential is uncertain, and recent has the morphology is similar to T. anatis
genetical insights have shown that this but it is slightly smaller.
species might be actually a complex of
Tritrichomonas eberthi (figure 2.25) has
cryptic species with more implications in
an elongated body, 8-14 x 4-7 µm, three
human health than in birds. Until more
free anterior flagella and a well-
clarification is available, we will follow
developed undulating membrane, lined
the classical concept and consider all
by the recurrent flagellum which ends
these species valid. Tetratrichomonas
freely at the posterior end. The axostyle
gallinae was reported from various
is relatively thick and extends the
domestic and wild species of birds
posterior end of the body.
(chicken, turkey, guinea fowl, quail,
pheasant, partridge, ducks etc.) and has Chilomastix gallinarum (figure 2.26) is
been recently incriminated in the etiology piriform, 11-20 x 5-12 µm, three anterior
of severe lung disorders in humans. flagella, and an additional spiraling
flagellum. The undulating membrane is
Tetratrichomonas anatis is the cause of
relatively narrow. In the case of this
small and large intestine trichomonosis
species, also cysts are known to be
in ducks. Tetratrichomonas anseris is
formed (7-9 x 4-6 µm).
responsible for the disease in geese.
Tritrichomonas eberthi and Chilomastix
Figure 2.24 Tetratrichomonas

gallinarum. Figure 2.25 Tritrichomonas eberthi.
Life cycle. All the species inhabit the

mucosa of the large intestine or small
intestine where they multiply by binary
fission. Transmission from a host to
another is via fecal-oral route, by fresh
feces. In the case of C. gallinarum,
transmission can be done through cysts.
Epidemiology. All the species have

global distribution. The resistance in the
environment is limited. Usually, young
birds seem to be more affected by the
clinical diseases.
Pathogenesis. There is serious debate on

the pathogenicity of certain species.
Generally, they are considered to be non-
pathogenic. However, most of them have
been isolated from birds with clinical
signs or lesions of enteritis.
Figure 2.26 Chilomastix gallinarum.
It is a question if they are the primary should be rather identified and

agents, or they just over multiply on eliminated.
lesions primarily induced by bacteria or
Control. Hygiene measures are essential,
viruses.
as contamination is usually via infected
Immunology. Unknown. water.
Clinical signs. With the same mentions

as stated above, clinical signs associated
with the presence of intestinal 2.3.2.5 Intestinal trichomonosis in
trichomonads vary from asymptomatic mammals
infections (in the vast majority of cases)
to mild, moderate or severe diarrhea, or Introduction. Intestinal trichomonads of
even sudden death (in ducks). domestic mammals include a great
variety of species, usually non-
Pathology. The lesions from birds pathogenic. If disease occurs, it is a result
infected with intestinal trichomonads are of multiple pathogen infections.
usually fibrinous or necrotic enteritis,
mainly in the cecum (typhlitis). Etiology. For a list of species and hosts
Sometimes, necrotic lesions on the liver please refer to Table 2.7.
have been described. In ducks, Morphology. Tritrichomonas enteritis
extraintestinal lesions were also has a small body, 6-12 x 5-6 µm, with
described: mucopurulent sinusitis, three free anterior flagella, and a
catarrhal rhinitis and tracheitis. medium-sized undulating membrane.
Diagnosis. In vivo, the flagellated Tetratrichomonas buttreyi is ovoid or
protozoans can be identified under the ellipsoidal, 4-7 x 2-5 µm, with four free
microscope in wet mounts from cloacal anterior flagella, an undulating
swabs. Their presence must be membrane with 3-5 waves and a
interpreted with caution, as usually the recurrent flagellum. The axostyle is
underlying cause of the symptoms are rather narrow.
more likely to be bacteria, viruses or even
Tetratrichomonas ovis has a piriform
other protozoans (i.e. Histomonas
body, 6-9 x 4-8 µm, with typical number
meleagridis). In dead animals, if they are
of flagella for the genus.
fresh, a wet mount from the cecal lesions
may reveal the presence of mobile Tetratrichomonas pavlovi has a pear-
organisms with the typical trichomonads shaped body, 11-12 x 6-7 µm, an
morphology. Otherwise, cytology or undulating membrane with 2-4 waves
histopathology are other options. and otherwise a similar morphology with
T. buttreyi.
Treatment. Usually the infections should
not be treated, as nitroimidazoles are Pentatrichomonas hominis is piriform, 5-
forbidden in animals intended for human 14 x 7-10 µm. There are five free flagella,
consumption. The underlying conditions four of which are grouped together and
oriented forward, and the fifth is separate
and somehow recurrent. The sixth was a major decline of the disease due to
flagellum, the true-recurrent one, runs the introduction of efficient drugs. First
along the undulating membrane ending report in chicken came in 1900 in USA.
with a free portion.
Etiology. The causative agent of black-
Trichomitus rotunda has wide piriform or head disease in turkeys and chicken is
ovoid shape, 7-11 x 5-7 µm Histomonas meleagridis. The same
species has been reported occasionally
Life cycle. Direct. No cysts stages are
from a great variety of birds, including
known.
ostriches and birds captive in zoos.
Pathogenesis. Clinical signs. Pathology. Another species (Parahistomonas
The pathogenic role of intestinal wenrichi) which is non-pathogenic was
trichomonads from mammals has not described more recently from turkeys
been clearly defined. All the species and other birds.
mentioned above have been isolated from
Morphology. Histomonas meleagridis
clinical cases with diarrhea and/or
(figure 2.27) has several developmental
enteritis.
forms (pleomorphism). However, all of
Diagnosis. Treatment. Control. See them are trophic stages; no cyst is known.
comments from Chapter 2.3.2.4. When they inhabit the lumen of the
cecum or when they are cultured, the
shape is irregular (or amoeboid), 5-30
2.3.2.6 Histomonosis of poultry µm in diameter and with a single
flagellum. Sometimes, during cell
Introduction. Known also as the black- division, two flagella can be observed.
head disease, histomonosis is a major Even during this stage they are able of
disease causing extensive economic moving by pseudopodia to invade tissues.
losses mainly in turkey farms with a very The tissue stages lack flagellum and
unusual way of transmission. resemble amoebae. Like trichomonads,
they lack mitochondria.
Historical notes. The disease was
described for the first time in Rhode Life cycle. The life cycle is considered
Island, USA in 1893, in turkeys. Two heteroxenous, with poultry as definitive
years later, Smith described the agent. hosts and nematodes from genus
Immediately after its discovery, Heterakis as intermediate hosts. Heterakis
Histomonas decimated turkey gallinae are nematodes parasitizing the
populations of USA from 11 million birds ceca of domestic poultry. When they feed,
in 1890 to 3.7 million in 1920, accounting they accidentally ingest the trophozoites
for one third of all the mortality cases in of Histomonas meleagridis. In the
this species. The mechanism of nematodes gut, they multiply and
transmission was fully understood only subsequently they invade the
in 1920, by Tyzzer. In 1926, the disease germinative area of the female ovaries.
was already known also in Europe, Asia They continue to feed and multiply and
and Australia. In the late 1960s, there
gradually they are incorporated in the Epidemiology. The distribution of

forming eggs of the nematode. histomonosis is global. It is distributed
virtually everywhere where large turkey
or chicken communities exist. Although
the main clinical importance of
Histomonas is in turkeys, the principal
reservoirs for the infections are chicken,
as asymptomatic carriers.
Infected Heterakis gallinae eggs can

survive in the environment at least two
years. However, if free trophozoites are
eliminated in the environment directly
with the feces of the birds they survive
for very short periods of time. Hence,
most transmission from host to host is
Figure 2.27 Histomonas meleagridis:
relying on Heterakis gallinae.
form in the lumen of the cecum (upper
Nevertheless, direct contamination is also
left); intermediate form (upper right);
possible and it is assumed that this
tissue form (lower).
situation is responsible for sudden
epizootics in dense flocks of turkeys.
More interestingly, it continues Young birds are the most susceptible and
multiplication even after the new the most infected age group is in turkeys
nematode embryo starts in ovo up to 14 weeks, with the higher
development, and H. meleagridis invades frequency of clinical cases between 3 and
the newly formed nematode larvae, still 12 weeks. Mortality can reach 100%. The
inside its egg. The larvated egg offers a main reservoirs for infection (directly for
perfect shelter to Histomonas. turkeys if kept together, or indirectly, by
infecting the vector nematodes) are
When the infective nematode eggs of
chicken, which are often asymptomatic
Heterakis gallinae are ingested by a bird,
carriers.
nematode larvae hatch, and Histomonas
meleagridis leaves its “Trojan horse”, Pathogenesis. After Histomonas
invading the avian host. To make things trophozoites emerge from the carrier
even more complicated, earthworms nematode hosts, they invade the ceca and
commonly act as paratenic hosts to from there, via blood they are carried to
Heterakis, and indirectly to Histomonas. various other internal organs (liver,
Parahistomonas wenrichi has the same kidney, bursa of Fabricius). During the
way of transmission, through Heterakis infection, the xanthophylls from the
gallinae. blood decrease and methemoglobinemia
increases, resulting in a dark coloration
Histomonas multiplies by binary fission.
of the skin (hence the name black head
No sexual stages are known.
disease). The symptoms are very
commonly exacerbated by the concurrent

infection with Escherichia coli or
Clostridium perfringens.
Immunology. As soon as histomonosis

has been identified as a severe
economical problem in farmed turkeys,
researchers have tried to figure out a way
for making them immune to the infection.
Infection does not confer immunity.
Moreover, reinfections can be as severe
as any infection and may even cause
death. Nevertheless, young turkeys are
more sensitive than adult ones, but it was
not shown if immunity plays a certain Figure 2.28 Liver of a turkey naturally
role in this. An interesting observation is infected with Histomonas meleagridis
that birds with some degree of immunity showing typical circular necrotic lesions.
against Heterakis gallinae are more (Photo Cristian Magdaș)
resistant to the infection with Histomonas
meleagridis.
On gross section, they extend also into
Clinical signs. The most common form of the internal parts of the hepatic tissue. In
the disease, mainly in young turkeys is chronic cases, these lesions might extent
acute. Infected turkeys have ruffled to contiguous organs like kidneys or
feathers, hanging wings and tail with lungs. These hepatic lesions may be small
yellowish (sulfur-colored) diarrhea. The and multiple or large and confluent. In
skin of the head might become dark other cases, they have a tumour like
colored, almost black, hence the name of appearance (differential diagnosis with
the diseases. If not treated, most birds die leucosis). Histology shows lymphocytic
in 1-2 weeks. In older turkeys, the disease and macrophage infiltration with the
is more often asymptomatic or chronic, presence of multinucleated giant cells in
but virulent strains can induce even in these. The parasitic organisms appear in
them an acute form. In chicken, the clusters. The cecal lesions in turkeys are
infection is usually mild or asymptomatic. also necrotic, with abundant white
Pathology. The main sites of lesions are fibrinous material filling the entire lumen
the liver and the ceca. The hepatic lesions (figure 2.29). The mucosa shows also
in turkeys are considered to be very small, hemorrhagic ulcers (figure 2.30).
characteristic or even pathognomonic. The ceca are often enlarged. Cecal
They consist of round, 1-2 cm areas of perforation may occur. In chicken, the
necrosis on the liver surface, yellowish cecal lesions can be necrotic, like in
and crater-like, with well-defined turkeys or hemorrhagic, resembling
margins (figure 2.28). Eimeria tenella coccidiosis.
From the hepatic and cecal lesions, the

direct microscopic examination (wet
mount) can demonstrate the presence of
live, highly motile Histomonas.
Alternatively, in cytological examination

or histological section the parasite is also
well visible and identifiable.
There are techniques available for the in

vitro cultivation of Histomonas
meleagridis. Several cultivation media can
be successfully used: Egg slant medium,
Laidlaw and Devolt medium or Dwyer
medium.
Figure 2.29 Cecum of a turkey naturally
infected with Histomonas meleagridis Recently, primers for the PCR diagnosis
showing necrosis of the mucosa and were designed and employed for
fibrinous content in the lumen. (Photo research, but their use in the routine tests
Cristian Magdaș) is not yet widely introduced.
Treatment. Despite of many successfully

in vitro tested compounds, no single drug
is available for in vivo use.
Most of them have high toxicity and their

use is forbidden due to human health
risks. Such products include: arsenical
compounds, nitroheterocyclic
compounds etc. The only drugs which are
allowed are those against the vector host,
the nematode Heterakis gallinae
(albendazole, fenbendazole).
Control. As no drugs for the treatment

are available, the only real control
measure is prevention. In general,
Figure 2.30 Cecum of a turkey naturally avoiding housing together turkeys and
infected with Histomonas meleagridis chicken, pasture rotation if grazing
showing multiple ulcerations of the systems are used, avoiding of
mucosa. (Photo Cristian Magdaș) overcrowding are some measure which
are somehow effective.
Diagnosis. The most common diagnosis Periodic treatment and

is based on gross lesions. Circular liver chemoprophylaxis against nematodes are
necrosis are considered pathognomonic. also very important.
Several attempts have been made to Medical importance. Genus Giardia is an

obtain a commercial vaccine. Live important pathogen of domestic animals
attenuated strains used during the early and humans, with zoonotic potential,
days offer some protection. However, causing digestive problems mainly in
they cannot be used, as prolonged culture young animals and children. Genus
induces the loss in their colonizing Hexamita is responsible for enteric
capacity. After the discovery of the lesions in colonies of laboratory rodents,
second, non-pathogenic species, in turkeys and pigeons. Both genera are
Parahistomonas wenrichi, it was believed considered opportunistic.
that it will induce cross immunity.
However, the results were inconsistent.
There were some moderate results 2.3.3.1 Giardiosis
following chemo-immunization (infection
followed by treatment to stop the disease Introduction. Giardiosis is a worldwide
before serious lesions appear). distributed zoonotic disease caused by
Giardia duodenalis, affecting hundreds of
mammal species, including domestic
2.3.3 Diplomonadids animals and humans, responsible for
diarrheal outbreaks and malabsorption
Introduction. The family Hexamitidae is mainly in children and young or
a member of order Diplomonadida. The immunosuppressed animals.
order includes flagellates with two
Historical notes. Giardia duodenalis has
separate nuclei, a simple cytoskeleton, no
a very important place in history. It was
plasmids and no mitochondria.
one of the first microscopic organisms to
The family Hexamitidae includes five be ever seen by the human eye. It was
genera. There are two medically observed for the first time by the Antonie
important genera, Giardia and Hexamita, van Leeuwenhoek with one of the first
the later not detailed in this textbook due microscopes, built by himself. He saw
to its limited importance in domestic Giardia in his own feces in 1681. For
animals. more than 200 years the parasite was
forgotten. In 1902, Stiles associated the
General morphology. The most striking
presence of Giardia with diarrhea in
aspect is the apparent bilateral symmetry
humans. His assumptions were correct,
(two symmetric nuclei, the position of the
as in the World War 1, many soldiers
even number of flagella). More aspects
suffering from diarrhea were passing in
will be discussed for members of genus
their stools Giardia parasites.
Giardia.
Etiology. The taxonomy of genus Giardia
Ecology and transmission. Some
is still a controversial issue in systematic
authors regard Hexamitidae as
parasitology. We will follow the opinion
commensals inhabiting the digestive tract
of the latest reviews which list 6 valid
of a variety of vertebrate species.
species: G. agilis (from amphibians), G.
Transmission is via fecal-oral route.
ardeae and G. psittaci (from birds), G. end and pointed posterior end. The body
muris and G. microti (from rodents) and is flattened dorsoventrally, and has a
G. duodenalis (from various mammals). convex shape towards the dorsal part
(spoon-like aspect). On the ventral side of
The only species with veterinary and
its surface, Giardia possesses an adhesive
zoonotic importance is G. duodenalis. All
disk. The adhesive disk (which is rigid
previous names used for this species in
due to the presence microtubules) is used
the past, some of them extensively (i.e. G.
for adherence to the host cells.
lamblia, G. intestinalis) must be regarded
now as invalid and considered synonyms. The trophozoite bears four pairs of
Today, G. duodenalis is divided into 7 flagella. One pair (known as ventral
assemblages, named from A to G: flagella) is located in the ventral groove.
Each flagellum originates from an
 assemblage A (zoonotic): primates
organelle called kinetosome. Posterior to
(including humans), livestock, cats,
the adhesive disk, Giardia has two
dogs, beavers;
structures with unknown function, called
 assemblage B (zoonotic): primates median bodies. Giardia has no
(including humans), dogs, beavers; mitochondria, no Golgi apparatus and no
axostyle.
 assemblage C (non-zoonotic): dogs;
The cysts (figure 2.32) are 8-12 x 7-10
 assemblage D (non-zoonotic): dogs;
µm, with 2-4 nuclei and inner structures
 assemblage E (non-zoonotic): cattle, corresponding to axonemes of the flagella
sheep, pigs; and median bodies.
 assemblage F (non-zoonotic): cats; Life cycle. The infective elements are
cysts from the environment (usually from
 assemblage G (non-zoonotic):
contaminated drinking water).
rodents
After ingestion, the excystation is
There are some attempts to use binomial
triggered by the low gastric pH and
specific names for each of these
pancreatic enzymes. From each cyst,
assemblages: G. canis (for C and D), G.
usually two trophozoites are emerging in
simondi (for G), G. cati (for F), G. bovis (for
the duodenum. They swim by rotational
E), G. enterica (for B) and G. duodenalis
movements towards the mucosal surface
(for A). As they are not widely accepted,
where they attach using the adhesive
their further use in this textbook will be
disks. Trophozoites inhabit the surface of
avoided.
the intestinal epithelium. Despite the
Morphology. Species of genus Giardia trophozoites of Giardia are highly mobile,
have two developmental stages: the they prefer to stay attached rather than
endogenous stage called trophozoite and swim.
the exogenous stage, known as cyst. The
They multiply by binary fission. Three
trophozoites of Giardia (figure 2.31) are
cellular divisions take place before the
piriform, with round and broad anterior
trophozoites are mature.
The speed and amount of multiplication

in Giardia is amazing. Estimates say that
diarrheic stools from infected humans
can contain around 14 billion Giardia
individuals.
As trophozoites move to the colon and

the intestinal content becomes
dehydrated, Giardia begins the
encystation process. They are eliminated
through the feces of the infected host in
the environment where they are
immediately infective to a new host.
The metabolism of Giardia is anaerobe.

However, it tolerates well the presence of
oxygen. Trophozoites feed on the mucus
produced by the host cell.
Epidemiology. Although not a severe or

life threatening disease, giardiosis is
among the most widespread infection of
humans and animals. The geographical
wide distribution, the large spectrum of
Figure 2.31 Trophozoite of Giardia hosts, the high prevalence in certain
duodenalis. areas makes giardiosis an important
public health problem. This large scale
importance is probably caused by the
relatively high resistance of cysts in the
environment and by the great variety and
ease of transmission mechanisms. The
transmission route is always fecal-oral,
and the possible mechanisms, direct or
indirect are: human to human, animal to
animal, animal to human or human to
animal. The infection sources are
represented in all cases by: contaminated
water (drinking or recreational),
contaminated food (from water used in
its preparation or from food handlers).
The most common source of infection for

humans is drinking water from various
Figure 2.32 Cyst of Giardia duodenalis. sources, including public systems. They
are usually caused by severe deficiencies malabsorption of other nutrients

in the water filtration process. The together with dehydration induces
contamination of water is through the weight loss.
discharge of human sewage or drainage
Immunology. Most of the knowledge on
of animal feces, mainly from farms (cattle,
the immune response in giardiosis is
sheep, goats, pigs and horses). Another
either from humans or laboratory animal
very common source of infection are
models. Infection with Giardia induces a
aquatic mammals (muskrats, beavers,
strong humoral immune response. The
otters and nutria). Consumption of fresh
most important antibodies are IgA, which
vegetables, fruits or shellfish has also
are secreted in the intestinal lumen. They
been reported as infection sources.
have good in vitro effect, but the
Cysts of Giardia can survive in the water antigenic variation of Giardia reduces
or soil for several months. Freezing their efficacy in vivo. The role of the
during winter destroys the cysts. Cysts immune system in the defense against
are sensitive to UV light. Exposure to Giardia is evident mainly in the light of
chlorine and chloramines during the several clinical signs in immunodeficient
water disinfection is ineffective against hosts. The role of cellular immunity is not
Giardia cysts. Cysts are sensitive to ozone fully understood, but it seems it plays a
treatment. less important role in protection.
Pathogenesis. The pathogenicity Clinical signs. Most of the infections in

depends on the strain (assemblage, animals and humans are inapparent. In
genotypes etc.) and on the host. Most of domestic animals, the clinical disease is
the cases are asymptomatic. reported occasionally in dogs, cats,
ruminants and pigs. Symptoms are more
Several mechanisms have been
common in young animals.
incriminated in the pathogenesis of
giardiosis in humans and animals. These In dogs and cats, the symptoms vary from
include: production of toxins, intestinal subclinical to moderate or severe
dysmicrobism, inhibition of normal abdominal discomfort and pain. Diarrhea
enzymatic activity of the enterocytes, is not constant, but when it is present it is
intestinal motility disorders. The soft, watery and coated with mucus and
permanent attachment of trophozoites to often with steatorrhea and strong odor.
the enterocytes induces mucus The diarrhea is self-limiting in dogs and
hypersecretion and destruction of cats with normal immune status.
microvilli.
As a result of long-term malabsorption
The anaerobic metabolism is responsible and diarrhea, chronic, persistent
for gas production resulting in flatulence infections are accompanied by
and intestinal distension with pain. The dehydration and weigh loss. Diarrhea can
results of all these is diarrhea and be continuous or intermittent. Flatulence
malabsorption. Impaired absorption of may be present, mainly in humans.
fats leads to fatty stools, while the Typically, the blood is not present in feces
of animals suffering from giardiosis. If

blood is present it might be the results of
concurrent bacterial or coccidian
infections. Some dogs and cats may
vomit. Fever is usually absent.
Differential diagnosis in dogs and cats
include pancreatic insufficiency or other
malabsorption syndromes.
In calves and other livestock, the clinical

picture is more or less similar to the
symptoms described above for dogs and
cats. Diarrhea which is not responsive to
antibiotic or anticoccidial treatment in
young animals (1-6 months) might be an Figure 2.33 Cyst of Giardia duodenalis
indication of giardiosis or crypto- from the feces of a dog. (Photo Viorica
sporidiosis (see Chapter 2.4.2.1). Mircean)
In such cases, confirmation must be using

laboratory methods. In livestock, the
economic impact of the disease is also
important, as infection results in a
decreased feed efficiency and weight
gain.
Hematology and biochemistry laboratory

values are usually within physiological
limits. They can reflect only dehydration
with loss of electrolytes if diarrhea is
severe.
Pathology. Gross intestinal lesions are

rarely evident. Microscopic lesions
consist in the villous atrophy of the
enterocytes. Figure 2.34 Trophozoites of Giardia
duodenalis from culture. (Photo Andrei D.
Diagnosis. The preferred method for the Mihalca)
diagnosis of Giardia cysts in feces is
ELISA, employed for detection of
coproantigens. Direct detection of cysts Other diagnosis methods include
(figure 2.33) or even trophozoites immunofluorescence and phase contrast
(figure 2.34) by microscopic microscopy. Identification of assemblages
examination is possible. Various methods and genotypes is done by molecular
are used, including flotation and staining techniques (e.g. PCR).
methods (iodine).
Treatment. Various drugs have been dogs and cats. Side effects include
used for the treatment of giardiosis in anorexia and vomiting.
animals. Most effective group of drugs are
 Furazolidone, 4 mg/kg body
benzimidazoles.
weight/day, orally, for one week is
There are no licensed drugs to be used in effective in dogs and cats.
farm animals. In pets (dogs and cats),
 Paromomycin, 50–75 mg/kg body
several protocols are approved and
weight/day, orally, for 5 consecutive
licensed. The following protocols can be
days is used in calves.
used:
 Fenbendazole, 50 mg/kg body

weight/day, orally for three These drugs may not eliminate
consecutive days. It is recommended completely the infection, but they reduce
for treatment of dogs, including significantly the oocyst shed and severity
pregnant and lactating females. It is of symptoms.
not approved for cats. In ruminants, Control. The most effective prevention is
the dose is 5-20 mg/kg body by avoiding ingestion of cysts. In humans,
weight/day, orally for three drinking pure water (boiled, filtered) is
consecutive days. Fenbendazole has the key. In animals, these general
also been used in birds. preventive measures are more difficult to
 Oxfendazole, 11.3 mg/kg body be applied. However, a good waste
weight/day, orally for three management in farms greatly reduce the
consecutive days is used also in dogs. environmental pollution.
It is not approved, but it is effective. Specific prevention is available for dogs
 Albendazole, 25 mg/kg body and cats as vaccination. The commercial
weight/day, orally for 4-5 product is a killed vaccine, efficient for
consecutive days in dogs and cats. It both, prevention and treatment.
is not approved but it is effective.
Bone marrow toxicity of albendazole
has been reported. In calves, the 2.4 Apicomplexa
same dose given for fenbendazole is
recommended. Phylum Apicomplexa includes exclusively
parasitic organisms, some of them with
 Pyrantel and febantel combination
huge medical importance in both human
(each at 30 mg/kg body weight/day,
and veterinary medicine. Prominent
orally, single dose, are effective in
examples of medically important
canine giardiosis.
apicomplexans are the agents of human
 Metronidazole, 25 mg/kg body malaria (genus Plasmodium) which are
weight/twice a day, orally, for 5-7 responsible for more than one million
consecutive days is 65% effective in deaths annually. In animals, genus
Eimeria has a huge economic impact on
poultry farming. Other species have subpellicular microtubules radiate

major zoonotic impact (e.g. Toxoplasma, posteriorly, parallel to the body axis.
Cryptosporidium).
 the conoid, consists of a conic spiral
The name Apicomplexa is derived from of fibrillar structures. It is not
the presence of a series of ultrastructural present in all apicomplexans. Based
cell organelles, known as the apical on its presence or absence, Phylum
complex (figure 2.35). The apical Apicomplexa is divided in two
complex is present only in “zoite”-like classes: Conoidasida (with conoid)
stage (e.g. sporozoites, merozoites). and Aconoidasida (without conoid).
The apical complex includes several  two or more rhoptries, under the
structures: shape of elongated bodies.
 one or two polar rings, which  micronemes, like smaller elongated
surround the apical tip of the cell; bodies.
from the polar rings, two
Table 2.8 Taxa of veterinary importance in phylum Apicomplexa
Most
Class Order Family important Disease (Chapter)
genera
Intestinal coccidiosis in
mammals (2.4.1.1)
Intestinal eimeriosis in
birds (2.4.1.2)
Eimeria
Hepatic eimeriosis in
rabbits (2.4.1.3)
Eimeriidae
Renal eimeriosis in geese
(2.4.1.4)
Isosporosis in pigs
(2.4.1.5)
Eimeriorina Isospora
Coccidia Isosporosis in carnivores
(2.4.1.6)
Sarcocystosis in domestic
Sarcocystis
animals (2.4.3.1)
Toxoplasmosis in
Toxoplasma domestic animals
Sarcocystidae
(2.4.3.2)
Neospora Neosporosis (2.4.3.3)
Hammondia Hammondiosis (2.4.3.4)
Besnoitia Besnoitiosis (2.4.3.5)
Adeleorina Hepatozoidae Hepatozoon Hepatozoonosis (2.4.4.1)
Cryptosporidiosis in
Cryptosporidea Cryptosporidiidae Cryptosporidium domestic animals
(2.4.2.1)
Babesiosis in domestic
Babesiidae Babesia
animals (2.4.6.1)
Haematozoea Piroplasmida
Theileriosis in domestic
Theileriidae Theileria
animals (2.4.7.1)
Micropores located along the body  Some groups (Eimeriidae,

margins of the “zoites” have role in the Cryptosporidiidae) have
ingestion of food by the parasitic homoxenous life cycle (black
organism. Movement cell organelles pathway in figure 2.36), with
(flagella, cilia, pseudopodia) are absent in endogenous and exogenous stages.
apicomplexans, with the exception of Infection of the host is made with
very few developmental stages (like some infectious stages from the
gametes). environment.
Additionally, the apicomplexan cell  Some others (Babesia, Theileria,
contains various cell organelles and Hepatozoon) are heteroxenous, with
structures typical to eukaryote cells: no stages in the external
nucleus, mitochondria, Golgi body etc. environment (red pathway in figure
Apicomplexans have a very complex life 2.36). These include vector-borne
cycle (figure 2.36), with three main species which are transmitted to the
types of pathways. vector by blood meal and to the host
by blood meal or ingestion of vector.
 The third group includes members of

Sarcocystidae family (Sarcocystis,
Toxoplasma, Neospora) with
heteroxenous development (blue
pathway in figure 2.36).
Transmission from the definitive
host (which is usually a carnivorous
species) to the intermediate host is
through the environment, and from
the intermediate host to the
definitive host by predatorism.
The multiplication in Apicomplexa takes

place in both ways: asexually (binary
fission, multiple fission or
endopolyogeny) and sexually (by male
and female gametes). The sexual
reproduction takes place always in the
definitive host. The vast majority of
species are intracellular parasites. All
domestic species are affected by diseases
produced by apicomplexans.
Figure 2.35 General structure of the cell The apicomplexan species of veterinary
in Apicomplexa. importance are included in three classes
A more detailed list of genera and merogony once again. Merogony is

associated diseases is shown in table 2.8. repeated several times, depending on
several factors. The last generation of
merozoites will transform into gamonts,
initiating the gametogony. There are two
types of gamonts (gametocytes):
microgametocytes (corresponding to
male cells) and macrogametocytes
(female). Each macrogametocyte
develops into one macrogamete. Each
microgametocyte divides by multiple
fission producing numerous biflagellated
microgametes. The macrogamete is
fertilized by a microgamete and this
produces the zygote. Zygotes develop
into oocysts. By sporogony, inside each
oocyst the sporozoites will be formed.
Figure 2.36 General life cycle paths in

Apicomplexa of domestic animals. H =
2.4.1 Eimeriidae
Host; DH = Definitive Host; IH =
Intermediate Host; E = Environment. For
Introduction. Family Eimeriidae include
detailed explanations please refer to the
thousands of species parasitic in
text.
vertebrates and invertebrates. There are
three genera of veterinary importance:
Eimeria, Isospora and Tyzzeria.
Coccidia and Cryptosporidea inhabit the
epithelium of digestive tube, the liver, General morphology. Each
kidney, blood cells and various other developmental stage has a typical
tissues of vertebrates and invertebrates. morphology. Nevertheless, the most
important stage from diagnostic point of
The typical life cycle of coccidia has three
view and for specific identification is the
phases: merogony, gametogony and
oocyst. The internal structure of the
sporogony. The infective stages are
sporulated oocysts is different in the
called sporozoites. These sausage-shaped
various genera of the family (figure
(or banana-shaped) cells infect the host
2.37).
via various routes and after entering the
host cell they become trophozoites and In genus Eimeria the sporulated oocysts
start the merogonic development. By contains 4 sporocysts, each with two
asexual multiplication, during merogony sporozoites. In genus Isospora, there are
numerous merozoites are produce which two sporocysts, each with four
escape from the host cell and infect other sporozoites. In genus Tyzzeria, there are
susceptible cells, re-starting the eight sporozoites, free in the oocyst and
not within a sporocyst as mentioned for

the previous two genera. The fine
structure will be detailed, as an example
for genus Eimeria (figure 2.38).
The oocyst wall has two layers. In many

species there is a small opening in the
oocysts wall called micropyle. This
opening is used for the emergence of Figure 2.37 General morphology of the
sporozoites when the oocyst reaches the most representative species of
digestive tube of the host. The micropyle, Eimeriidae: left - Eimeria (four
if present is covered by a cap. A refractile sporocysts, each with two sporozoites);
structure called polar granule may be center - Isospora (two sporocysts, each
also present. The internal structure of with four sporozoites); right - Tyzzeria
typical sporulated oocysts comprises (asporocystic oocyst, eight free
sporocysts in different numbers. sporozoites).
Figure 2.38 Diagrammatic representation of a typical sporulated oocyst of Eimeria.
Between sporocysts, an oocyst residuum other livestock, affecting mainly the

may be present, as a result of young animals. Their economic impact is
unincorporated cytoplasmic material huge and losses are due to mortalities or
during sporogony. expenses for prophylaxis and treatment.
Similarly, inside each sporocyst, as

sporocyst residuum is evident. Each
sporocyst is delimited by a sporocyst
wall. At the anterior end of the sporocysts
a small plug-like structure known as
Stieda body may be visible. Less typical is
the general morphology of the
unsporulated oocyst. Unsporulated
oocysts (figure 2.39) are present in fresh
fecal material and they have similar
morphology in all Eimeriidae genera. It is
impossible to identify the species based
on the morphology of unsporulated
oocysts. They contain one single round
central body called sporont, which has a
fine granular structure.
Ecology and transmission. All species

inhabit the intracellular environment of
epithelial cells, usually enterocytes. They Figure 2.39 Diagrammatic
can be parasitic intracytoplasmatically or representation of an unsporulated oocyst
intranuclearly. As a rule, all species are of Eimeriidae.
homoxenous, although exceptions are
documented. Merogony and gametogony
take place within the host, while 2.4.1.1 Intestinal coccidiosis in
sporogony occurs in the external mammals
environment. The infective stage is the
sporulated oocyst. Transmission is by Introduction. Intestinal coccidiosis in
ingestion of infective oocysts. Usually domestic mammals are globally
they are highly specific parasites, and distributed in infections responsible for
interspecific transmission is very limited. hemorrhagic diarrhea in young
Eimeriidae are not zoonotic. Moreover, in individuals, with possible mortality and
certain host species (like chicken for with important economic losses. Under
instance) there is also a very pronounced the name of “eimeriosis” we include
organ specificity. diseases caused by species of genera
Eimeria and Isospora.
Medical importance. Members of
Eimeriidae are responsible for severe Historical notes. The first oocysts of
intestinal infections in poultry but also in Eimeria were seen in the liver of an
infected rabbit, by Antonie van carnivores harbor only genus Isospora.

Leeuwenhoek in 1674 but it was not Pigs are the only domestic species to be
described as a new species during those infected with both genera. Previous
times. The first description of a species in reports of genus Eimeria in carnivores
genus Eimeria came in 1870, when Eimer, are probably pseudoparasitic species
a German zoologist, named a small from their prey which are passed
organism found in house mice as passively through the feces.
Gregarina falciformis. Five years later
Johann Gottlob Schneider, another
German naturalist erected a new genus in Table 2.9 Species of genus Eimeria parasitic in
domestic ruminants
the memory of Eimer and named it
Eimeria. In the following years many Species Host
E. alabamensis Cattle, Buffalo
other species parasitic in domestic and
E. auburnensis Cattle, Buffalo
wild animals have been described. Genus E. bovis Cattle
Isospora was proposed by the same E. brasiliensis Cattle
E. bukidnonensis Cattle
Schneider, in 1881. E. canadensis Cattle
E. cylindrica Cattle
Etiology. The diversity of the species in E. ellipsoidalis Cattle
genus Eimeria parasitic in domestic E. illinoisensis Cattle
E. pellita Cattle
mammals is huge. The quasi-complete list E. subspherica Cattle
of them is shown below for ruminants E. thianethi Cattle, Buffalo
E. wyomingensis Cattle
(table 2.9), equids and camelids (table
E. zuernii Cattle, Buffalo
2.10), pigs (table 2.11), rabbits (table E. ankarensis Buffalo
2.12) and laboratory rodents (table E. bareillyi Buffalo
E. gokaki Buffalo
2.13). E. ovoidalis Buffalo
E. ahsata Sheep
In domestic animals, the species of genus E. crandallis Sheep
Isospora are parasitic only in pigs and E. danielle Sheep
E. faurei Sheep
carnivores (table 2.14). E. gilruthi Sheep
E. gonzalezi Sheep
The taxonomic value of genus Isospora is E. granulosa Sheep
being under debate for some years. In E. intricata Sheep
E. marsica Sheep
1977, a new genus was proposed E. ovina Sheep
(Cystoisospora) to include species E. ovinoidalis Sheep
parasitic in carnivores with facultative E. pallida Sheep, Goat
E. parva Sheep
heteroxenous life cycle. For educational E. punctata Sheep, Goat
purposes, these taxonomic debates are E. absheronae Goat
E. africiensis Goat
more confusing, hence we will use in this E. alijevi Goat
textbook the name Isospora for all E. arloingi Goat
E. caprovina Goat
species.
E. christenseni Goat
E. gilruthi Goat
One should note that in ruminants, E. hirci Goat
horses and rabbits the only parasitic E. jolchijevi Goat
genus of Eimeriidae is Eimeria while E. kocharii Goat
E. ninakohlyakimovae Goat
Morphology. The general morphology Table 2.13 Species of genus Eimeria parasitic
in laboratory rodents
for Eimeriidae was described previously.
Species Host
E. caviae Guinea pig
Table 2.10 Species of genus Eimeria parasitic E. amburdariana Golden hamster
in domestic equids and camelids E. aurata Golden hamster
E. razgovica Golden hamster
E. arasinaensis House mouse
Species Host
E. baghdadensis House mouse
E. leuckarti Horse
E. falciformis House mouse
E. solipedum Horse
E. ferrisi House mouse
E. uniungulati Horse
E. hansonorum House mouse
E. bactriani Camels
E. hindlei House mouse
E. cameli Camels
E. keilini House mouse
E. dromedari Camels
E. krijgsmanni House mouse
E. pellerdyi Camels
E. musculi House mouse
E. rajasthani Camels
E. musculoidei House mouse
E. alpacae Llama, Alpaca
E. papillata House mouse
E. lamae Llama, Alpaca
E. paragachaica House mouse
E. macusaniensis Llama, Alpaca
E. schueffneri House mouse
E. peruviana Llama
E. vermiformis House mouse
E. punoensis Llama, Alpaca
Table 2.11 Species of genus Eimeria parasitic

in domestic pigs
Table 2.14 Species of genus Isospora parasitic
in domestic mammals
Species Host
E. almaataensis Swine
Species Host
E. betica Swine
I. suis Swine
E. debliecki Swine
I. burrowsi Dog
E. guevarai Swine
I. canis Dog
E. ibrahimovae Swine
I. neorivolta Dog
E. neodebliecki Swine
I. ohioensis Dog
E. perminuta Swine
I. felis Cat
E. polita Swine
I. rivolta Cat
E. porci Swine
E. residualis Swine
E. scabra Swine
E. spinosa Swine Specific morphology for sporulated
E. suis Swine oocysts is given for selected species in
tables 2.15, 2.16, 2.17, 2.18 and 2.19.
in domestic rabbits Identification of species can be done
solely if the oocysts are sporulated.
Species Host
E. coecicola Rabbit
Measurements are necessary for such a
E. elongata Rabbit purpose not only for the oocyst but also
E. exigua Rabbit for internal structures (sporocyst,
E. flavescens Rabbit
E. intestinalis Rabbit sporozoites). Other specific
E. irresidua Rabbit characteristics must be also observed:
E. magna Rabbit
E. matsubayashii Rabbit presence or absence of the micropyle,
E. media Rabbit Stieda body, polar granule, aspect of
E. neoleporis Rabbit
oocyst and sporocyst residuum etc. In
E. perforans Rabbit
E. piriformis Rabbit fresh feces, the oocysts are not
100 | P r o t o z o a
sporulated and their specific Table 2.15 Basic morphology of Eimeria

parasitic in domestic ruminants
identification is not achievable.
Species Oocyst shape Size
Life cycle. The common aspects of the (µm)
life cycle were described under general E. alabamensis subellipsoidal 13-24 x
considerations about Eimeriidae 11-16
E. auburnensis elongated- 32-46 x
(Chapter 2.4.1). Intestinal Eimeria species ovoidal 20-25
develop intracellularly in epithelial cells E. bovis ovoidal 23-34 x
17-23
of the intestine (enterocytes) (figure E. brasiliensis ovoidal 34-42 x
2.40). Each species has a specific habitat. 24-29
E. bukidnonensis piriform 33-41 x
Some species inhabit the small intestine, 24-28
some other the large intestine. Other E. canadensis ellipsoidal 28-37 x
20-27
species are very limited (only duodenum) E. cylindrica cylindrical 16-27 x
others are more generalist and can infect 12-15
E. ellipsoidalis ellipsoidal 12-27 x
portion of the intestine. Hosts acquire the 10-18
infection when ingesting sporulated E. pellita ovoidal 32-42 x
22-27
oocysts (figure 2.40 - 1). Sporozoites
E. subspherica subspherical 9-13 x
escape (figure 2.40 - 2) through the 8-12
opened micropyle. In the species which E. wyomingensis ovoidal 37-45 x
26-30
lack micropyle, the oocyst wall ruptures E. zuernii spherical 15-22 x
in order to release the sporozoites. 13-18
E. ankarensis elongated- 32-43 x
Sporozoites will enter a host cell (figure ovoidal 25-29
2.40 - 3) and start the merogony. They E. bareillyi piriform 23-29 x
16-22
soon become enlarged trophozoites E. gokaki ovoidal 22-32 x
(figure 2.40 - 4), divide their nucleus and 18-25
E. ovoidalis ovoidal 32-40 x
become multinucleated cells (called 20-28
meronts (figure 2.40 - 5). Each nucleus E. ahsata
ellipsoidal 29-37 x
17-28
will be incorporated in the structures of ellipsoidal 17-23 x
E. crandallis
the merozoites (figure 2.40 - 6). 17-22
ovoidal 25-36 x
Merozoites than rupture the host cell E. faurei
19-28
(figure 2.40 - 7) and actively search for a ellipsoidal 26-38 x
E. gonzalezi
new cell which they infect, repeating the 20-26
ellipsoidal 22-35 x
merogony (figure 2.40 - 8). The last E. granulosa
17-25
generation of merozoites (figure 2.40 - 9) ellipsoidal 39-53 x
E. intricata
27-34
will enter enterocytes (figure 2.40 - 10 ellipsoidal 23-36 x
E. ovina
and 11) and become macrogametes 16-24
subspherical 12-23 x
(figure 2.40 - 12) and biflagellated E. parva
10-19
microgametes (figure 2.40 - 13). The E. punctata
ellipsoidal 18-25 x
16-21
microgametes will fertilize the E. arloingi ellipsoidal 17-42 x
macrogamete (figure 2.40 - 14) forming 13-27
E. christenseni ovoidal 34-41 x
the zygote (figure 2.40 - 15) which 23-28
eventually becomes an oocyst (figure E. hirci round 18-23 x
14-19
2.40 - 16).
101 | P r o t o z o a
Table 2.16 Basic morphology of Eimeria Table 2.18 Basic morphology of Eimeria
parasitic in domestic equids and camelids parasitic in domestic rabbits
Species Oocyst shape Size Species Oocyst shape Size

(µm) (µm)
E. leuckarti piriform 75-88 x E. exigua subspherical 10-18 x
50-59 9-16
E. solipedum spherical 15-28 x E. intestinalis piriform 27-32 x
15-28 17-20
E. uniungulati oval-ellipsoidal 15-24 x E. irresidua ovoidal 31-43 x
12-17 22-27
E. bactriani subspherical 32 x 25- E. magna ovoidal 31-40 x
27 22-26
E. cameli oval 81-99 x E. matsubayashii ovoidal 22-29 x
63-94 16-22
E. dromedari ovoidal 23-33 x E. media ovoidal 27-36 x
20-25 15-22
E. pellerdyi ellipsoidal 22-24 x E. neoleporis subcylindrical 33-44 x
12-13 16-23
E. rajasthani ellipsoidal 34-39 x E. perforans ellipsoidal 15-29 x
25-27 11-17
E. alpacae ellipsoidal 22-26 x E. piriformis piriform 26-32 x
18-21 17-21
E. lamae ovoidal 30-40 x
21-30
E. macusaniensis ovoidal 81-99 x Table 2.19 Basic morphology of Isospora
61-80 parasitic in domestic mammals
E. peruviana ovoidal 28-37 x
18-22 Species Oocyst shape Size (µm)
E. punoensis ellipsoidal 17-22 x I. suis subspherical 20-24 x
14-18 18-21
I. burrowsi ellipsoidal 17-22 x
16-19
Table 2.17 Basic morphology of Eimeria I. canis ellipsoidal 34-42 x
parasitic in domestic pigs 27-33
I. neorivolta oval 15-19 x
Species Oocyst shape Size (µm) 13-16
E. debliecki ellipsoidal 18-24 x I. ohioensis oval 23-25 x
15-20 19-20
E. guevarai piriform 26-32 x I. felis oval 39-48 x
15-19 26-37
E. neodebliecki ellipsoidal 17-26 x I. rivolta oval 20-25 x
13-20 15-20
E. perminuta ovoidal 11-16 x
10-13
E. polita ellipsoidal 22-31 x The time needed for sporulation is
17-22
E. porci ovoidal 18-27 x variable, from species to species and it
13-18 depends a lot on various environmental
E. scabra ovoidal 22-36 x
16-26 factors like temperature and humidity.
E. spinosa ellipsoidal 16-22 x The average sporulation times for
13-16
selected species of Eimeria and Isospora
are given in tables 2.20, 2.21, 2.22, 2.23
Oocysts are eliminated into the and 2.24.
environment through the feces of the
In genus Isospora, the general life cycle is
host (figure 2.40 - 17) where they
similar with the one described for
sporulate (figure 2.40 - 18).
102 | P r o t o z o a
Eimeria. However, in several species Table 2.21 Sporulation times of Eimeria

parasitic in domestic equids and camelids
infecting carnivores, the presence of
paratenic hosts (facultative heteroxenous Species Sporulation time
life cycle) has been reported. In this case, (days)
E. leuckarti 14-21
the final hosts (dogs, cats) become E. bactriani 10
infected after preying on infected hosts. E. cameli 10-15
E. dromedari 15-17
Moreover, in species of genus Isospora E. pellerdyi 5
parasitic in carnivores, extraintestinal E. rajasthani 7
replication can take place in mesenteric
lymph nodes, spleen or liver. Table 2.22 Sporulation times of Eimeria
parasitic in domestic pigs
Species Sporulation time

Table 2.20 Sporulation times of Eimeria
(days)
parasitic in domestic ruminants
E. debliecki 7
E. guevarai 10
Species Sporulation time E. neodebliecki 13
(days) E. perminuta 9-11
E. alabamensis 4-5 E. polita 8-9
E. auburnensis 2-3 E. porci 9
E. bovis 2-3 E. scabra 9-12
E. brasiliensis 6 E. spinosa 10-12
E. bukidnonensis 4-7
E. canadensis 3-4
E. cylindrica 2 Table 2.23 Sporulation times of Eimeria
E. ellipsoidalis 2-3 parasitic in domestic rabbits
E. pellita 10-12
E. subspherica 4-5
Species Sporulation time
E. wyomingensis 5-7
(days)
E. zuernii 2-3
E. intestinalis 1-2
E. ankarensis 3-4
E. irresidua 2
E. bareillyi 3-4
E. magna 2-3
E. gokaki 7
E. matsubayashii 1-2
E. ovoidalis 4-5
E. media 2
E. ahsata 2-3
E. neoleporis 2-3
E. crandallis 1-3
E. perforans 3-5
E. faurei 1-2
E. piriformis 1-2
E. gonzalezi 5-6
E. granulosa 3-4
E. intricata 3-5
Table 2.24 Sporulation times of Isospora
E. ovina 2-4
parasitic in domestic animals
E. parva 2
E. punctata 1-2
E. arloingi 1-2 Species Sporulation time
E. christenseni 6 (days)
E. hirci 2-3 I. suis 3-5
E. ninakohlyakimovae 1-4 I. canis 2
I. neorivolta 2
I. ohioensis 4
I. felis 2
Epidemiology. In general, intestinal I. rivolta 4
eimeriosis in mammals is distributed
worldwide. However, some species are
It is beyond the scope of this textbook to
known only from certain parts of the
provide detailed information on the
world.
103 | P r o t o z o a
distribution of each mammalian Eimeria Intestinal Eimeria of domestic rabbits is

or Isospora species. Generally, they are extremely common. Virtually all rabbits
more prevalent in areas with warmer and are infected. Coprophagia has been
humid climate (i.e tropics, subtropics). incriminated as a cause for such a high
Usually, infection is present in all age prevalence. The rabbits are susceptible
groups, at lower intensities in adult from the age of 16 days.
animals which are asymptomatic carriers
In dogs and cats, younger individuals are
and a permanent source of infection for
more commonly affected. Cats under four
young animals. Severity of the disease is
years are at increased risk. Purebred
exacerbated by various stress factors like
animals are more susceptible.
overcrowding, poor nutrition, post-
weaning stress, transportation etc. The The resistance of oocysts in the
disease is hence more common and more environment is normally high, with
severe in farmed animals than in specific limits for each species. In general,
backyard ones. Oocysts survive up to one year at
temperatures between -30°C and +40°C.
In cattle the disease occurs all over the
Prolonged freezing and direct sun light
world. It causes huge economic losses.
kill most oocysts on the pastures.
Mortality can reach up to 50%. Infection
is rare in suckling calves. The most Pathogenesis. It is believed that the
affected age group is 9-12 months. severity of symptoms is correlated with
the relative length of the intestine and the
In sheep and goats, the disease is very
potential number of host cells. This is
common, with moderate to high mortality
why species affecting the large intestine
in young animals. It is distributed
or specific portions of the small intestine
worldwide and responsible for important
(which have rather low lengths) are
economic losses. The most susceptible
usually more pathogenic than those with
age is 6-12 weeks, usually in the first few
less selective histotropism. Moreover, the
weeks after the first contact with the
large intestine has a much lower turn-
pasture. Outbreaks are acute, and they
over rate of the epithelial cell population
usually affect a substantial part of the
and as consequence, a lower regenerative
flock.
potential.
In horses, the infection with Eimeria is
The pathogenic effect is mostly caused by
sporadic, and it has been reported so far
the direct damage of the enterocytes
only Europe and parts of Asia. All species
during the merogonic phase of the life
can infect horses, donkeys and their
cycle. Hence, the acute form of the
hybrids.
disease is during parasitic merogony.
The infection in pigs is very common, This has a practical impact on the
although rarely symptomatic. Suckling diagnosis, as during the acute diarrhea
piglets acquire the infection from the skin the typical oocysts are absent from the
around the mammary glands. feces.
104 | P r o t o z o a
Figure 2.40 Life cycle of genus Eimeria. For the meaning of numbers, please refer to the
text.
105 | P r o t o z o a
Denudation of the intestine with the diarrhea is catarrhal in the beginning and
destruction of the epithelial lining results hemorrhagic during the merogonic
in intestinal hemorrhage, reduced water development of the coccidia.
resorption with consecutive diarrhea.
In bovines the most common species
Chronic infections with catarrhal
involved in clinical cases are E. zuernii
inflammation are responsible for
and E. bovis. The first two days of clinical
malabsorption and various consequent
infection are characterized by catarrhal
nutritional deficiencies.
diarrhea, followed by hemorrhagic
Immunology. As only young animals are discharges. Other symptoms reported in
susceptible and stress is a favoring factor cattle include: anorexia, accelerated
it is evident that the immune system has respiration, convulsions, emaciation and
a well-established role in the active tremors. Fever is rarely present. In dairy
protection against coccidial infection. The cows, milk production might be affected.
main problem with post-infective Cows with chronic infection display
immune protection is the lack of cross- intermittent/recurrent diarrhea.
immunity between the different species
Eimeriosis of sheep is a very severe
of Eimeria infecting certain hosts.
parasitic problem, with significant
There are no extensive studies on all mortality in lambs and less severe in
species of Eimeria. However, some goats (kids). Lambs with acute infections
aspects can be concluded based on show a profuse diarrhea, often
several experimental studies. It is hemorrhagic, with almost liquid feces,
thought that certain species are highly which lasts several days. Debilitated
immunogenic and the infection with very lambs become weak, they cease eating
few oocysts (less than 10) can induce a and some die.
strong immunity.
In horses, the infection is usually
Both components of the immune system asymptomatic. If clinical cases occur in
are involved in the anti-eimerial foal, they are generally mild, with
protection. IgG antibodies and moderate and self-limiting diarrhea.
lymphocytes are responsible for
Coccidiosis in pigs is rarely a clinical
protection. A strong immune response
problem. Diarrhea is not usually
can be detected at around 14 days after
hemorrhagic. More severe cases show
the initial infection.
loss of appetite, emaciation and retarded
Clinical signs. Despite the diversity of growth. Mortality is very rare.
etiological agents in the various domestic
The main symptoms in domestic rabbits
hosts, the clinical signs of coccidiosis are
are diarrhea and bloating. Mortality is
rather uniform. In adult animals the
high, sometimes even superacute,
infection is usually asymptomatic. Clinical
without any prodromal signs.
signs in young animals are
predominantly digestive, with diarrhea, In dogs and cats, diarrhea is uncommon,
dehydration, anemia and weight loss. The unless associated with
106 | P r o t o z o a
immunosuppressive condition or petechial hemorrhages and necrotic

concurrent infection. In kennels, enteritis with edema of the intestinal
outbreaks can be enzootic. wall.
Pathology. The main lesions are located The lesions in horses were described
in the intestine. Generally, they consist in after experimental infection. They consist
an inflammation of the intestinal in catarrhal enteritis, with whitish foci
epithelium (enteritis). Their severity and easily visible at gross examination.
location depends on the age of the animal
In pigs, the gross lesions consist in
and the species of coccidia involved.
catarrhal enteritis mainly in the large
Some species are located deeply, under
intestine.
the lamina propria of the enterocyte
lining and are responsible for Domestic rabbits show catarrhal
hemorrhagic lesions. Some other are enteritis, with whitish deposits.
more superficial and the lesions are In dogs and cats, lesions are usually
catarrhal. Often, whitish spots are easily catarrhal, rarely hemorrhagic.
visible on the intestinal surface. They
represent the merogonic stages of the Diagnosis. Based on clinical signs,
eimerids. diagnosis must be confirmed
microscopically. The presence in the
In cattle, the body of animals which died samples of any of the developmental
of acute eimeriosis is weak, with the stages of Eimeria or Isospora has
posterior parts (perianal area, ventral diagnostic value. During the acute stage
surface of the tail) soiled with red- of infection, when the life cycle has barely
colored feces. In the abdominal cavity reached its merogonic or gametogonic
there are small amounts of reddish phases, the oocysts (which appear after
exudate. The body is generally anemic, the gametogony) are absent from the
with pale colored organs. Mesenteric feces. During this clinical stage, other
blood vessels are hyperemic. The most developmental forms can be detected in
characteristic lesions are at the level on the feces (e.g. meronts). Examination of
intestinal mucosa. The luminal surface of large number of samples from the same
the intestines is coated with reddish flock can be helpful. For the detection of
mucus, congestion is present and the most Eimeria and Isospora oocysts,
mucosa is congested, mainly in the flotation methods are recommended. In
terminal part of the ileum and in the large certain Eimeria species (i.e. E. leuckarti
intestine (cecum and colon). The from horses) better results are obtain
intestinal content is liquid and using sedimentation.
malodorous. The hemorrhages on the
intestinal mucosa can be punctiform or The oocysts from feces are normally not
confluent. sporulated (figure 2.41), thus their
specific identification is impossible at this
In sheep and goats, the lesions are stage. For detailed morphological studies
different depending on the causative and specific diagnosis, they can be
species. In general they consist of
107 | P r o t o z o a
sporulated in the laboratory at room

temperature, using a 2.5% solution of
potassium dichromate in the presence of
oxygen. In older fecal samples, the oocyst
can begin the sporulation process and
they are found in various stages (figure
2.42).
The presence of oocysts in the feces of

ruminants, horses, and rabbits normally
means genus Eimeria. In swine, both
genera can be present (Eimeria and
Isospora). The most controversial
coproscopic diagnosis is in dogs and cats,
as domestic carnivores pass in feces Figure 2.42 Unsporulated oocyst of
oocysts of several species of intestinal Isospora sp. from the feces of a cat. Note
coccidia: Isospora, Toxoplasma, Neospora, the oocyst beginning the sporulation
Hammondia and Besnoitia. Usually, the process (lower right). (Photo Andrei D.
differentiation should be made on the Mihalca)
basis of size. In dogs, “Isospora”-like
oocysts which are larger than 15 µm are
with high probability members of genus In cats, oocysts larger than 20 µm are
Isospora. If they are smaller, they belong likely to be Isospora, while those smaller
to Neospora caninum (10-12 µm) or than 12 µm are one of the heteroxenous
Hammondia heydorni (11-12 µm). species (Toxoplasma gondii, Hammondia
hammondi, Besnoitia darlingi or Besnoitia
oryctofelisi).
However, Besnoitia wallacei also reported

in cats has slightly larger oocysts than its
congeners (17 x 12 µm).
Post-mortem diagnosis is achieved by

direct examination of the intestinal
content from the parts with lesions or by
histopathology, when all developmental
stages can be identified. For dogs and
cats, differentiation of small oocysts can
be achieved also by PCR.
Treatment. The number of available

drug used for the treatment of coccidial
Figure 2.41 Unsporulated oocyst of infections in mammals is huge. They are
Eimeria sp. from the feces of a domestic known generically as anticoccidial drugs.
rabbit. (Photo Andrei D. Mihalca)
108 | P r o t o z o a
Table 2.25 Drugs used for the treatment of coccidiosis in domestic mammals
Drug Species Dose (mg/kg) Route Duration (days)

cats, dogs 50-60 PO 5-20
Sulfadimetoxine
sheep 50-100 PO 5
cattle 140 PO 3
Sulfadimidine
sheep 25-50 PO 3
cats, dogs 100-200 PO 5
Sulfaguanidine sheep 250 PO 7
swine 200 PO 3-4
cattle 110 PO 5
Sulfamethazine
sheep 60 PO 3-5
cattle 6 PO 3-5
Sulfaquinoxaline
sheep 60 PO 3-5
dogs 30-60 PO, SC 5
Trimethoprim-sulfonamide
cats, dogs 15-30 PO, SC 5
Ormetoprim-sulfadimethoxide dogs 66 PO 7-23
Furazolidone cats, dogs 8-20 PO 5
cats, dogs 300-400 PO 5
cats, dogs 110-200 PO 7-12
cats 60-100 PO 7
cattle 10 PO 5
Amprolium
cattle 65 PO 1
sheep 50-65 PO 4-7
swine 25-65 PO 3-4
rabbits 25 PO 4-5
Quinacrine cats, dogs 10 PO 5
Clindamycin cats 10 PO, SC, IM 7-28
dogs 15-30 PO 1-6
cattle 15 PO 1
Toltrazuril
sheep 20-40 PO 1
rabbits 20 PO 1-3
Diclazuril cats 25 PO 1
dogs 30-50 PO 1-7
Ponazuril
cats 15 PO 7
cattle 1 PO 10
Monensin
sheep 1.5 PO 21
Treatment must be implemented for exposed to risk, chemoprophylaxis. The

treating animals with clinical symptoms most important factor for avoiding the
or to eliminate asymptomatic carriers, as onset of clinical disease is to maintain a
a control measure. Drugs can be used as good overall health status in young
chemoprophylaxis. animals. Neonates should be given
colostrum. Proper environmental
A check-list of available drugs and their
conditions, microclimate, a balanced
dosage for various domestic mammals is
nutrition and avoidance of overcrowding
given in table 2.25.
are essential factors. Moreover,
Control. The most efficient way for sanitation, disinfections, use of clean
controlling coccidiosis in mammals is water and watering devices are also
prevention. This can be achieved by using important.
general measures and in the animals
109 | P r o t o z o a
Unlike in birds, the use of Not only they are host specific, but they
chemoprophylaxis is not compulsory only have different tropism for various
when outbreaks are imminent (i.e. segments of the intestine (figure 2.43).
previous history of disease, introduction Other species of Eimeria parasitic in birds
of new animals). In principle, the same are shown in tables 2.27, 2.28 and 2.29.
molecules which are used for treatment
Morphology. General morphology of
can be used for chemoprophylaxis, but in
Eimeria parasitic in poultry is concordant
lower doses and long-term
with genus characteristics, discussed
administration. In ruminants, the use of
above. Specific morphology for selected
decoquinate and ionophores was shown
species parasitic in chicken is given in
to be effective. During the first month in
table 2.30. No data will be provided for
calves exposed to infection, lasalocid,
species parasitic in other domestic bird
monensin or amprolium are efficient. In
species.
pigs, sulfonamides and amprolium were
successfully used.
in chicken
2.4.1.2 Intestinal eimeriosis in birds Species Intestinal segment

E. acervulina Duodenum
E. brunetti Large intestine
Introduction. Eimeria infections in
E. dispersa Small intestine
poultry, mainly in chicken, are among the E. hagani Duodenum
most important diseases in industrial E. maxima Small intestine
E. mitis Duodenum
farms. They have a huge economical E. mivati Duodenum
dimension, mainly by expenses with the E. necatrix Small intestine
E. praecox Duodenum
prophylaxis. The estimated annual cost E. tenella Cecum
related to poultry eimeriosis is situated
around 2 billion euros.
Historical notes. The first description of

Life cycle. The life cycle follows the same
a coccidian life cycle from birds came in
phases and developmental stages as for
1910, when Fantham published his work
species parasitic in mammals. In birds,
on red grouse. In 1929, Tyzzer described
the life cycle is somehow faster that in
the life cycle for several species of
species parasitic in mammals. For some
Eimeria parasitic in chicken (E.
species (i.e. E. tenella) the entire
acervulina, E. mitis, E. maxima, E. tenella).
development takes 4-6 days.
The first anticoccidial drugs have been
introduced in 1948, when FDA approved Epidemiology. The disease is present
in USA the use of sulphaquinoxaline and everywhere where the hosts are
nitrofurazone. The first commercial presents. Their distribution is hence
vaccine was introduced in 1952. global. As the parasitism is strictly host-
specific, the only sources of infection are
Etiology. There are ten species of
conspecific birds.
coccidia parasitic in chicken (table 2.26).
110 | P r o t o z o a
Table 2.27 Species of genus Eimeria parasitic in poultry farms is mechanical, by

in other galliformes
personnel.
Species Host
E. adenoeides Turkey
E. dispersa Turkey Table 2.28 Species of genus Eimeria parasitic
E. gallopavonis Turkey in ducks and geese
E. innocua Turkey
E. meleagridis Turkey
Species Host
E. meleagrimitis Turkey
E. abramovi Duck
E. subrotunda Turkey
E. anatis Duck
E. gorakhpuri Guinea fowl
E. battakhi Duck
E. grenieri Guinea fowl
E. boschadis Duck
E. numidae Guinea fowl
E. danailovi Duck
E. colchici Pheasant
E. mulardi Duck
E. dispersa Pheasant
E. nottion Duck
E. duodenalis Pheasant
E. saitamae Duck
E. langeroni Pheasant
E. schachdagica Duck
E. megalostomata Pheasant
E. anseris Goose
E. pacifica Pheasant
E. fulva Goose
E. phasiani Pheasant
E. hermani Goose
E. mandali Peacock
E. kotlani Goose
E. mayurai Peacock
E. magnalabia Goose
E. patnaiki Peacock
E. nocens Goose
E. pavonina Peacock
E. stigmosa Goose
E. pavonis Peacock
E. striata Goose

in pigeons
Species Host
E. columbae Pigeon
E. columbarum Pigeon
E. kapotei Pigeon
E. labbeana Pigeon
Table 2.30 Basic morphology of Eimeria

parasitic in chicken
Species Oocyst shape Size (µm)

E. acervulina ovoidal 17.7-20.2 x
13.7-16.3
E. brunetti ovoidal 20.7-30.3 x
18.1-24.2
E. maxima ovoidal 21.5-42.5 x
16.5-29.8
Figure 2.43 Location of Eimeria species E. mitis subspherical 11.7-18.7 x
11.0-18.0
in chicken. E. mivati ellipsoidal 11.1-19.9 x
10.5-16.2
E. necatrix ovoidal 13.2-22.7 x
11.3-18.3
As a consequence, unlike in other E. praecox ovoidal 19.8-34.7 x
bacterial or viral disease of poultry, wild 15.7-19.8
E. tenella ovoidal 19.5-26.0 x
birds are not infection sources. The most 16.5-22.8
important way for spreading the coccidia
111 | P r o t o z o a
There is a clear age predisposition. The and lesions below). The pathogenicity is
most sensitive age is variable in each also host-dependent (age, immune status,
Eimeria species. For instance in the case species) and is influenced by the
of the most commonly occurring species presence of concurrent infections.
in chicken, E. tenella (cecal eimeriosis), Although the lesions are generally local,
the most affected age is 5-7 days in birds they affect the whole organism.
are exposed to high infective doses
The most important pathogenic effect is
immediately after hatching. Normally,
due to destruction of enterocytes and
cecal eimeriosis appears at 21-25 days.
other associated tissues (e.g. lamina
Cecal coccidiosis is also among the most
propria, submucosal layers, blood
severe forms of disease, with an acute
vessels) by the merogonic development.
onset and high mortalities (50-100%) in
Massive destructions are responsible for
few days, if not treated. Infection with E.
intestinal hemorrhages. Intestinal tissue
necatrix produces clinical infection in 5-7
damage results in motility disorders,
weeks old chicken, and the onset and
altered absorption of nutrients,
evolution is slower. Mortality is much
decreased water resorption, malnutrition
lower. Infections with E. brunetti are rare
etc. Their severity is variable and
but the onset is very fast. Eimeria
depends on the surface of damaged
acervulina affects mainly older chicken
epithelium. Epithelial destruction allows
and even adults, while E. maxima is
undisturbed access of other pathogens
responsible for coccidiosis in laying hens.
(mainly bacteria) to the blood stream and
Turkeys are less sensitive to clinical tissues. Chronic infections, although not
eimeriosis, and outbreaks are less severe life-threatening produce long-term
than in chicken. The most susceptible age debilities (i.e. rickets).
is 6-8 weeks. In ducks and geese, the
In order to assess the severity of
infection is sporadic. In pigeons, the
infection, mostly in experimental trials
infection is common and mortality is high
for testing anticoccidial drugs or
(15-70%) at the age of 3-4 months.
vaccines, a scoring system has been
Resistance of oocysts in the environment developed (please refer for details to
is relatively high. Alternation of freezing- Conway and McKenzie (2007).
defreezing or direct sunlight exposure
Immunology. The knowledge on the
kills them rapidly. However, the most
immunology of eimeriosis in chicken is
important aspect regarding oocyst
very extensive, as the quest for safer and
resistance is within the
more ecological preventive measures (i.e.
microenvironment of the farm. Common
vaccination) is permanent. There is an
disinfectants have limited efficacy on the
evident acquired immunity, as adult birds
oocysts. Most of them inhibit sporulation;
are non-receptive to clinical infection and
hence unsporulated oocysts are more
the development in their intestine is self-
sensitive.
limiting. Local intestinal cellular
Pathogenesis. Some species are more immunity from the associated lymphoid
pathogenic than others (see symptoms tissues are responsible for the post-
112 | P r o t o z o a
infective resistance. B cells produce anti- The most pathogenic species in turkeys
Eimeria antibodies shortly after the debut is E. adenoides. The feces are liquid and
of infection. However, their protective may be coated with hemorrhagic mucus.
role is limited. The most important Mortality can be present if infective doses
components seem to be intraepithelial are high. Chronic infections are
and lamina propria cytotoxic T responsible for significant weight loss.
lymphocytes.
In ducks and geese, the signs of infection
Clinical signs. Clinical signs are mainly with E. anseris are: anorexia, weight loss,
digestive and certainly not characteristic. general weakness, distress, diarrhea and
even mortality.
Clinical signs in chicken range from
asymptomatic infections in adult birds to In pigeons, the common signs of infection
mild, moderate or severe disease in are greenish diarrhea, anorexia,
young birds. Clinical eimeriosis in dehydration and extreme weight loss.
chicken varies from chronic forms with The feces may be hemorrhagic. Chronic
decreased growth rate to severe diarrhea, eimeriosis can cause mineral deficiencies
often with high and fast mortality. There (figure 2.44).
are some differences in the clinical signs
between Eimeria species involved. In the
case of cecal eimeriosis (caused by E.
tenella), the diarrhea is watery and
contains often hemorrhagic droppings. As
a consequence, chicken are anemic and
may exhibit even nervous signs.
Hemorrhagic feces can be present also in
infections caused by other species of
Eimeria, but they are not as severe as in
the case of E. tenella. In the case of E.
brunetti, E. necatrix, E. acervulina, E.
maxima or E. mivati, the hemorrhage in
the feces is weaker and it appears as
discrete streaking on the droppings.
Moreover, in these later species, the feces Figure 2.44 Typical “S” shaped keel as a
are rarely watery, or even with normal result of secondary calcium deficiency in
consistence and soaked with slightly a pigeon suffering from chronic
hemorrhagic mucus. eimeriosis. (Photo Andrei D. Mihalca)
Sometimes the infection with Eimeria in
chicken does not result in changes in the
Pathology. The lesions in poultry
consistence of feces, nor other evident
coccidiosis are different for the various
symptoms. However, even low levels of
species of Eimeria involved. Their
infection can induce low weight gain or
location and gross aspect are of great
decreased feed conversion rate.
113 | P r o t o z o a
diagnostic value, some almost

pathognomonic. In cecal coccidiosis (E.
tenella) the most prominent finding is a
severe hemorrhagic typhlitis (figure
2.45), with a dilated cecum (figure 2.46)
containing liquid or partially clotted
blood.
The extent of the lesion might be reduced

to some patches which in severe forms
are confluent and affect both ceca, totally.
Sometimes the lesions consist in
hemorrhagic-necrotic typhlitis or even
with the presence of fibrinous material.
Figure 2.46 Dilated ceca with focal
hemorrhagic typhlitis caused by Eimeria
tenella in chicken. (Photo Adriana Györke)
The same situation is encountered in the

infection with E. brunetti, but the
punctiform hemorrhages are located in
the rectum and cloaca. Necrosis of the
rectal wall may be present.
Figure 2.45 Hemorrhagic typhlitis

caused by Eimeria tenella in chicken.
(Photo Adriana Györke)
The infection with E. necatrix is

responsible for intestinal congestion,
with pinhead-sized hemorrhagic spots
(figure 2.47). In severe cases, these spots
become confluent and the middle part of
the small intestine becomes entirely
hemorrhagic (figure 2.48). Sometimes Figure 2.47 Small intestine enteritis
the lesions are fibrinous or necrotic caused by the infection with E. necatrix.
(figure 2.49). (Photo Adriana Györke)
114 | P r o t o z o a
The lesions in other bird species vary

from catarrhal enteritis to various
degrees of hemorrhagic enteritis (focal or
generalized) or fibrinous-necrotic
inflammations.
Diagnosis. Based on clinical signs and

necropsy, the etiology must be confirmed
Figure 2.48 Severe hemorrhagic enteritis
in the laboratory. This is done by direct
caused by the infection with E. necatrix.
identification of various stages of Eimeria
in the feces of living birds or in the
lesions in the case of dead birds (figures
2.50, 2.51, 2.52, 2.53).
Eimeria maxima is responsible for
hemorrhagic enteritis in the anterior and Please refer to the diagnosis section from
medial segment of the small intestine, the previous Chapter (2.4.1.1) on
very clearly delimited from the healthy mammal coccidiosis.
contiguous intestinal segments.
Eimeria acervulina and E. mivati produce

more or less similar lesions, with focal
(petechial) hemorrhagic enteritis in the
small intestine with the presence of
whitish colonies.
Figure 2.50 Meronts of Eimeria sp. in wet

mount from intestinal lesions of chicken.
Treatment. The disease in chicken is

very severe. Treatment in large bird
communities (farms) is most often
Figure 2.49 Fibrinous-necrotic enteritis impossible, mainly because of logistic
caused by the infection with E. necatrix. reasons.
115 | P r o t o z o a
Figure 2.51 Merozoites of Eimeria sp. in Figure 2.53 Various developmental

wet mount from intestinal lesions of stages of Eimeria sp. in histological
chicken. (Photo Adriana Györke) section from intestinal lesions of chicken.
Several drugs have been used in chicken

in traditional (backyard), free-range
systems. Sulfaquinoxaline (125 mg/kg)
or Sulfadimidine (150-200 mg/kg) for 3-
5 days are effective against E. tenella. In
pigeons, sulfonamides and clazuril are
used in the drinking water.
Control. Prevention of eimeriosis in

chicken is crucial in the poultry industry.
It represents the only viable solution for
controlling outbreaks. Otherwise, any
clinical outbreaks are equivalent with
economic disaster.
Figure 2.52 Merozoites of Eimeria sp. in General hygiene methods and specific
stained smear from intestinal lesions of methods are used for controlling
chicken. (Photo Adriana Györke) eimeriosis in birds.
General measures include: maintaining

Even if the parasites are successfully the general health status of birds at
eliminated using specific anticoccidial optimal levels, decreasing the level of
medication, the lesions do not heal fast stress, use of proper and balanced diet,
enough in order to allow full recovery. optimal environment, avoiding of
overcrowding, good lighting and
116 | P r o t o z o a
ventilation and general biosecurity  robenidine (inhibits development of

measures (strict access control, cleaning, meronts).
disinfections).
(2) Polyether antibiotics or ionophores
Specific measures include
Their mechanism of action is by
chemoprophylaxis (with low and long
interfering with the metabolism of
term/continuous administration of
sodium and potassium. Three types are
anticoccidial drugs) and immune
known:
prophylaxis (using vaccines) or an
alternation of them.  monovalent ionophores (monensin,
narasin, salinomycin);
Various anticoccidial drugs are
currently being used in the  monovalent glycosidic ionophores
chemoprophylaxis of eimeriosis in (maduramicin, semduramycin);
chicken. They are grouped in two
 bivalent ionophores (lasalocid).
categories, based on their chemical
structure (classification based on Peek Ionophores cannot be associated with
and Landman, 2011). certain other antibiotics (e.g. tiamulin,
chloramphenicol, erythromycin,
oleandromycin, sulphonamides).
(1) Synthetic compounds
Additionally, there are various
 amprolium (competes for the commercial products where a
absorption of vitamin B1 by the combination of the aforementioned
parasites); products is used. The poultry category
and the concentration to be given to
 aprinocid (interferes with DNA
chicken in food for each drug is listed in
synthesis);
table 2.31.
 clopidol (inhibits development of
The main problem when using
sporozoites);
chemoprophylaxis is the emergence of
 decoquinate (inhibits development of resistant strains. In the case of chicken
sporozoites); eimeriosis, resistance is known for all
compounds and it has been reported
 diclazuril (blocks the excretion of
worldwide. Despite this, severe
oocysts);
outbreaks are occasional, as the insidious
 dinitolmide (inhibits development of presence of Eimeria due to resistance
meronts); stimulates immunity.
 halofuginone (inhibits maturation of To reduce the impact and occurrence of
merozoites); resistance, rotation of anticoccidial drugs
is recommended. Each drug should be
 nequinate;
used for maximum 2 months, or in
 nicarbazin (inhibits development of broilers, for maximum two fattening
meronts) cycles.
117 | P r o t o z o a
Table 2.31 Anticoccidials used in the expressed from DNA) of different

prophylactic treatment of eimeriosis in chicken
(after Peek and Landman, 2011) developmental stages (sporozoites,
merozoites, gametogonic stages). There is
Concentration a single subunit commercial vaccine
Poultry
Drug in fodder
category available (CoxAbic). It is used for
(ppm)
Amprolium Broiler, 125-250 vaccination of mother hens and immunity
rearing
Amprolium+ Broiler, 125-250+ is transmitted to broiler chicken via
ethopabate rearing 4 trans-vitelline route.
Aprinocid Broiler 60
Clopidol Broiler, 125 (2) Live vaccines contain non-attenuated
rearing
Decoquinate Broiler 30 or attenuated sporulated oocysts of
Diclazuril Broiler, 1 various species of Eimeria. Two
rearing
Dinitolmide Broiler, 125 vaccination strategies are employed:
rearing single shot (high dose) or multiples shot
Halofuginone Broiler, 3
rearing
(low dose). The vaccinal strains might be
Nequinate Broiler, 20 sensitive to anticoccidial drugs. Thus,
rearing
discontinuation of these is essential in
Nicarbazin Broiler 125
Robenidine Broiler 33 vaccination strategies are to be
Lasalocid Broiler 75-125 implemented.
Maduramicin Broiler 5-6
Monensin Broiler, 100-120 Non-attenuated vaccines have been used
rearing
Narasin Broiler 60-80 for long time (CocciVac, Inovocox,
Salinomycin Broiler, 44-66 Advent, Imunocox), but their
rearing
Semduramycin Broiler 25 administration is risky, as they can
induce clinical infection if protocols are
not followed strictly.
Shuttle programs (simultaneous use of
two or more drugs with different Attenuated vaccines (with decreased
mechanism of action during the same virulence obtained by repeated in vitro
technologic cycle) are also recommended. passages on chicken embryos) are safer
but they lose immunogenicity over time
Before implementing chemoprophylaxis
and their production is more costly.
programs, it is highly recommended to
Examples of attenuated vaccines include
perform in vivo Anticoccidial Sensitivity
Livacox or Paracox.
Tests, using local strains.
However, antigenic variability between
New approaches to the management of
various Eimeria species restrict the
anticoccidial drug resistance include the
commercial value of live vaccines. Some
rotation of chemoprophylaxis with
of the vaccines are also available for
immune-prophylaxis (vaccination).
turkeys (e.g. Coccivac, Immunocox).
There are several types of vaccines
available today.
(1) Subunit vaccines contain antigens

(either native or recombinant proteins
118 | P r o t o z o a
2.4.1.3 Hepatic eimeriosis in rabbits via blood through the portal, free or in
macrophages. The sporozoites reach the
Introduction. Hepatic eimeriosis is a sinusoid veins between liver cells 1-6
severe condition of rabbits caused by E. days after the infection. They
stiedai, with high mortality in young subsequently migrate to the biliary ducts
animals. and penetrate the epithelial cells where
Historical notes. E. stiedai is probably they start the merogony. Merogony takes
the first ever unicellular “animal”-like around 12 days. Gametogony lasts for 4
organism ever observed (by Antonie van more days. Unsporulated oocysts appear
Leeuwenhoek in 1674). The species was in feces as early as 16 days after the
described as Monocystis stiedae by infection. In the environment, the
Lindemann, in 1865. The first study on its sporulation takes 2-3 days.
life cycle date from 1903 (Metzner). The Epidemiology. Eimeria stiedai is present
first reports of disease date back from the all over the world, affecting various
mid-19th century. species of rabbits and hares. Adult
Etiology. The causative agent of hepatic rabbits are the source of infection for
eimeriosis in rabbits is Eimeria stiedai. young rabbits. Wild rabbits can also
Except domestic rabbits, E. stiedai is harbor the infection and contaminate the
parasitic in various wild rabbit and hare environment. Contaminated grass fed to
species (Lagomorpha): European rabbit rabbits can bring the infection. After
(Oryctolagus cuniculus), European brown elimination through the feces, they
hare (Lepus europaeus), Snowshoe hare become infected in 2-3 days. Rabbits up
(Lepus americanus), mountain hare to two weeks old are resistant to
(Lepus timidus) and Eastern cottontail infection. The rabbits are normally
(Sylvilagus floridanus). receptive to the infection with E. stiedai
after 16-18 days of life up to 4 months.
Morphology. The oocysts are oval or After this age, they become completely
narrow oval, sometimes asymmetrical resistant, and clinical cases are normally
and they have a micropyle. The size of absent.
oocysts is 28-40 x16-25 µm.
Pathogenesis. As parasites are invading
Life cycle. Eimeria stiedai follows the the biliary ducts and merogonic stages
typical life cycle of genus Eimeria, as are developing, the epithelial cells are
described in Chapter 2.4.1.1. However, being destroyed. The biliary ducts
there are few particular aspects which become distended and filled with cellular
require some attention. First of all, their debris and nodules appear in the liver
typical habitat is the epithelial lining of parenchyma. These changes are most
biliary ducts. After sporulated oocysts are prominent by day 16, when merogonic
ingested by rabbits they typically excyst gametogonic phases are already complete
in the duodenum. Sporozoites leave the (figure 2.54). If rabbits survive and no
intestine by penetrating the mucosa and massive reinfection takes place, all these
reach the liver via lymphatic system or lesions heal completely. These lesions are
119 | P r o t o z o a
able to produce significant functional the liver is severely affected, jaundice,

disorders. The main alteration seems to ascites and fever may be present.
be in the metabolism of vitamin E. Mortality can be present.
Pathology. The gross lesions in rabbits

which died of coccidiosis consist in
hepatomegaly with the presence of
numerous, disseminated white or grey-
white nodules (figure 2.55) even in the
more profound regions of the liver
(figure 2.56).
There are various degrees of lesion

severity. In mild forms, the nodules are
few and small, while in the most severe
cases nodules are confluent and normal
liver tissue is almost absent. The bile is
full of debris. Bile ducts are fibrous and
enlarged.
Figure 2.54 Various developmental Liver lesions must be differentiated from
stages of Eimeria stiedai in histological the white and fibrous migratory routes or
section rabbit liver. (Photo Andrei D. the vesicle-like cysts of the larval stages
Mihalca) of Taenia pisiformis (i.e. “Cysticercus
pisiformis”).
Immunology. All infections, regardless

they produce clinical disease or not are
ultimately inducing a strong immunity.
Experimental data suggest that
development of protective immunity
requires around 21-30 days. It seems the
most important component of this post-
infective resistance is humoral immunity.
Cross immunity with intestinal Eimeria
have been suspected (i.e. with E. magna).
Clinical signs. Infection with E. stiedai

may be asymptomatic, may cause various
clinical signs or may even result in
Figure 2.55 Typical gross lesions in the
sudden death without any prodromal
liver of rabbits suffering of hepatic
signs. Symptoms can vary from only
eimeriosis: hepatomegaly with the
moderate weight loss to more evident
presence of multiple whitish nodules.
signs like bloating, loss of appetite,
diarrhea or constipation. If function of
120 | P r o t o z o a
Figure 2.56 More detailed view of the Figure 2.57 Wet mounts from the
lesion pictured previously. (Photo Andrei hepatic lesions reveal usually high
D. Mihalca) number of oocysts. (Photo Andrei D.
Mihalca)
Diagnosis. In living rabbits, the positive

diagnosis is based on the demonstration Control. Asymptomatic carriers can be
of oocysts in the feces. By the time clinical treated to eliminate the infections
signs are present, the oocysts are already sources for the young susceptible rabbits.
present in stools. They must be Sulfaquinoxaline (0.04% in drinking
differentiated from intestinal Eimeria. water for 30 days or 0.025% in food for
20 days), sulfadimetoxine (0.06% in
In dead animals, the lesions are almost
drinking water), sulfadimerazine (0.2%
pathognomonic. Fresh preparations (wet
in drinking water) or amprolium 9.6% (in
mounts) done directly from the whitish
drinking water) are all effective for
nodules from the liver or from the bile
chemoprophylaxis. Withdrawal time for
reveal the presence of various
sulfaquinoxaline is 10 days.
developmental stages but mainly of
unsporulated oocysts in impressive General hygiene measures (frequent
numbers (figure 2.57). removal of feces from pens and
disinfection with 10% ammonia help in
Treatment. Suffering rabbits are treated
reducing the infective preasure.
using oral medication. The anticoccidial
drugs recommended for treating clinical
cases in rabbits is toltrazuril (25 ppm in
drinking water for two days). 2.4.1.4 Renal eimeriosis in geese
Other anticoccidials may be used. Introduction. It is a locally relatively

common protozoal infection of domestic
121 | P r o t o z o a
geese which is responsible for acute of debris and possible micro-obstructions

symptoms and high mortality in goslings. of the tubules. This results in significant
increase of the kidneys’ size and
Historical notes. The etiological agent,
deposition of urates.
Eimeria truncata was described as
Coccidium truncatum by Railliet and Immunity. No studies are available, but
Lucet in 1891 from domestic geese. birds which survive the infection become
refractory to new infections.
Etiology. The only known species able to
infect the epithelial layer of the renal Clinical signs. The usual form of the
tubules in domestic geese is Eimeria disease is acute. Renal coccidiosis may be
truncata. The species was reported a very serious disease of goslings, with
subsequently from various other wild severe depression, general weakness,
avian hosts. whitish diarrhea and anorexia. During
more chronic forms, birds have
Morphology. The oocysts of E. truncata
polydipsia and nervous signs may be
are oval but with a truncation of the
present (gait). Neurologic sequelae
narrow end. The size is 20-22 x 13-16
include vertigo and torticollis.
µm. A micropyle is present.
Pathology. The most characteristic
Life cycle. All stages develop in the
lesion is the enlarged aspect of kidneys
tubular epithelial cells of the kidneys. As
which have a greyish-yellow to yellowish
experimental infection is difficult, it is not
red colored surface (normal color is
yet fully understood how the infective
reddish brown). Kidneys often protrude
sporozoites reach from the intestine to
from their sacral bed. The surface is
the kidneys. The contamination route is
covered with small pinhead-sized
oral, although some authors have
grayish-white foci. Hemorrhagic lesions
questioned this. Oocysts can be recovered
can be occasionally present.
from the feces 5-6 days after the
infection. Sporulation takes 1-2 days. Diagnosis is based on clinical sign and
lesions, followed by demonstration of
Epidemiology. The disease seems to be
oocysts in the droppings or in the kidney
spread worldwide. Outbreaks are
lesions.
sporadic, but when they occur, they are
able to affect a significant number of Treatment and control. No reliable
animals. The most susceptible age groups experimental studies are available.
are goslings between 3 weeks and 3 Anecdotal reports suggest sulfonamides
months old, in which mortality can reach as being effective. Keeping goslings
high values. The prepatent period is 5-6 separated from the adults reduces the
days. infective pressure.
Pathogenesis. Development of the

various stages in the epithelial cell of the
renal tubules is responsible for
desquamation followed by the presence
122 | P r o t o z o a
2.4.2 Cryptosporidiidae 2.4.2.1 Cryptosporidiosis
Introduction. The family includes a Introduction. Cryptosporidiosis is a

single genus, genus Cryptosporidium, with widespread zoonotic parasitic infection
20 species parasitic in all vertebrate of all vertebrate groups, produced by
classes. small apicomplexan parasites from genus
Cryptosporidium. It affects mainly very
The name (Greek: kryptos = hidden; spora
young or immunosuppressed individuals,
= seed) suggests its very small size and
producing severe diarrhea and
the difficulty in detecting it.
dehydration.
General morphology. The morphology
Historical notes. The first observations
is discussed in more detail in the
of these parasites came in 1907 by
corresponding section from Chapter
Tyzzer, when he described
2.4.2.1.
Cryptosporidium muris from mice.
Ecology and transmission. All species
The first association of Cryptosporidium
are primarily parasitic in the digestive
with clinical cases of diarrhea in turkeys
tract of all vertebrates groups, but some
has been reported in 1955 and in cattle
may inhabit also other organ systems
came only more than half century after its
(e.g. respiratory).
discovery, in 1971. The first human cases
They have a homoxenous life cycle and were reported in 1976 and two years
are transmitted from host to host via later, Cryptosporidium parvum was
fecal-oral contamination. designated as a zoonotic species. In 2004,
Medical importance. Species of genus the complete genome of a couple of
Cryptosporidium are distributed Cryptosporidium species was published.
worldwide and are able to produce Etiology. Although the taxonomy of
clinical infection in a large variety of genus Cryptosporidium is still debated,
hosts. Some species are host specific, generally 20 named species are currently
some others not. recognized (valid) (table 2.32).
In general, there is a relative host class Additionally, there are several other
specificity. This means that species genotypes which do not have assigned a
parasitic in reptiles are not able for specific epithet.
instance to infect birds or mammals. A new genus (Piscicrytposporidium) was
On the other hand, some species seem to erected to designated two species
lack host specificity and infect a wide parasitic in fish: P. cichlidis and P.
range of species within a class. One reichenbachklinkei.
prominent example is Cryptosporidium Morphology. The number of studies on
parvum which has been reported from the morphology of various species of
more than 150 mammal species. Cryptosporidium produced huge amount
of information.
123 | P r o t o z o a
Table 2.32 The species of genus environment by infected hosts (figure

Cryptosporidium
2.58 - 1). Infection of the host takes place
Species Hosts by ingestion of these sporulated oocysts
C. molnari fish (figure 2.58 - 2). Immediately after
C. scophthalmi fish
C. fragile amphibians ingestion by a suitable host, the oocysts
C. serpentis reptiles will start excystation (figure 2.58 - 3) and
C. varanii reptiles
C. meleagridis birds, mammals
the free motile sporozoites approach the
C. bailey birds apical end of the potential host-cells
C. galli birds (figure 2.58 - 4) and invade them (figure
C. andersoni cattle, camels,
humans 2.58 - 5). After attachment, the
C. bovis cattle sporozoites become oval or spherical and
C. canis canids, humans
C. fayeri marsupials, sheep vacuoles form inside them (figure 2.58 -
C. felis cats, humans 6). This stage is called trophozoite. The
C. hominis humans, cattle, goats
C. macropodum marsupials
newly formed parasitophorous vacuoles
C. muris rodents, camels, are located intracellularly in the host cell,
goats, primates, pigs,
dogs
but as they are not in direct contact with
C. parvum various mammals its cytoplasm their location is called
C. ryanae cattle epicellular. The next stage is the
C. suis pigs, cattle, humans
C. wrairii guinea pigs merogony, which is the phase of intense
asexual multiplication. This phase is
different in the various species of
Nevertheless, the identification of species
Cryptosporidium. In general, the nucleus
is more routinely based nowadays on
of the trophozoite will divide several
molecular data.
times (figure 2.58 - 7), resulting in
The most important stage from multinucleated structures called meronts.
diagnostic point of view is the oocyst. In Each nucleus will eventually be
general, oocysts are very small (2-6 µm in incorporated in the structure of the
diameter). The shape is usually spherical. forming merozoites (figure 2.58 - 8).
Under direct light, they are highly
The mature merozoites will leave the
refractile. Each sporulated oocyst
surface of the infected host cells (figure
contains 4 free, slender or fusiform
2.58 - 9) and will re-infect other cells
sporozoites. Unlike most other coccidian
(figure 2.58 - 10). The number of
parasites (Eimeria, Isospora, Sarcocystis,
merozoites per meronts is different from
Toxoplasma etc.) oocysts of
species to species, but it is usually eight.
Cryptosporidium lack a sporocyst.
These meronts are called type I meronts.
Life cycle is homoxenous (figure 2.58), The last generations of meronts (type II)
typically with three phases: merogony, always contain only four merozoites and
gametogony and sporogony. The only these will be responsible for the initiation
exogenous stages known are sporulated of the next phase of the life cycle, the
oocysts, which are eliminated to the gametogony (figure 2.58 - 11).
124 | P r o t o z o a
Figure 2.58 Life cycle of Cryptosporidium. For the meaning of numbers, please refer to the
text.
125 | P r o t o z o a
Hence, the last generation merozoites days for calves infected with C. bovis, 2-9
will differentiate into female days in pigs infected with C. suis and 5-6
macrogamonts (syn. macrogametocytes) days for cats infected with C. felis.
(figure 2.58 - 12) and male microgamonts
The sources of infection are oocysts from
(syn. microgametocytes) (figure 2.58 -
the environment and the route of
13). Microgamonts will develop into
infections is ingestion. Oocysts of
microgametes and will penetrate the
Cryptosporidium are sporulated when
female gametes (figure 2.58 - 14) in order
they are eliminated so they are
to produce fertilization with formation of
immediately infective. The sources of
the egg cell (zygote) (figure 2.58 - 15) and
environmental pollution are infected
ultimately unsporulated oocysts (figure
animals (wild or domestic) or humans.
2.58 - 16).
Farm husbandry practices which enhance
Oocyst will sporulate in situ (figure 2.58 -
the transmission cycles include shared
17), hence in Cryptosporidium the
feeding of neonates with older animals
sporulation is typically endogenous. This
not necessarily conspecific. Improper
important from epidemiological point of
disposal of manure and other fecal
view, as the oocysts from the feces of
wastes is contaminating water the
infected animals will be immediately
sources. Raw sea food (i.e. oysters, clams)
infectious to new hosts. Sporulated
have been incriminated is several human
oocysts are released from the host-cell
outbreaks.
(figure 2.58 - 18) and are eliminated in
the feces (figure 2.58 - 1). Susceptibility is higher in very young
animals and decreases with the age.
Some sporulated oocysts might excyst
Immunodeficient individuals are
before being eliminated in the feces, and
particularly sensitive. Calves are sensitive
the released sporozoites are responsible
between 1 and 4 weeks of age for the
for autoinfection (figure 2.58 - 19).
infection with intestinal species.
Cryptosporidium species are responsible
Cryptosporidium andersoni infects only
for the infection of various parts of the
cattle older than 5 months. In sheep and
digestive system. In mammals, some
goats, young animals can be infected and
species inhabit the distal small intestine,
seriously affected from the first days of
cecum and colon. Cryptosporidium
life. In pigs, the highest susceptibility is
andersoni is found in the digestive glands
between weaning time up to the age of 2
of the abomasum. In birds, some species
months. In horses, the susceptible age
are able to infect also the respiratory
group is 5-8 weeks.
system, conjunctival mucosa or the bursa
of Fabricius. Cryptosporidium oocysts are relatively
resistant in the environment. At optimal
Epidemiology. The distribution of
temperatures (5-15°C) and humidity they
Cryptosporidium in domestic animals is
remain infective for 6 months. Deep
global. Prepatent periods are 2-7 days in
freezing destroys them in 24 hours.
calves infected with C. parvum, 10-12
126 | P r o t o z o a
Pathogenesis. Unlike other Immunology. The role of immunity is

apicomplexans, Cryptosporidium is not an very important in the case of
intracellular parasite. They are typically cryptosporidiosis. It is very evident that
located on the epithelial surface (figure immunocompromised hosts are severely
2.59), and their pathogenicity is related affected by the infection. In humans with
to the villous atrophy (loss and AIDS, cryptosporidiosis can be a
shortening of microvilli) or even potentially lethal complication. The first
detachment of enterocytes. This results in line of defense is the innate immunity.
diarrhea, intestinal malabsorption and Toll-like receptors on the intestinal
hypersecretion of chloride and water. epithelial cells are enabling the pathogen
After attachment to the cell, C. parvum is recognition. In the case of C. parvum, the
able to use the host cell’s membrane recognition activates the nuclear factor
transport systems for its own metabolic kappa-light-chain-enhancer of activated
processes. Abomasal infection with C. B cells pathway and expression of pro-
andersoni causes inhibition of proteolytic inflammatory cytokines. Interferon-γ and
enzymes. Moreover, the epicellular natural killer (NK) cells have a significant
location (between the cell membrane and effect against C. parvum. The phagocytic
cell cytoplasm) makes them very system also plays an important role in
refractory to chemotherapy. Significant cryptosporidiosis. The production of the
part of the pathogenetic process is free radicals of the nitric oxide by
dependent on the host’s immune system neutrophils and macrophages is
and will be detailed in the section on increased during the infection with C.
immunity. parvum. The complement system is
activated by C. parvum on the classical
and lectin pathways.
The acquired immunity plays crucial role

in the defense against the parasite but
also in the pathogenesis. T lymphocytes
are mediating the microvillus atrophy.
Clinical signs. The most important

symptom in clinical cryptosporidiosis is
diarrhea in unweaned animals, mainly
livestock (calves, lambs, goat kids). In
adult animals the infection is regularly
asymptomatic, while in very young ones
the diarrhea is severe (scouring).
Mortality is uncommon and it if is
Figure 2.59 Oocysts of Cryptosporidium present, it is usually because of
parvum covering the intestinal coinfections with other pathogens.
epithelium in a naturally-infected goat Infected calves may cause various
kid. (Photo Alexandru Bejan) associated symptoms: dehydration,
127 | P r o t o z o a
anorexia, dullness, weight loss and even The main lesion in calves infected with C.
fever. parvum is enteritis in the small intestine,
atrophy of villi with the presence of
Cryptosporidiosis of pigs is a rare
various developmental stages on the
condition. The clinical signs described
surface of the epithelial cells. Histological
after experimental infections are:
lesions consist of cellular infiltrates in
inappetence, depression, vomiting,
lamina propria and hyperplasia of
diarrhea. Clinical cryptosporidiosis has
epithelial cells of the intestinal crypts.
been reported also in other livestock, but
The infection with C. andersoni invades
rarely.
the peptic and pyloric glands in the
In dogs and cats the clinical infection is stomach, producing their dilatation with
rare, but even inapparent infections pose hypertrophy of the gastric mucosa.
an increased zoonotic risk. Clinical Similar intestinal lesions are found in
symptoms in pets include: diarrhea, small ruminants and pigs. In dogs and
anorexia, weight loss, tenesmus, etc. Cats cats, lesions can be found also in the large
infected with FeLV or FIV are more prone intestine.
to develop clinical cryptosporidiosis. In
Diagnosis. Clinical signs of diarrhea in
horses the infection is relatively common
young animals is an indication for
but rarely causes serious problems.
cryptosporidiosis, mainly if the usual
In birds, the infection with C. baileyi is treatments are not efficient. Diagnosis
rarely responsible for digestive signs. should be based on the identification of
More commonly it produces respiratory oocysts in the feces of animals. As oocysts
symptoms: sneezing, coughing, are very small, their detection in feces is
orthopneic position. The respiratory not always an easy task. Regular
signs can last up to 4 weeks. coproscopic methods (i.e. salt flotation)
Cryptosporidium meleagridis infects the are not very sensitive. Moreover, when
ileum of turkeys and other birds the number of oocysts in the feces is very
producing severe diarrhea. low their detection is even harder.
Cryptosporidium galli infects the There are three main method of choice
proventriculus and the clinical infection for the detection of Cryptosporidium in
in chicken (even adults) results in puffed the feces, or other sample types.
plumage and decreased growth.
(1) Direct detection (visualization) of
In quails, unnamed Cryptosporidium oocysts in the feces is based either on
species produce similar digestive and their concentration from fecal material,
respiratory signs. or special staining methods. The most
Pathology. Lesions are located at the site commonly used concentration methods
of infection. Usually no other systemic are: sucrose flotation or formalin-ether
lesions are found, except situations method. For stools which have large fat
where bacterial or viral pathogens contents, the formalin-ether method is
complicate the diseases. recommended. As oocysts are very small
and conventional light microscopy does
128 | P r o t o z o a
not allow accurate identification, staining Usually animals recover if only given
methods have been developed. The most symptomatic treatment (i.e. preventing
commonly used staining method for fecal dehydration and correcting electrolyte
smears is the Ziehl-Neelsen modified by balance). The minimum duration of
Henriksen and Pohlenz. Using this chemical treatment should be at least 5
method, the oocysts appear bright red on days.
a green background (figure 2.60).
Table 2.33 Drugs used in the treatment of

cryptosporidiosis in domestic animals (after
Stockdale et al., 2008; Scorza and Lappin,
2012)
Drug Animal Dose (/kg)

Paromomycin calf 25-100 mg
goat kid 100 mg
dogs, cats 125-165 mg
Halofuginone calf 30-500 µm
lactate
Lasalocide calf 6-15 mg
Sulfadimidine calf 200 mg
Sulfaquinoxaline goat kid 100 mg
β-Cyclodextrin lamb 500 mg
Nitazoxanide dogs, cats 100 mg
Azithromycin dogs 5-10 mg
cats 7-15 mg
Figure 2.60 Oocysts of Cryptosporidium In birds, anticoccidial drugs can be used,

sp. in a fecal smear as they appear at Ziehl but with low moderate success.
Neelsen modified by Henriksen and Control. Controlling the disease is not
Pohlenz method. (Photo Andrei D. easy. Although there are some
Mihalca) chemoprophylaxis protocols, they are
rarely used. General hygiene methods are
recommended. As infection is potentially
(2) Immunological methods include
dangerous during the first days of life, the
direct immunofluorescence, ELISA or
maternity area of the farms should be
other immunochromatographic methods,
kept as clean as possible. Colostrum must
all used to identify antigens in fecal
be fed to newborns, mainly in calves. In
material. ELISA tests are available also
farms where imminent risk exists (i.e.
for detection of serum antibodies.
history of recent cryptosporidiosis)
(3) Detection of DNA are highly sensitive newborn calves must be kept separated,
and they are used mainly for genotyping. with no calf-to-calf contact during the
first two weeks of life. Sick animals with
Treatment. Various chemical
diarrhea must be isolated from the
compounds are used for the treatment of
healthy ones. All in-all out system with
cryptosporidiosis in animals (table 2.33)
thorough disinfection between animal
but their efficacy is often moderate.
series must be strictly followed. As host
129 | P r o t o z o a
barrier for some species is low, the farm hosts are usually carnivorous species
must be kept free of free ranging dogs, which acquire the infection after
cats and rodents. Water sources must be ingesting infected intermediate hosts. In
clean. the definitive host, the gametogony
typically takes place in the intestinal
As zoonotic risk is high, rules and
epithelial cells.
regulations for waste management must
be strictly followed. The differentiation between the two
subfamilies is based on the nature of
stages found in the intestine of their
2.4.3 Sarcocystidae definitive hosts and the type of cysts from
the tissues of intermediate hosts. In
Introduction. Family Sarcocystidae subfamily Sarcocystinae gametogony and
includes several genera of great sporogony are both endogenous while in
veterinary and public health importance. Toxoplasmatinae the sporogony is
The family currently includes two exogenous.
subfamilies: Sarcocystinae (with genera The infective stage for the intermediate
Sarcocystis, Frenkelia) and host is the sporulated oocyst. After it is
Toxoplasmatinae (with genera ingestion, the sporozoites infect various
Toxoplasma, Neospora, Hammondia, tissues and rapidly produce the first
Besnoitia and others). generation of merozoites known as
General morphology. All species have tachyzoites (Greek: tachy- = swift, fast,
Isospora-like oocysts. This means, that speed). They subsequently infect other
sporulated oocysts contain two tissues of the intermediate hosts and
sporocysts, each with four sporozoites. continue merogony by a slow asexual
Members of genera Toxoplasma, multiplication resulting in the production
Neospora, Besnoitia and Hammondia have of later generations of merozoites known
relatively small oocysts. Their as bradyzoites (Greek: brady- = slow).
differentiation by morphological criteria They typically remain in this stage
is virtually unachievable. Except oocysts, (known as tissue cysts) until a new
the morphology of the other suitable definitive host preys on the
developmental stages is also important infected intermediate host. In the
for diagnosis purposes, as some of them intestine of the definitive host, the
are commonly found in various tissues of “zoites” (tachyzoites or bradyzoites) are
their intermediate hosts. released and invade the enterocytes
Ecology and transmission. All species where they finish their merogonic
are intracellular parasite in various development and undergo gametogony
tissues and organs of animal and human with the formation of unsporulated
hosts. They are parasitic in a great variety oocysts. In genera Toxoplasma, Neospora,
of vertebrate species, including Besnoitia and Hammondia, the
amphibians, reptiles, birds and mammals. unsporulated oocysts are shed with the
Life cycle is heteroxenous. Definitive feces and they undergo sporulation in the
130 | P r o t o z o a
environment, becoming infective for a skeletal muscle of their intermediate

new intermediate host. hosts and the intestinal epithelium of the
definitive host with little clinical impact.
In genus Sarcocystis, gametogony is
However, their zoonotic transmission
followed by endogenous (intraintestinal)
confers them a public health importance.
sporogony with the formation of typical
sporulate Isospora-like oocysts. The Historical notes. In 1843, Miescher
oocyst wall of Sarcocystis is very thin and found some white thread-like structure in
fragile and it ruptures releasing the the skeletal muscle of house mice. He did
sporocysts. The definitive hosts in this not realize they are parasites, and for
case shed through their feces the more than 20 years, they were known as
infective sporocysts (each of them with the “Meischer’s tubules”. Similar
four sporozoites). structures were found in the muscle of
domestic pigs in 1865 and described as
For some genera (i.e. Toxoplasma), other
Synchytrium miescheriana by Kühn. In
complex transmission mechanisms are
1892, Lankester erected the genus
described, like for instance the
Sarcocystis and in 1899, Labbé
transmission from an intermediate host
transferred the species earlier described
to another intermediate host, without the
in pigs to this new genus and named it
presence of definitive hosts. The life cycle
Sarcocystis miescheriana. In the beginning
for each genus will be detailed in the
they were considered to be fungi. Their
following chapters.
correct taxonomic position was
Medical importance. The members of established in 1967. The heteroxenous
Sarcocystidae are important human and life cycle was discovered only in 1970.
animal pathogens. Some of them are First clinical cases of equine protozoal
responsible for systemic disease myeloencephalitis were described in
(Toxoplasma, Sarcocystis neurona), others 1970, but its etiology was clarified only in
produce mild intestinal infections 1974, when Dubey and his team
(Hammondia, Sarcocystis) or concluded the agent was a Sarcocystis
reproductive and congenital disorders species. The name S. neurona was
(Toxoplasma, Neospora). Toxoplasma proposed in 1991 by the same American
gondii and certain species of genus author, Dubey. Its life cycle was
Sarcocystis are of zoonotic importance. elucidated only at the end of the 1990s.
Etiology. The diversity of species

parasitic in domestic animals is shown in
2.4.3.1 Sarcocystoses tables 2.34 (dogs as definitive hosts),
2.35 (cats as definitive hosts), 2.36
Introduction. Sarcocystoses are (humans as definitive hosts) and 2.37
extremely common parasitic infections (wild or unknown definitive hosts).
produced by member of genus Sarcocystis
Morphology. Two developmental stages
(Greek: sarx- = meat, flesh; kystis =
are important from morphologic point of
bladder, pouch). They generally infect the
view.
131 | P r o t o z o a
Table 2.34 Species of genus Sarcocystis with Table 2.37 Species of genus Sarcocystis with
domestic dogs as definitive host domestic animals as intermediate hosts and
wild or unknown definitive hosts
Species Intermediate
host Species Intermediate
S. bertrami, S. fayeri Equids host
S. cruzi, S. levinei Cattle S. neurona Horse
S. arieticanis, S. micros, S. Sheep S. novaki Cattle
mihoensis, S. tenella S. ippeni Dromedary
S. capracanis, S. hircicanis Goats S. asinus Donkeys
S. miescheriana Swine S. canis Dog
S. alceslatrans, S. Cervids S. felis Cats, Dogs
capreolicanis, S. gracilis, S.
cervicanis, S. sybillensis, S.
wapiti, S. grueneri, S. In the intestine and feces of the definitive
hemionilatrantis, S.
odocoileocanis hosts (carnivorous mammals) two
S. aucheniae Llamas, Alpaca developmental stages can be found:
S. cameli Camels
S. poephagicanis Yaks oocysts and sporocysts.
S. baibacinacanis Squirrels
S. erdmanae Skunks The sporulated oocyst contains two
S. wenzeli Chicken sporocysts, each of them with four
S. peckai Pheasants
sporozoites (“Isospora”-like). The oocysts
are thin-walled and they normally
Table 2.35 Species of genus Sarcocystis with
domestic cats as definitive host
rupture while still inside the intestine
and release the two sporocysts.
Species Intermediate Sporocysts (figure 2.61) found in feces
host
S. buffalonis, S. fusiformis, Cattle
are small stages, and their morphology is
S. hirsuta relatively similar, regardless the species.
S. gigantea, S. medusiformis Sheep
They contain four sporozoites and well-
S. moulei Goats
S. porcifelis Swine visible sporocyst residuum.
S. cuniculorum, S. leporum Rabbits
S. muris, S. rodentifelis, S. Rodents The size of sporocyst found in the feces is
neotomafelis, S. cymruensis
variable from species to species (table
S. odoi Cervids
S. wenzeli Chicken 2.38).
The stages found in the muscle of the

Table 2.36 Species of genus Sarcocystis with intermediate hosts are called muscular
humans as definitive host and domestic
animals as intermediate hosts cysts or sarcocysts. Biologically they are
the last generation of meronts. Their size,
Species Intermediate
shape and location is variable, but as a
host
S. hominis Cattle rule all are whitish, cyst-like structures
S. suihominis Swine located in the skeletal muscles of various
animals (figure 2.62). A practical
These are the stages in the striated classification based on their size classifies
muscles of intermediate hosts and the them in macrocysts (visible with the
stage in the feces of the definitive hosts. naked eye) and microcysts (visible only
under the microscope) (figure 2.63).
132 | P r o t o z o a
Figure 2.62 Muscular cysts of Sarcocystis

sp. from a naturally infected pig are
visible during meat inspection. (Photo
Andrei D. Mihalca)
Figure 2.61 Sporocyst of Sarcocystis sp.
Table 2.38 Sporocyst size of selected species

of Sarcocystis found in feces of dogs, cats and
humans
Species Size (µm)

S. cruzi 10.8 x 16.3
S. hominis 9.3-14.7
S. tenella 9.9 x 14.8
S. fusiformis 7.8 x 12.5
S. gigantea 8.1 x 12.4
S. miescheriana 9.6 x 12.6
S. suihominis 10.5-13.5
S. bertrami 10.0 x 15.2
S. neurona 10 x 8
Figure 2.63 Microcysts of Sarcocystis sp.
are visible only under the microscope.
Sometimes, sarcocysts are very long and
thin, like for instance certain species
found in rodents (figure 2.64).Internally,
muscular cysts contain variable number
Meronts and S. cruzi (dog-cattle cycle)
of bradyzoites (figure 2.65).
from the endothelial cells are very small,
The sarcocysts are usually located 2-8 µm. The cyst in the muscle is fairly
longitudinally, along the length and in large (0.5-5 mm) and often visible with
between of the muscle fibers. the naked eye.
133 | P r o t o z o a
bigger (37 x 22 µm with 100 tachyzoites

first generation meronts; 14 x 6.5 µm
with 35 tachyzoites the second
generation meronts). Muscular cysts of
Sarcocystis hominis (human-cattle cycle)
are microscopic, with a thin wall (6 µm)
with radial striations.
First generation meronts of S. tenella

(dog-sheep cycle) are 19-29 x 7.5-24 µm,
with 120-280 tachyzoites. The muscular
cysts are relatively small (0.1-0.6 mm),
have a thick and radially striated wall.
Endothelial meronts of S. gigantea (cat-
Figure 2.64 In some hosts, the muscular sheep cycle) are small (2-8 µm) but their
cysts of Sarcocystis are very thin and long, muscular cyst is very large (hence the
like in this laboratory mouse. (Photo name) and measure up to 1.5 x 0.5 cm.
Andrei D. Mihalca)
Sarcocystis capracanis (dog-goat cycle)
develops small muscular cysts (130-800 x
50-70 µm) with a thick (2.5 µm) and
radially striated wall. On the other hand,
the second species with dog-goat cycle, S.
hircicanis produces larger muscular cysts,
of around 2.5 µm but with thinner and
smooth wall. The muscular cysts of S.
moulei (cat-goat cycle) are even bigger
(12 mm) with a thick and striated wall.
Muscular cysts of S. miescheriana (dog-

pig cycle) are large, 0.5-2.2 mm x 160-
260 µm. In S. suihominis the muscular
cysts are thin-walled (4-9 µm) and visible
with the naked eye (1.5 mm).
Figure 2.65 Content of a squashed In S. bertrami (dog-horse cycle), the
muscular cyst of Sarcocystis reveals the muscular cysts are large, up to 10 mm in
presence of the sausage-like bradyzoites size, with a smooth and very thin wall.
(Photo Andrei D. Mihalca) Sarcocystis fayeri (dog-horse cycle) has
smaller muscular cysts (0.9 mm x 70 µm)
and a thin, striated cyst wall. Sarcocystis
The cyst wall is thin and smooth.
neurona develops small meronts (5-20 x
Muscular cysts of S. hirsuta (cat-cattle
4-40 µm) in various tissues of naturally
cycle) are relatively big (8 mm) and have
or experimentally infected hosts
a striated wall. Endothelial meronts are
134 | P r o t o z o a
Life cycle. The life cycle of Sarcocystis is hours after the infection. They fuse
heteroxenous (figure 2.66). Each species (figure 2.66 - 7) resulting in the sexual
is relatively host specific. formation of the zygote (figure 2.66 - 8).
Each zygote will become on oocysts
The definitive hosts (dogs, cats, humans,
(figure 2.66 - 9).
wild carnivores) eliminate through their
feces the already infective sporocysts. If The oocysts will sporulate in the intestine
they are ingested by a suitable of the host (figure 2.66 - 10) with the
intermediate hosts (figure 2.66 - 1), in formation of two sporocysts each with
their intestine the sporocyst wall four sporozoites. The very fine oocyst
ruptures and the free sporozoites migrate wall ruptures (figure 2.66 - 11) and the
through the epithelium of the gut and two sporocysts are freed in the intestinal
invade the endothelial cell of blood lumen. They are subsequently eliminated
vessels in various internal organs (figure in the environment together with the
2.66 - 2) host’s feces (figure 2.66 - 12).
Sarcocystis miescheriana will be used as Sarcocystis neurona is one of the most

example in this section. Inside the interesting species of the genus. Its
endothelial cells, they undergo usually natural life cycle includes two species of
two merogonic developments. opossums (Didelphis virginiana and D.
albiventris) in North and South America.
The first merogony (figure 2.66 - 3) takes
The natural intermediate host is not
place at 5-6 days. The first generation of
known, but the infection was found in a
merozoites (tachyzoites) invade other
great variety of mammal and bird species.
endothelial cells (figure 2.66 - 4) and
Among domestic animals, the natural
undergo the second merogony at 12-17
infection was reported in horses, cats,
days after infection.
and dogs. All are however considered
The second generation of merozoites aberrant (accidental) intermediate hosts.
(tachyzoites) travels via the blood stream
The life cycle is not yet fully understood.
and when they reach the striated muscles
Asexual merogonic stages develop in the
they undergo the final merogony and
central nervous system (brain and spinal
become tissue (muscular) cysts with
cord) of horses and other intermediate
bradyzoites (figure 2.66 - 5). They remain
hosts. A single neuron can harbor as
in this stage for a long time, until the
many as 13 meronts with altogether
hosts or its flesh (raw meat) are
several hundred merozoites. In
consumed by a suitable carnivorous
experimental infection in cats, cysts
definitive host (figure 2.66 - 6).
developed also in the skeletal muscles.
After being ingested by the definitive
Epidemiology. All species parasitic with
host, muscular cysts are broken, the
domestic life cycles (both, the definitive
bradyzoites invade intestinal epithelial
host and the intermediate host are
cell and start the gametogonic
domestic animals) have a global
development with the formation of
distribution.
micro- and macrogametes as early as 14
135 | P r o t o z o a
Figure 2.66 Life cycle of genus Sarcocystis. For the meaning of numbers, please refer to
the text.
136 | P r o t o z o a
Sarcocystis neurona has been reported encephalomyelitis. In pregnant females,

only in the Americas, its distribution heavy infections with certain species (S.
being determined by its strict specificity cruzi, S. tenella) are able to induce
to the definitive hosts. abortions. Sarcocystis suihominis
develops in the endothelial cells of blood
The data regarding prevalence of
vessels from the liver. Sever muscular
infection in intermediate hosts is very
destruction is responsible for gait and
abundant in the literature. However,
myalgia.
most studies did not attempt to identify
the species; hence their zoonotic Sarcocystis neurona was found in
potential is not fully known. The neurons, mononuclear cells and glial cells
prevalence of muscular cysts in but not peripheral nerves. Although not
slaughtered cattle is very high in certain too many information are available on
areas, but the most common species is S. the migration route, experimental
cruzi which is infective for dogs. infection in ponies by Elitsur et al. (2007)
Intestinal sarcocystosis in humans is the revealed the presence of S. neurona in
most common in Europe (between 7.3 lymph nodes, liver and lungs. At 9-21
and 10.4%). The main source of infection days after the infection, parasites reach
for humans is raw meat from cattle and the central nervous system and infect
pigs. various parts: cerebellum (with
depression, seizures, behavioral
In the case of S. neurona, the disease is
changes), brainstem and spinal cord
most commonly reported in racing
(abnormal gait) or damage of the cranial
animals aged between 3 and 6 years. In
nerve nuclei (various paralysis).
USA, the seroprevalence of anti-S.
neurona is between 30 and 50%. The intestinal development of
gametogonic and sporogonic stages of
Resistance of sporocysts is high.
Sarcocystis in the definitive host is usually
Sporocysts of S. cruzi remain infective if
non-pathogenic. The main difference
kept at -22°C for 10 days or at 56°C for 10
from the severe impact of Eimeria and
minutes. Sporocysts of S. miescheriana
Isospora on the intestinal mucosa
are destroyed in the meat after 20
consists in the different phase of the life
minutes at 60°C, after 15 minutes at 70°C
cycle taking place here. In Eimeria and
and in 5 minutes at 100°C. Freezing does
Isospora, the repeated merogony is
not inactivate sarcocysts.
responsible for the epithelial destruction,
Pathogenesis. In the intermediate hosts while in Sarcocystis only the gametogony
the most important pathogenic effect is and sporogony take place here, both of
caused by the first and the second them being non-repetitive.
merogonic development which takes
Immunology. In intermediate hosts, the
place in the vascular endothelial cells. In
immune reaction during the muscular
certain species (i.e. S. tenella in sheep),
phase of the life cycle is predominantly
merogonic development can be also
cellular. In time, the organism is able to
responsible for severe myositis
eliminate the infection. Definitive hosts
137 | P r o t o z o a
are easily susceptible to reinfections, Sarcocystis miescheriana produces

demonstrating a decreased immune enteritis with diarrhea, myositis with
response. impaired movement and lameness, fever,
anorexia and weight loss. Infections wirh
Clinical signs. With the exception of S.
S. suihominis can be acute, with two fever
neurona, sarcocystoses are benign
peaks (days 5-9 and 11-15), apathy,
muscular infections in intermediate hosts
dyspnea, anemia, cyanosis, muscles
and asymptomatic or light intestinal
spasms and tremors, hyperexcitability,
infections in their definitive host. Clinical,
prostration and abortion.
signs are very rare, and they are reported
mostly after very high infective doses. In horses, two forms of sarcocystoses
The pathogenicity and symptoms in such have been described. As in all other
cases are variable from species to species. domestic animals, horses usually develop
asymptomatic muscular sarcocystosis
In cattle heavily infected with S. cruzi
(with S. bertrami or S. fayeri, both from
anorexia, fever, weight loss, anemia and
dogs). However, S. fayeri may be
difficulty in movements have been
responsible for myalgia (associated with
reported. Loss of hair on the tip of the
myositis).
tail, submandibular edema,
exophthalmia, lymphadenopathy and The second type of sarcocystosis in horse
abortion are also possible. This particular is the very severe infection with S.
condition has been known also as the neurona causing a distinct parasitic
Dalmeny disease. Infection of cattle with disease known as equine protozoal
the species of cat-origin (S. hirsuta) is myeloencephalitis. This is a debilitating
usually asymptomatic, but heavy disease, with progressive clinical
infective disease may induce anorexia, evolution, responsible for a variety of
weight loss, anemia, fever and even nervous signs. The disease may be acute
diarrhea. Sarcocystis hominis infection is or chronic. In general, the first observed
asymptomatic. symptoms are lameness which gradually
increases in intensity leading to ataxia.
Massive infection with S. tenella in sheep
One of the most typical clinical signs are
can be responsible for anorexia, loss of
the asymmetrical gait disorders with
weight, fever, anemia, recumbency and
focal muscular atrophy. Some horses
abortions in pregnant ewes. The cat-
have abnormal upper respiratory
origin species parasitic in sheep (S.
function, difficulties in standing or
gigantea, S. medusiformis) are rarely
walking, dysphagia. Neurologic
responsible for clinical infections. In
examination reveals asymmetric signs of
goats, S. capracanis and S. hircicanis can
weakness, spasticity, hypoalgesia or
produce similar clinical signs, including
complete loss of sensitivity. If the
abortions. Infection with S. hircifelis is
function of cranial nerves is affected
asymptomatic.
horses have tilted head and facial nerve
From the three species parasitic in pigs, paralysis. During all the course of the
only two seem to be pathogenic. disease, the animals are bright and alert.
138 | P r o t o z o a
Affected horses usually die during the inflammatory cells, mainly macrophages
acute stage of the disease. Dogs and cats and lymphocytes. Older cysts are
can be also infected with S. neurona and surrounded by thick capsules and may
they develop similar signs of fatal degenerate. Muscular cysts of S. hirsuta
myeloencephalitis. are easily visible and are located mainly
in the striated muscle fibers from the
In dogs infected with S. canis the parasite
esophagus.
produces a systemic disease involving the
central nervous system and liver
necrosis.
In the definitive hosts, heavy infections

are responsible for mild diarrhea.
Humans infected with S. miescheriana
after eating raw infected pig meat can
develop bloat, diarrhea, stomach ache,
nausea, vomiting or loss of appetite. In
dogs and cats with intestinal
sarcocystosis, the infection is normally
asymptomatic. However, the author of
this book has found sporocysts in dogs
with diarrhea.
Pathology. In the intermediate hosts, the

merogonic stages produce lesions of Figure 2.67 Histological aspect of a
different degrees, dependent mainly on muscular cyst of Sarcocystis. Bradyzoites
the infective dose. The most striking are clearly visible. (Photo Andrei D.
aspect during the gross necropsy is the Mihalca)
disseminated presence of white nodules
in the skeletal muscles, in the striated
muscle of the esophagus in ruminants In sheep, goats and pigs, the lesions are
and even in the cardiac muscle. Histology similar to those described in cattle. Cysts
reveals the presence of intramuscular of some species (S. tenella, S. capracanis,
parasitic cysts (figure 2.67) associated S. hircicanis) can be found also in the
with myositis, myodystrophy or cardiac muscles.
myocarditis. Cellular inflammatory Diagnosis. The diagnosis in the definitive
infiltration around the cyst can be host is based on the detection of
present. sporocysts in the feces (figure 2.68) by
In bovines, meronts of S. cruzi are flotation methods. Differentiation of
responsible for destructions of the species based on sporocyst morphology
endothelial lining of capillaries. The is not easy.
muscular stage produces myositis, with Diagnosis of muscular cysticercosis in
the parasitic cysts surrounded by intermediate hosts is usually post-
139 | P r o t o z o a
mortem, during the compulsory meat Diagnostic of equine protozoal

inspection in slaughterhouses. The myeloencephalitis caused by S. neurona is
detection of large white cysts in the done by serological confirmation
striated or cardiac muscles has diagnostic (immunoblotting) of cases clinically
value. corresponding to the disease. The
presence of the parasite can be
They have to be differentiated from other
demonstrated also in the cerebrospinal
cystic structure like for instance from the
fluid by western blot.
bladder-like cysts of “Cysticercus bovis”
(the larval stage of Taenia saginata) in Treatment. Animals infected with
cattle or “Cysticercus cellulosae” (the muscular sarcocysts are not usually
larval stage of Taenia solium) in swine. treated, as the diagnosis is most
However, the detection of microcysts is commonly done post-mortem. There are
impossible when examining the meat by several therapeutic studies done in
naked eye. In pigs microcysts can be experimental infections. In acute
accidentally detected during the sarcocystosis of lambs, amprolium (50-
microscopical examination of meat for 100 mg/kg) decreased the intensity of
Trichinella. clinical signs. Salinomycin (1-2 mg/kg)
and halofuginone (0.67 mg/kg) had the
In vivo, the infection (asymptomatic or
same protective value in sheep and goats.
not) can be detected using serological
Monensin was found to be effective for
tools (immuno-fluorescence, ELISA) or by
the treatment of acute bovine muscular
correlating the clinical signs (if present)
sarcocystosis.
with increased serum levels of bilirubin,
creatine phosphokinase and lactic acid. The treatment of equine protozoal
myeloencephalitis is an emergency, and if
it is applied in time and correctly, the
success rate is up to 75%. The most
common therapeutic protocol for horses
is the use of sulfadiazine (20 mg/kg, PO)
once or twice per day combined with
pyrimethamine (1 mg/kg, PO) once per
day. The duration of treatment is long
(84-120 days) and it must be
discontinued only when the
cerebrospinal fluid is negative by western
blot. In the case that this treatment fails
to yield good results, the drugs of choice
are diclazuril, toltrazuril or nitazoxanide.
The treatment of intestinal sarcocystosis

Figure 2.68 Sporocyst of Sarcocystis sp. in the definitive host is similar to the
from the feces of a grey wolf. (Photo Călin treatment of other intestinal coccidiosis
M. Gherman) (see Chapter 2.4.1.1).
140 | P r o t o z o a
Control. The most important means for toxoplasmosis in humans was reported in
prevention are the general hygiene 1938 in an infant girl who died at the age
measures which interrupt the life cycle of of one month in New York. However,
the parasite. Free-ranging dogs and cats previous reports of human congenital
must be excluded from farms. The chorioretinitis and encephalomyelitis,
infected meat should not be given to initially attributed to some other agents,
carnivores. There is no specific were later shown to have been caused by
prophylactic method yet, but vaccines are Toxoplasma. The first case of human
being developed for immune-prophylaxis acquired toxoplasmosis has been
of the infection with S. neurona in horses. identified in 1940. Nevertheless, first
reports of animal toxoplasmosis date
back to 1910, when Mello described an
2.4.3.2 Toxoplasmosis acute case in a dog from Italy. Although
recognized as a widespread and
Introduction. Toxoplasmosis is one of sometimes severe zoonotic infection, the
the most widely distributed parasitic full life-history and the role of the cats in
infections on Earth, affecting humans and the biology and transmission of T. gondii
animals as well. Its highly zoonotic was not fully understood until the 1970s,
potential and the severity of infection in when Dubey and Frenkel described the
certain host categories make it one of the entire developmental cycle.
most intensively studies parasites. The Etiology. The only known species is
most important aspect of toxoplasmosis Toxoplasma gondii. It has a worldwide
is probably its congenital transmission, distribution and an immense host
the subsequent clinical problems in spectrum. Virtually it can undergo its
children and the resulting social impact. asexual development in any warm-
Historical notes. The description of the blooded host, mammal or bird.
parasite came in 1908, when Nicolle and The genetic analysis of various strains of
Manceaux, two researchers from Pasteur Toxoplasma gondii from Europe and
Institute in Tunis have noticed protozoan North America revealed the presence of
stages in the tissues of a laboratory kept three major genotypes (I, II and III).
rodent known as the common gundi, Subsequently, new genetic variants were
Ctenodactylus gundi. Initially, they identified worldwide and they were
misidentified the parasite as Leishmania classified into 12 haplogroups. All these
but subsequently, in 1909, they described genetic variants differ in their
it as a new species, Toxoplasma gondii. pathogenicity on various hosts.
The generic name was given according to
the morphology of the stages they found Morphology. Toxoplasma gondii is a very
(Lat. toxo = arc or bow; plasma = life) and common parasite of humans and animals
the specific epithet is an erroneous and its diagnosis in the definitive and
spelling of the host’s name. The first case intermediate hosts is based on the
of correctly diagnosed congenital detection of various developmental
stages.
141 | P r o t o z o a
Figure 2.69 Sporulated oocysts of Figure 2.70 Tissue cyst of Toxoplasma

Toxoplasma gondii from the feces of a cat. gondii in the nervous system of an
(Photo Jana Juránková) infected mouse. (Photo Jana Juránková)
The typical stage found in the intestine of

cats as definitive hosts is the
unsporulated oocysts. In older feces, the
oocysts are sporulated and they are
”Isospora”-like (two sporocysts, each with
four sporozoites) (figure 2.69).
The tachyzoites are crescent-shaped

(Greek: toxon = arc or bow), 2-6 µm with
pointed anterior and rounded posterior
end. The nucleus is in central position.
They are found intracellularly in almost
any cell type, except red blood cells. The
group of tachyzoites resulting after
repeated multiplication by endodyogeny Figure 2.71 Tissue cyst of Toxoplasma
inside a cell is also known as pseudocyst. gondii freed from its host tissue.
Numerous bradyzoites are visible inside
Bradyzoites (5-8.5 x 1-3 µm, posterior
(Photo Břetislav Koudela)
nucleus, more slender than tachyzoites)
are found in tissue cysts. Tissue cysts are
also intracellular. They multiply by Small tissue cysts (~5 µm) contain two
endodyogeny within the tissue cysts bradyzoites while larger cysts (70-100
(figure 2.70). The size of the tissue cysts µm) contain thousands of them (figure
is variable and it depends on the number 2.71). The shape and size of the tissue
of contained bradyzoites. cysts depend also on the host tissue.
142 | P r o t o z o a
Tissues in the brain are usually smaller (4) Diversity of infected tissues is great,
(~70 µm) and round while those in the and as the parasite has systemic
muscles for instance are larger (~100 distribution, virtually any organ can
µm) and elongated. The tissue cyst wall is be infected and infective. However,
elastic and thin (<0.5 µm). In older tissue they are more common in the brain,
cysts, the wall may be hardly visible. eyes, skeletal muscles and
myocardium.
Life cycle. The biology of Toxoplasma
gondii typically includes two obligatory (5) Infected pregnant females (including
host, the cats and other felids as women) are able to pass the infection
definitive hosts and rodents as natural to the fetus via transplacentary
intermediate hosts (figure 2.72). In route.
many aspects, this typical life cycle is
Toxoplasma gondii is an obligatory
similar to Sarcocystis spp. However,
intracellular parasite, with tropism
several particular biology aspects make
mainly for nervous and muscular tissues.
Toxoplasma gondii a unique parasite:
However, it can be found occasionally in
(1) Extremely broad host specificity for any other organs. It is usually located in
its asexual stage (merogony). the cytoplasm of the infected cells, but
Toxoplasma gondii can use virtually sometimes it can invade also the nucleus.
any mammal and any bird for its
Typically, intermediate hosts are infected
merogonic development.
after ingesting sporulated oocysts from
(2) Natural transmission can be done the cat’s feces (figure 2.72 - 1). After
directly from an intermediate host ingestion, the oocyst wall ruptures
to another intermediate host, releasing the sporozoites which, after
without the presence of the definitive passing through the intestinal wall will
host. For instance, humans (which penetrate into various types of cells
are intermediate host) can get the (macrophages, endothelial cells,
infection after eating infected tissues fibroblasts etc.) (figure 2.72 - 2) where
from livestock (also intermediate they multiply by endodyogeny (figure
hosts). 2.72 - 3) producing the tachyzoites.
Tachyzoites may rupture the host cell and
(3) All “zoite” stages are infective to
invade other cells (figure 2.72 - 4) or
any susceptible host. Sporozoites
migrate through the host’s body, reaching
(from the feces of cat definitive
various tissues (including the fetus)
hosts), and tachyzoites or
where they continue their multiplication
bradyzoites (from the tissues of
in a slower rate. The result is the
intermediate hosts) are infective to
formation of tissue cysts with bradyzoites
any other intermediate host. Cats are
(figure 2.72 - 5). If cats or other felids
also susceptible to infection with any
feed on tissue cysts originating from an
of these stages, but depending on
infected intermediate host (figure 2.72 -
which stage is ingested, they act as
B2), they become infected (2.72-6).
intermediate or definitive hosts.
143 | P r o t o z o a
Figure 2.72 Life cycle of Toxoplasma gondii. For the meaning of numbers and letters,
please refer to the text.
144 | P r o t o z o a
The tissue cyst wall is dissolved by oocysts will ultimately shed oocysts in
proteolytic enzymes from the feline their feces. The prepatent period in cats
stomach and intestine, realizing the is different according to the infection
bradyzoites. The bradyzoites invade the source. After ingesting tissue cysts
epithelial cells of the small intestine of (bradyzoites), cats shed oocysts after 3-
cats and undergo repeated asexual 10 days. After being infected with oocysts
multiplication (figure 2.72 - 7), passing or tachyzoites, the prepatent period is
through multiple generations of meronts, longer (18 days).
classified in five types (type A to E). After
One of the most important life cycle
this supplementary asexual merogony
pathways is the possibility of
takes place in the intestine, the sexual
transmission form an intermediate host
gametogonic development starts (figure
to another intermediate host by
2.72 - 8) with the formation of the
carnivorism (figure 2.72 - C). According
zygotes (figure 2.72 - 9) and ultimately
to numerous opinions, this is the most
the unsporulated oocysts (figure 2.72 -
common way of infection for humans (i.e.
10). Unsporulated oocysts are eliminated
following eating raw or undercooked
through the feline feces (figure 2.72 - 11)
meat from infected animals). This
intro the environment where they
bradyzoites-induced cycle in the
sporulate in 1-5 days (figure 2.72 - 12),
intermediate host is following similar
becoming infective.
patterns to that of the oocyst-induced
Except this typical heteroxenous life cycle infection. However, the infectivity of
(figure 2.72 - A and B), there are several bradyzoites to intermediate hosts is
other pathways which can be followed by lower than the infectivity of sporozoites.
Toxoplasma gondii. If cats are infected This is why oocyst and their hosts (cats)
following ingestion of tachyzoites (figure are an absolutely essential link in the
2.72 - B1) the life cycle in the cat is complex transmission chains of
slower. It is considered that tachyzoites Toxoplasma gondii.
are less acid-resistant than bradyzoites
From clinical point of view, the most
but they can be still infective.
important contamination route is the
If cats ingest oocysts (figure 2.72 - A1) vertical transmission of tachyzoites
the course of infection is different. In this (figure 2.72 - D), mainly in humans.
case, in the first stage the cat acts as an Various studies have shown that the
intermediate host with the formation of transplacental infection occurs only if the
tachyzoites and bradyzoites in the tissue. mother is primo-infected during the
In some of the cats infected with oocysts, pregnancy. The chances of transplacental
after almost three weeks, oocysts can be transmission are low if the women
found again in the feces. The acquire the infection just before the
hypothesized scenario is that some pregnancy or during older, pre-natal
bradyzoites reach back the intestine and chronic infections. Nevertheless, in
start gametogony in the enterocytes. immunosuppressed pregnant women
However, not all cats infected with with chronic infection, transplacental
145 | P r o t o z o a
infection is possible. Transplacental sporulation success at lower

infection was also reported in domestic temperatures.
animals. The risk of congenital infection
The infections sources are various. The
is lowest when maternal infection is in
direct sources of infective oocysts are
the first trimester (10–15%) and highest
always cats. However, cat owners are not
when infection occurs during the third
more exposed to infective oocysts
trimester (60–90%). If maternal infection
compared to people who never had a cat,
occurs early in pregnancy, it results in
as oocysts from cat feces can contaminate
fewer infected babies, but they are more
fruits and vegetables. Dogs can also shed
severely affected than the greater
T. gondii oocysts following coprophagia
number of infected babies born when
of cat feces. Dogs which rolled over
infection is acquired later in pregnancy.
infected cat feces pose also a risk for
The highest risk to the fetus is when
humans. Defecation sites in public parks
infection is acquired between the 10th
are important and oocysts may be
and 24th week of gestation. Fortunately
mechanically carried on shoes.
about 60–70% of babies born of infected
mothers escape infection. Another source of infective oocysts is
represented by wild felids which acquire
In certain species (i.e. laboratory
the infection from their wild prey. Hence,
rodents) transplacental transmission
the wildlife reservoirs can be locally
occurs even if the infection is chronic and
important also.
took place before the pregnancy. In
domestic animals (i.e. sheep), various The main sources of infection with
observation suggest that the situation is Toxoplasma for humans are not the same
similar to humans, and only tachyzoites everywhere. In the areas where cats are
can pass transplacentally (i.e. infection abundant and live in close contact with
must be during pregnancy). people the oocysts are probably the
Transplacental transmission was not principal infection sources. In developed
documented in all domestic species. countries, where cats are mostly indoors
There are no confirmed reports from and they feed on commercial food, the
dogs, horses or cattle. most probable source for human
infection is raw or undercooked meat.
Epidemiology. As stated before,
Raw goat milk was reported as a source
Toxoplasma gondii is probably the most
of infection for humans. Raw cow milk or
common parasite on Earth. It is present
uncooked chicken eggs are not
wherever cats are present which means
considered dangerous for the
everywhere where humans are present.
transmission of Toxoplasma.
Despite its global distribution,
Toxoplasma is more common in warmer Other sources of infection are
climates than in colder ones and in uncommon. Tachyzoites accidentally
lowland compared to highlands. This is reaching the cornea during laboratory
most probably related to the lower manipulation can induce the infection.
survival of oocysts and their lower Transfusion of whole blood is not
146 | P r o t o z o a
infective as the number of circulating less aversion to cat odor. This host-
tachyzoites is very low and the period of manipulation makes infected mice easier
parasitemia is low. However, transfusion preys to cats.
of packed leukocytes can be a risk. Organ
The values for the infection prevalence in
transplants are also incriminated. The
cats are variable. If we assess this
presence of tachyzoites has been
epidemiologic parameter on the basis of
demonstrated in semen and saliva but no
the presence of oocysts in the feces the
venereal or salivary transmission were
prevalence is very low (average less than
reported.
1%). However, if we assess the
The prevalence in humans is not prevalence of anti-Toxoplasma antibodies
necessarily related to the prevalence in (seroprevalence) it can reach an
cats, but rather to cultural habits. In astonishing 100% in certain cat
nations where eating raw or population. This can be explained if we
undercooked meat is a common practice consider the biology of T. gondii in its
(i.e. France) the seroprevalence of definitive host, as the time for oocysts
toxoplasmosis in humans is higher. elimination in cat’s feces is very short (1-
Eating raw meat seems to be a more 2 weeks) and the number of oocysts can
common habit in more developed be low, under the coproscopic detection
countries. In third-world countries, meat threshold (<1000 oocysts per gram).
is usually well cooked because of other Nevertheless, PCR detection of
health risks. This explains the lower Toxoplasma DNA in feline feces can yield
prevalence in humans from Africa and higher prevalences (up to 11%) and is
Asia. The prevalence in humans is also able to differentiate between other small
influenced by the species they most intestinal coccidia like Hammondia.
commonly eat. In countries where
Another very important epidemiological
mutton is a common dish, the prevalence
question is if cats shed oocysts more than
of human toxoplasmosis is higher. Viable
once in their lifetime or they acquire kind
Toxoplasma cysts are commonly found in
of immunity. Data from experimental
pigs and sheep; in cattle, viable cysts are
studies are controversial. Even though,
very rare. Reported values for
probably the number of oocysts
seroprevalence in humans are very
eliminated by cats during their first
heterogeneous and they depend on
infection is much higher than during
various factors. The higher values have
subsequent infection. More details are
been reported in South America, and the
given in the immunity section.
lowest in Eastern Asia.
Quantitative assessments found
The prevalence of infection in cats is impressive number of oocysts in cats
dependent on various factors, but the with primary infection (up to 13 million
most important factor seems to be the oocysts per gram of feces). The average
presence and availability of infected values are of course lower, but still
rodents. Interestingly, mice infected with impressive (around 10 million oocysts
T. gondii are less neophobic and show per cat).
147 | P r o t o z o a
The seropositivity in cats increases with Seropositivity greatly depends on the

the age and it is higher in feral cats than farming system. The infection is virtually
in indoor cats. Prevalence of cats with absent from intensive farms and more
tissue cysts is between 5 and 70% in common in free-ranging birds.
various countries.
Surprisingly, the resistance of T. gondii
In sheep the infection was also found oocysts in the environment is not too well
worldwide. Except cats, seroprevalence known under natural conditions. Under
in sheep is among the highest from all experimental conditions they proved to
domestic animals. In certain adult be relatively resistant. At -21°C in water
populations, it can easily reach 95%. In they were not killed. They also resisted
intensive farming system the 4.5 years in water at 4°C and more than 1
seroprevalence is lower than in semi- year in water at 22°C. Warmer aquatic
intensive systems. Risk factors include medium kills them faster (1 month at
mostly the age, presence of free-ranging 40°C; 2 minutes at 55°C; 1 minute at
cats in the farm and history of abortions. 60°C). If kept in cat feces, they resist
It is estimated that between 10 and 23% several years at temperature between 15
of abortions in sheep are caused by T. and 35°C. In dry condition they die faster
gondii. Toxoplasmosis in goats is also (11 days in air at 11% relative humidity
globally distributed, with variable and 2 days at 0% relative humidity).
seroprevalence which is generally lower Unsporulated oocysts are generally more
than in sheep. In cattle the global sensitive to environmental factors than
seroprevalence is generally lower than in sporulated oocysts. Oocysts are also very
sheep. resistant to disinfectants. Kept in 10%
formalin they resist 48 hours. The 5%
The same worldwide distribution was
ammonium hydroxide kills them in 30
reported in pigs. The seroprevalence is
minutes but not in 10 minutes. Iodine
much higher in backyard and free-range
tincture (2%) kills oocysts in 3 hours but
pigs and almost absent in pigs from
not in 10 minutes. Oocysts survive
intensive farm system. There is also a
standard water chlorination for at least
clear age related distribution of
24 hours.
seropositivity values. Adult saws show
higher prevalences than market-age pigs. Tissue cyst resistance is a key
epidemiologic factor. Treatment and
In dogs the distribution is global.
injection with salt of meat-based
Seropositivity is variable and higher in
products kills bradyzoites from tissue
older dogs and in rural dogs. In general,
cysts. Tissue cysts are sensitive to
the seroprevalence in dog is high (up to
conventional cooking. They are killed as
almost 90%). In horses the
the internal temperature is over 60°C.
seroprevalence is generally low.
Freezing also kills tissue cysts (at -12°C in
Multiple seroprevalence studies are 1 day). In decomposing carcasses
available for chicken, as their meat forms bradyzoites survive for several days.
a significant part of human diet. Resistance of tachyzoites is very low
148 | P r o t o z o a
compared to the resistance of cattle). Other determinant factors for the

bradyzoites or oocysts. pathogenicity are the route of infection,
the source of infection and the parasite
Pathogenesis. Despite the huge attention
strain. Oocyst-induced infections are
given to T. gondii, clinical infections are
more severe that bradyzoites-induced
rare. After the infection with “zoites”
infections. Type I genotype is pathogenic
(bradyzoites from tissue cysts,
for mice, but not type II and III. In
tachyzoites from pseudocysts,
humans, the most pathogenic genotypes
sporozoites from oocysts in cat feces),
are I and III, but in France, severe cases
they penetrate the intestinal wall and
were reported also with type II. Certainly
multiply locally in adjacent tissues
the immune system of the host plays also
including mesenteric lymph nodes. They
a great role (see next section).
cause here local necrosis. Similar necrotic
lesions are produced in various other Parasitemia with tachyzoites during
organs by the asexual development of pregnancy is a key factor for
tachyzoites. Necrosis is the result of transplacental transmission. After
intracellular development cellular death invading the placenta, they produce
and not the result of toxins. No toxin has placental necrosis associated with
been so far detected in T. gondii. The embryonic death, fetal resorption,
initial necrosis may kill the host if it is mummification, abortion or stillbirth. If
extensive enough and affects vital organs. the fetus survives, tachyzoites invading
Otherwise, the necrosis is gradually the fetal tissue are able to cause necrotic
replaced by local chronic inflammation lesions. As some cases of severe placental
and the host develops immunity. necrosis did not result in abortions, also
Tachyzoites usually disappear from the hormonal imbalances have been
internal organs in three weeks after the incriminated in the pathogenesis of
infection and afterwards, bradyzoites are toxoplasmic abortion.
located in cysts mainly in the muscular
Behavioral alterations in laboratory
tissue (striated and cardiac) and central
rodents and humans are linked to
nervous system.
perturbations in dopamine production.
Tissue cysts remain arrested awaiting a
Immunology. Immunity against
carnivorous predator to prey on the host.
Toxoplasma is very complex. It involves
However, in certain situations (mainly
both types of immunity, innate and
related to a sudden decrease in
acquired. The intracellular location
immunity) the tissue cysts can rupture
protects the parasite from the direct
and the released bradyzoites invade
contact with the host’s immune effectors.
other tissues forming new cysts.
The fact that clinical cases are rare
Pathogenicity is dependent on various suggests that the immune system work
factors. Certain host species (New World effectively against Toxoplasma in most of
monkeys, Australian marsupials) are the cases. This is supported by the
more susceptible to develop clinical signs extremely high and widespread
than others (Old World cattle, horses, seroprevalence values reported in
149 | P r o t o z o a
various hosts worldwide. However, the oocysts formation is lost after several
ubiquity of this parasite and also high years if no reinfections take place. An
prevalence values for the presence of interesting immunologic interaction with
infective viable tissue cysts suggest that other feline coccidia was reported in cats
despite not being able to produce clinical with latent toxoplasmosis. When infected
infection, Toxoplasma is capable of with Isospora felis, the bradyzoites from
surviving in the host and remaining the cat’s tissue cyst become active again
infective. and start to shed Toxoplasma oocysts in
feces. On the other hand, another
Cellular response is also very strong.
coccidian parasite of cats, I. rivolta is not
CD4+ and CD8+ T-cells are crucial in the
able to induce the relapse in oocyst
recovery form the primary infection. The
shedding.
protective role in subsequent infection is
probably held by antibodies. This theory Clinical signs. Despite most of the
of cellular-mediate immunity is also infections are asymptomatic,
sustained by the increased susceptibility toxoplasmosis still remains a major
of human patients suffering from AIDS, a disease.
condition caused by the HIV virus which
Symptoms are not characteristic and this
causes depletion of CD4+ cells.
may account for false negative diagnosis
In general, the humoral response is and subsequent limitation of its clinical
strong. In cats infected with tissue cysts, importance. Moreover, certain signs of
the seroconversion appears after 10 days infection in humans are not considered to
and is very persistent. Antibodies can be be real symptoms of a disease (decreased
detected even years after the infection. reaction times, tendency for accidents,
Seropositive mother cats transfer personality changes, lower guilt
protective antibodies to kitten. This proneness, higher chance for more
situation is probably valid also for other promiscuous lifestyle) and their
animal species but it has not been correlation with toxoplasmosis is quasi-
investigated in detail. This is why post- impossible in practice. In animals, these
natal infection in newborns is rare, and “hidden” signs are even more difficult (if
most animal become susceptible to oral not impossible) to trace. In mice infected
infection after several weeks of life. In to T. gondii, various behavioral changes
cats for instance, the passive maternally - which enhance the chance of being
acquired immunity disappears by the age predated by cats have been recorded:
of 3 month. decreased learning capacity, higher
activity levels, lower ability to
Various experimental trials showed that
differentiate familiar and novel
cats shed massive number of oocysts only
surroundings or reduced predator
during the first (primary) infection. All
avoidance.
subsequent infection of already immune
cats result in no or very low levels of fecal Clinical signs and severity of disease vary
oocyst elimination. The immune with the host species, age and immune
protection responsible for inhibition of status.
150 | P r o t o z o a
In cats with tissular infections, the resorption are also reported in infected
clinical signs consist in one or more of the sheep. Sterility is also possible in
following symptoms: fever, anorexia, Toxoplasma-infected ewes. In sheep
respiratory abnormalities (dyspnea, flocks in which toxoplasmic abortions are
polypnea), abdominal pain (due to present, a great number of lambs born-
hepatitis or pancreatitis), icterus, alive can suffer of subclinical congenital
neurologic signs (blindness, anisocoria, toxoplasmosis. Except abortion, other
slow pupillary light reflex, ear twitch, symptoms associated with post-natal
circling, torticollis, seizures, infection in sheep are fever and diarrhea.
incoordination, increased affection,
In goats, clinical toxoplasmosis is similar
stupor, atypical cry, central
with the situation described for sheep.
hypothermia), cutaneous signs (nodules,
Abortions and neonatal mortality are not
ulcerations), locomotory problems
uncommon. Goats are more susceptible
(lameness, articular pain), and ocular
to clinical toxoplasmosis than sheep.
signs (iritis, mydriasis, hyphema, retinal
Mortality following natural infection was
hemorrhages). A statistical analysis on
reported even in adult goats.
100 feline cases showed that 36% had
systemic infection, 26% showed Clinical toxoplasmosis in pigs is a rare
pulmonary involvement, 16% abdominal condition. Clinical signs of the acute form
lesions, 12% hepatic involvement, 7% (postnatal) include fever, anorexia,
neurologic involvement, 4% ocular dyspnea, weakness of the limbs,
involvement while other location neurologic signs and abortions. Generally,
(cutaneous, pancreatic, cardiac) were less pigs recover after 3 weeks. Mortality is
common. Clinical tissue infections in cats possible, but rare. Congenital (neonatal)
might result in sporadic cases of toxoplasmosis is associated with gait
mortality. Cats infected with FIV might abnormalities, dyspnea, diarrhea and
have aggravated symptoms and chronic mortality up to the second week of life.
asymptomatic cases may become acute. In dogs clinical cases are usually
Congenital toxoplasmosis results in associated with lower immunologic
significant mortalities in kitten. status, mainly after surviving canine
No clinical signs were described in cats distemper. Reported symptoms include:
with intestinal infection with oocysts. orchitis, respiratory signs, nervous signs
Lesions of severe enteritis were and death. Toxoplasmosis usually is
described in cats but they were caused by diagnosed post-mortem and it seems to
tissue cysts. complicate canine distemper cases in
puppies. Rare cases of acute
In sheep, the most important clinical sign
toxoplasmosis in adult dogs included
is abortion. Toxoplasma gondii is one of
ocular and hepatic involvement. No
the main causes of infective abortion
congenital cases are known.
worldwide. Toxoplasmic abortions in
sheep are in the mid or last term of Except very few cases of abortion, in
gestation. Mummified fetuses or fetal cattle clinical toxoplasmosis is a rare
151 | P r o t o z o a
condition. Clinical toxoplasmosis in Focal myocarditis and encephalitis with

horses is virtually absent. However, in the presence of bradyzoites in tissue
both these cattle and horses, any cysts are the main lesions in chronic
reported case of toxoplasmosis must be toxoplasmosis.
regarded suspicious. Instead, the other
Diagnosis. Diagnosis has different
related conditions are definitely more
approach in the feces of the definitive
prevalent: neosporosis in cattle (see
host or in the samples from intermediate
Chapter 2.4.3.3) and equine protozoal
hosts.
myeloencephalitis (see Chapter 2.4.3.1).
Detection of oocysts in the feces of cats is
In chicken, there are very few known
done by classical flotation methods.
cases of clinical toxoplasmosis. These
However, finding non-sporulated or even
scarce reports include sudden death and
sporulated oocysts with Toxoplasma-like
nervous signs (torticollis, lateral
morphology is not enough to say it is
recumbency).
Toxoplasma. As shown in other sections
Pathology. The lesions associated with of this textbook (see Chapters 2.4.1.1 and
Toxoplasma infection are located in 2.4.3.4), various coccidia are parasitic in
various organs and tissues. During acute the small intestine of cats. Their
toxoplasmosis, tachyzoites are differentiation cannot be done relying
responsible for producing necrotic strictly on morphological features (table
lesions in various tissues (mesenteric 2.39).
lymph nodes, liver, intestinal lamina
propria, spleen, pancreas, lungs, adrenal
glands, kidneys). Same tachyzoites- Table 2.39 Oocyst size of coccidia found in
feces of cats (after Dubey and Greene, 2012)
induced lesions are present in internal
organs of early aborted or stillborn Species Average size
(µm)
fetuses or in newborns suffering of Isospora felis 40 x 30
congenital toxoplasmosis. Isospora rivolta 22 x 20
Toxoplasma gondii 12 x 10
Additionally, necrotic or degenerative Hammondia hammondi 12 x 11
encephalitis, endocarditis and retinitis Besnoitia wallacei 17 x 12
Besnoitia darlingi 12 x 11
have been described in congenital Besnoitia oryctofelisi 12 x 11
toxoplasmosis in goat kids, lambs, kittens, Sarcocystis spp.* 11 x 9
*sporocysts
puppies and piglets. Histologically, in all
the affected organs tachyzoites are
visible. For safety reasons, all small oocysts
Tachyzoite infection in pregnant females found in the feces of cats must be
results in degenerative lesions of the regarded as Toxoplasma. Specific
placenta. The main lesion is necrotizing identification can be done only by
placentitis with the presence of large molecular biology (copro-PCR) or after
amounts of tachyzoites in the sporulation by ultrastructural studies or
trophoblastic layer. xenodiagnosis.
152 | P r o t o z o a
The diagnosis in systemic infections of and peribronchial markings. Abdominal

intermediate hosts is more complex. As radiology shows the enlarged mesenteric
clinical signs are not characteristic, lymph-nodes. Other imagery techniques
diagnosis must rely on detection of the used mainly for detection of lesions in the
organism or its DNA in various tissues or central nervous system include
the detection of antibodies. The most myelography, computer tomography (CT)
difficult task is the differentiation of and magnetic resonance imaging (MRI).
subclinical from clinical toxoplasmosis Clinical laboratory findings are not
and to correlate the presence of specific but they may help in the
Toxoplasma with the symptoms. diagnosis. They include: anemia,
leukocytosis with neutrophilia,
For diagnosing clinical toxoplasmosis,
eosinophilia, lymphocytosis and
various symptoms must be correlated
monocytosis. Terminally ill cats present
with imagery and clinical laboratory
leukopenia (with absolute lympho-
followed by identification of the organism
cytopenia and neutropenia). Usually the
from various samples, including biopsies
leukocytosis is indicative of recovery and
by cytology, histology, PCR,
a better prognosis.
xenodiagnosis (artificial infection in
rodents) or serology. Clinical biochemistry shows
hypoproteinemia, hypoalbumin-emia,
In vivo diagnosis of clinical
increase of alanine amino-transferase,
toxoplasmosis is important for acute
aspartate aminotransferase and alkaline
post-natal cases and congenital
phosphatase associated with hepatic and
infections. It is mainly of interest in pets.
muscular necrosis. The serum level of
Fever in cats, correlated with
creatine kinase is increased when
unresponsiveness to antibiotic treatment
muscular necrosis is present. In animals
is one of the most common findings of
with acute hepatic necrosis, the levels of
acute toxoplasmosis. The procedure in
serum bilirubin are also increased.
this case is to continue with further
Increased serum amylase and lipase
clinical procedures. Fundic ocular
activities are indication of pancreatic
examination reveals multifocal
involvement. All these clinical laboratory
iridocyclochoroiditis. Cytology during the
findings are not enough for a positive
acute disease can reveal the presence of
diagnosis of toxoplasmosis.
free tachyzoites in various tissue and
body fluids. Tachyzoites are more Isolation of the agent from aborted
common in thoracic and peritoneal fetuses and fetal membranes is routinely
pathologic effusions but they can be done by inoculation to laboratory mice.
rarely detected also in other samples For this scope, the fetal brain and
(blood, cerebrospinal fluid, tracheal placental cotyledons yield optimal
washings). These samples should be results.
further analyzed by PCR for confirmation.
Identification in tissue section is done by
Thoracic radiology can also help, showing
histology and more specifically by
a diffuse interstitial to alveolar pattern
immunohistochemistry. Histopathology
153 | P r o t o z o a
is essential for concluding on the cause- In cats with systemic infection the
effect association. treatment is done by combining two
drugs. Sulfonamides (20-30 mg/kg,
Serologic diagnosis include detection of
orally, every 6-24 hours, for 2-4 weeks)
humoral antibodies: Dye test known also
in combination with pyrimethamine (0.5-
as Sabin-Feldman test, indirect
1 mg/kg, orally, every 24 hours, for 2-4
hemagglutination test, complement
weeks) are the drugs of choice.
fixation test, modified agglutination test,
Pyrimethamine can be given parenterally,
latex agglutination test, indirect
after dilution. Sulfonamides can be also
fluorescent antibody test, ELISA,
used in combination with trimethoprim.
immunoglobulin M immunosorbent
The use of these drugs may induce
agglutination assay test and Western
thrombocytopenia and/or leukopenia. In
blotting.
such a case, treatment should not be
An ELISA method has been developed for discontinued but the cats should receive
detection of Toxoplasma antigens in cats. folinic acid and yeast supplement.
Molecular techniques are employed for Clindamycin (8-17 mg/kg, orally or
the detection of parasite DNA. PCR is intramuscularly, every 8-12 hours, four 4
widely used on various samples mainly weeks) is also highly effective in feline
for diagnosing abortions and for toxoplasmosis.
molecular epidemiology surveys. The treatment of choice in dogs is similar
For details on the technique of isolation, with the one in cats, but doses are slightly
cultivation and serologic procedures different: clindamycin (3-13 mg/kg,
refer to Dubey (2010) and to OIE (2012). orally or intramuscularly, every 8 hours
or 10-20 mg/kg, same routes, every 12
Differential diagnosis is variable in each hours) for 4 weeks.
species. Because of the great variety of
clinical signs in cats, the list of diseases to As in the other domestic animal species
be considered for the differential acute toxoplasmosis is rare, no
diagnosis is too long to be given here. therapeutic protocols are recommended.
Readers should refer to a more general In the case of toxoplasmic abortion,
feline medicine book. In the case of chemoprophylaxis must be performed in
toxoplasmic abortion, differential pregnant animals.
diagnosis must include all the other Treatment of cats which shed oocysts is
causes (infectious and non-infectious). In done by: clindamycin (25-50 mg/kg,
dogs the differential diagnosis must be orally or intramuscularly, every 12-24
done against neosporosis. hours, for 1-2 weeks); a combination of
Treatment. Treatment has two major sulfonamides (100 mg/kg, orally, every
indications: to treat the clinical systemic 24 hours, for 1-2 weeks) with
cases and two treat the cats with pyrimethamine (1 mg/kg, orally, every
intestinal infection to stop the oocyst 24 hours, for 1-2 weeks); toltrazuril (5-
elimination. 10 mg/kg, orally, every 24 hours, for 2
weeks). Monensin given in food for one
154 | P r o t o z o a
two weeks is also effective and stops Chemical prevention is done mainly in
oocysts shedding. humans in certain cases when patients
are exposed to risk of clinical infection or
Control. Preventing infection with
the risk of congenital toxoplasmosis is
Toxoplasma is essential in all host
high. If a human patient is serological
categories (humans, cats, livestock).
negative, meaning there is no protection
Prevention in cats is easy if they are kept
against Toxoplasma, and an
indoors and never receive uncooked
immunosuppressive treatment must be
meat, bones or organs from animals, even
applied (i.e. before transplants), the
if these are bought from grocery stores.
prophylactic therapy is recommended.
In the case cats do not eat dry or canned
Prophylactic treatment has been used
food or cooked food, the option of choice
also in sheep, in flocks with history of
is to give them raw meat which was deep-
toxoplasmic abortion. The drug of choice
frozen before or beef which is usually
in this case is monensin (17-28 mg/kg,
free of infective cysts. Raw liver is an
daily, for five days), given in the last half
essential part of feline diet, as it is a
of gestation. Other drugs (sulfamethazine,
perfect dietary supplement of vitamin A.
pyrimethamine, decoquinate) have been
As infective Toxoplasma cysts are very
shown to have similar effects in sheep.
common in the liver, in such cases the
organs must be deep frozen before fed to One commercial vaccine (Toxovax) is
cats. Owners must avoid letting cats to available for prevention of toxoplasmic
hunt outside or to scavenge in the trash abortions in sheep.
can. In farms, cat populations must be
controlled. In farms where abortions
occur, fetuses and fetal membranes must 2.4.3.3 Neosporosis
be eliminated promptly to avoid
placentophagia by cats or other animals. Introduction. Neosporosis is a disease of
Outdoor cats must be under permanent cattle and dogs with huge economic
surveillance and treated if they are impact in dairy and beef cow farms. It is
shedding small coccidian oocysts. considered one of the most important
Prevention of infection in humans infectious causes of abortion in cattle,
include: washing the hands after handling worldwide. It has been estimated that
meat or after petting cats and dogs. Fruits annual global losses due to neosporosis
and vegetables must be washed are between 1.2 and 2.3 billion US
thoroughly. Any consumed meat must be dollars. Additionally, another Neospora
properly cooked. Tasting of food during species is responsible for a neurologic
cooking is not recommended. Microwave disease in horses.
cooking does not kill the bradyzoites. Historical notes. The history of
Freezing meat at -12°C kills the tissue neosporosis is very recent. Until 1988
cysts in few days. Pregnant women when the etiological agent was
should avoid contact with cats, raw meat discovered, it was confused with
and unwashed fruits or vegetables. Toxoplasma gondii. The first case of
155 | P r o t o z o a
neosporosis was described in 1984, in intermediate hosts (see life-cycle). Their

dogs from Norway by Bjerkas et al. Three typical shape is crescent-like (figure
years later, in 1987, O’Toole and Jeffrey 2.73). Bradyzoites (8 x 2 µm) are found
described a clinical case in a newborn in tissue cysts surrounded by a thick-wall
calf. Both reports were designated to be (4 µm), located in muscular and nervous
caused by an unidentified protozoan, tissues.
similar to Toxoplasma and Sarcocystis.
The agent was described only in 1988 by
Dubey and named Neospora caninum. Table 2.40 Oocyst size of coccidia found in
feces of dogs (modified after Dubey and
This does not mean the disease is new, Greene, 2012)
but that until 1988, all cases (except the
Species Average size
two listed above) were considered to be (µm)
toxoplasmosis. Isospora canis 38 x 30
Isospora ohioensis 24 x 20
More recently, in 1998, a new species, Isospora neorivolta 17 x 15
Isospora burrowsi 20 x 17
Neospora hughesi was described from the
Neospora caninum 12 x 10
central nervous system of a horse in Hammondia heydorni 12 x 11
California by Marsh et al. Sarcocystis spp.* 11 x 9
*sporocysts
Etiology. Two species are known in
genus Neospora. Neospora caninum is
typically parasitic in dogs (which act as
definitive hosts) and cattle (intermediate
hosts). Several other species have been
found naturally infected with viable N.
caninum (sheep, buffaloes, horses, bison,
deer). The second species, Neospora
hughesi is responsible for a form of
equine protozoal myeloencephalitis.
Morphology. Oocysts are small (10.6-

12.4 x 10.6-12.0 µm) and morphologically
not differentiable from other small
oocysts found in canine feces (see table
2.40). Oocyst wall is colorless. Sporulated
oocysts contain two sporocysts (7.4-9.4 x Figure 2.73 Tachyzoites of Neospora
5.6-6.4 µm), each with four sporozoites caninum in cell culture. (Photo Ovidiu
(5.8-7.0 x 1.8-2.2 µm). Oocysts Șuteu)
(“Isospora”-like) can be found in the feces
of dogs and other canids.
Although many genetic strains of N.
Tachyzoites (3-7 x 1-5 µm) are found in caninum have been described, little is
intracellular parasitophorous vacuoles in known on their variation in virulence. In
the cytoplasm of various cells in the the case of N. hughesi, only the asexual
156 | P r o t o z o a
stages in the intermediate host (horses) muscle cells where they can remain for
are known. Tachyzoites are located in a all the life of the animal.
parasitophorous vacuole inside host cell
The typical life cycle continues when
cytoplasm. Bradyzoites (2-3 x 4-7 µm)
tissue cysts with bradyzoites are ingested
are within a tissue cyst (7-16 x 10-19
by a canine definitive host. What happens
µm), surrounded by a wall (0.1-1 µm
here is still largely unknown, but it is
thick).
presumed that part of the bradyzoites
Life cycle. In many aspects, the life cycle reconvert into tachyzoites and produce
of Neospora caninum is similar to that of systemic infection which ultimately result
Toxoplasma gondii. The life cycle of N. in the formation of tissue cysts.
caninum is heteroxenous (figure 2.74).
Systemic infection with tachyzoites can
Domestic dogs and other canids (coyotes,
result in the transplacental transmission
grey wolves, dingoes) are definitive
to puppies. Other bradyzoites will invade
hosts. The typical intermediate hosts are
the epithelial cells of the dog’s intestine
cattle, but various other warm-blooded
and they probably follow a similar
vertebrates can serve as hosts for the
development as Toxoplasma gondii does
asexual stages. However, the spectrum of
in cats, continuing merogony, and then
recorded intermediate hosts is not as
gametogony with oocysts formation.
diverse as in the case of T. gondii. One
Infected dogs shed through their feces
very important aspect is the lack of
unsporulated oocysts 5 days after
human infections reported. So far,
ingestion of tissue cysts.
neosporosis is not considered a zoonotic
disease. The oocyst elimination by dogs is at a
much lower rate than in cats infected
Dogs shed in their feces unsporulated
with T. gondii. It has been estimated that
oocysts which eventually undergo
dogs shed around 500,000 oocysts
exogenous sporogony (24-72 hours) and
(compared to 1 billion oocysts excreted
become infectious (sporulated) oocysts. If
by one infected cat). In dogs, the time
sporulated oocysts are ingested by a
they shed oocysts extends up to 4 months
suitable intermediate hosts (e.g. cattle),
(unlike in cats which shed T. gondii only
they excyst and the freed sporozoites will
for 1-2 weeks). Considering the lower
penetrate the intestinal wall and invade
overall number of eliminated oocysts and
various cell types: macrophages, neural
the longer period, the chance of finding
cells, fibroblasts, endothelial cells, muscle
Neospora caninum oocysts in dog feces is
cells and hepatocytes where the multiply
very low. Another difference from
by endodyogeny and producing
Toxoplasma gondii is that dogs are not
tachyzoites. Tachyzoites divide around
susceptible for the infection with N.
twenty times before becoming
caninum oocysts or tachyzoites (like cats
bradyzoites in tissue cysts (in cca. three
are for T. gondii). Dogs can be infected
weeks after the infection). Tissue cysts
only with tissue cysts with bradyzoites
with bradyzoites are found typically in
from intermediate hosts.
the central nervous system and striated
157 | P r o t o z o a
Figure 2.74 Life cycle of Neospora caninum. Contamination of dogs as definitive hosts
takes place after ingestion of tissue cysts from meat or organs of infected intermediate
hosts (including aborted fetuses and fetal membranes). Intermediate hosts acquire the
infection after eating sporulated oocysts passed by dogs in the feces. Infected intermediate
host females are able to pass the infection to their offspring which will develop lifelong
infection. Subsequently they are able to transmit the infection transplacentally again and
again (dotted contour arrow). After ingesting tissues cysts, dogs develop both
enteroepithelial and systemic infection and are able to pass tachyzoites transplacentally to
puppies.
Additionally, the only known way of Except this typical life cycle involving
horizontal transmission to intermediate alternation of the definitive and
hosts is by ingestion of oocysts. intermediate hosts, Neospora caninum
can be transmitted vertically, from
Although placentophagia in cows was
infected pregnant females to the fetus.
suggested as a mode of transmission
There are two types of transplacental
(horizontal, intermediate to intermediate
transmission described for N. caninum in
host), no experimental trials support this
cattle: (1) The exogenous transplacental
theory yet.
158 | P r o t o z o a
transmission occurs when non-infected breeds. The highest seroprevalence in

pregnant cows ingest infective oocysts. In cattle has been found in those farms
this case, the tachyzoites will invade the where dogs were more abundant.
fetus, transported probably by the
Seroprevalence data in dogs is reported
mononuclear phagocytes via the blood
worldwide. In random populations it is
stream. (2) The endogenous
usually less than 20%. Purebred dogs are
transplacental transmission happens in
more likely to develop seropositivity than
cows which are already infected before
mixed breeds. Stray dogs with access to
pregnancy. In such a case, bradyzoites
raw organs and meat have significantly
from tissue cyst are reactivated and they
higher prevalence than indoor dogs fed
differentiate into tachyzoites which
exclusively with commercial diet.
ultimately infect the fetus. The
Serologic prevalence is higher in cattle
endogenous transplacental transmission
farm dogs than in dogs living in cities.
explains why female calves with
congenital neosporosis are able to pass The most important epidemiological
the infection to their offspring when they factor from clinical point of view is the
become reproductive females. prevalence of abortions caused by N.
caninum in cows. Two epidemiologic
It is not known if congenital transmission
patterns of Neospora-induced abortions
follows the same rule in dogs or other
are known: endemic abortion and
hosts. Infected female dogs can give birth
epidemic abortions. The endemic pattern
to infected puppies during several
consists of persistent abortion rate
pregnancies.
(around 5-10%, all year around). The
Transmission is not possible through most dramatic situation (epidemic
milk or venereal route. pattern) is the so called “abortion
storm”, when more than 10% of the
The life cycle of N. hughesi is not known,
pregnant cows from a single farm abort
as only the asexual stages in the
within a time frame on 12 weeks.
intermediate hosts were described.
Abortions can persist from several
Probably the definitive host is a
months to several years.
carnivorous mammal.
As dogs shed a very low number of
Epidemiology. Neosporosis is
oocysts, the main source of infection for
distributed worldwide in cows and dogs,
cows is the transplacental transmission
as numerous seroprevalence and
from their mothers. However, not all
molecular epidemiology studies show.
infected cows transmit the infection to
Antibodies were found also in small
their offspring. The transplacental
ruminants, but the clinical importance in
transmission rate varies roughly from 30
ovine abortion is still debated. The
to 60%. It is not known if the
prevalence of neosporosis is highly
transmission rate is different between
variable between countries, between
endogenous and exogenous
regions of the same country and between
transplacental transmission routes. Some
beef and dairy cows and between cattle
authors suggest that post-natal infection
159 | P r o t o z o a
is equally important, as seropositivity tachyzoites is thought to be related to

may increase dramatically in certain hormonal and immune factors of the
flocks at a given time. In the recent years, pregnant cow.
wildlife reservoirs increased in their
The pathogenesis of abortion is related to
epidemiologic importance. Abortion
the damage of the placenta by rapidly
storms are likely caused by exogenous
multiplying tachyzoites. They initially
transplacental transmission following
invade the maternal caruncular septum
exposure to oocysts.
and subsequently the fetal placental villi.
Resistance of oocysts of N. caninum in the The abortion occurs in two situations.
environment is considered to be more or When the placenta is severely damaged,
less similar with T. gondii. High the fetus receives insufficient oxygen
temperatures (100°C) inactivate them in supply and nutrition. Other situation is
one minute and treatment with 10% when tachyzoites destroy directly the
sodium hypochlorite in 1 hour. fetal tissues. Immune-mediated fetal
Bradyzoites in tissue cysts remain expulsion has been also suggested,
infective in tissues for 7-10 days. associated with maternal pro-
inflammatory cytokines (IL-10, gamma
Pathogenesis. It is not fully understood
interferon).
why some infected cows are able to give
birth normally while others abort. Pathogenesis in dogs is caused by the
Various factors have been incriminated, rapid multiplication of tachyzoites in
including the infective oocyst dose. It is various tissues. This can occur mainly
also not known if there are any during primary infections but also if
correlations between the clinical bradyzoites are reconverted to
outcome and the mode of transplacental tachyzoites during persistent infection
infection (endogenous or exogenous). (e.g. stress, pregnancy, immuno-
Other hypothesized factors include the suppressive diseases). Development in
existence of N. caninum strain with the brain of dogs causes monocyte-
different virulence or the susceptibility of mediated lesions with altered function of
cows under metabolic stress (e.g. dairy the nervous centers involved. Lower
cows). The factors affecting the risk of motor neuron damage and severe
abortion were summarized by Goodswen myositis are the causes of gradual hind
et al. (2013). limb paralysis in puppies with congenital
neosporosis. Destruction of the muscular
For the exogenous transmission cycle, the
layers of the esophagus can result in
risk factors are the number of oocysts
megaesophagus with dysphagia.
ingested and the gestation stage. In the
case of endogenous transmission cycle, Immunology. Immunity plays a crucial
cows with higher antibody titers are role in the development of neosporal
more likely to abort. infection. Weather the infected cows
abort or they transmit the infection
Reactivation of bradyzoites from tissue
transplacentally is greatly dependent on
cysts and their reconversion to
the immune response. Moreover, some
160 | P r o t o z o a
offspring which are born alive display Post-abortion sterility is not considered a
signs of disease, some others not. The problem.
immune response in cows infected with
Neospora caninum is associated with high
levels of IFN-γ, IgG-2 antibodies and Th1
cells. IFN-γ inhibits the growth of
tachyzoites. IFN-γ activates the response
of macrophages which play a major role
in the differentiation of tachyzoites to
bradyzoites and vice-versa (during
reactivation of infection).
The immunological maturity of the fetus

when it is infected determines probably
its survival chance. As most organs
involved in fetal immunity (thymus
spleen, lymph nodes) mature in the last
period of gestation, the risk of fetal death
and abortion is higher during the early Figure 2.75 Six months old bovine
gestation. The immunity can be aborted fetus caused by Neospora
protective as seropositive cows are less caninum. (Photo Ovidiu Șuteu)
likely to abort. Based on this, vaccination
has been developed.
Congenital neosporosis in calves (<2
Clinical signs. Most infections are months old) include variable clinical
asymptomatic. In cows, the characteristic signs: inability to rise, ataxia, flexed or
clinical sign is abortion (figure 2.75). hyperextended for or hind limbs,
The outcome of gestation resulting from decreased patellar reflex, loss of
infected cow can be: fetal resorption, fetal proprioception, exophthalmia and
mummification, fetal autolysis, stillbirth, decreased weight. Calves can be born
born alive with clinical signs, born with alive, but with severe congenital
no clinical signs but with persistent life- deformities (like hydrocephalus) which
long infection and born without infection. are incompatible with life. Other calves
About 80-90% of the infected cows are born with neonatal encephalomyelitis
produce apparently normal calves, part of and are paralyzed.
them infected.
The infection in dogs is usually
Abortion can be present in cows of any asymptomatic. It can affect dogs of all
age, from the age of gestation of three ages (post natal infection) but also
month to term. However, most abortions neonates (congenital neosporosis).
are reported to be between 4 and 6 Though, most cases are congenital.
months of gestation. Repeated abortion is Puppies born from infected mothers do
uncommon, and usually it is encountered not necessarily develop clinical signs. If
in less than 5% of the aborting cows.
161 | P r o t o z o a
they do, anyhow they are usually born cerebrospinal fluid. There are no
with no evident sign of infection. recorded clinical cases of canine
intestinal neosporosis caused by the
First clinical signs of congenital
enteroepithelial cycle.
neosporosis in puppies appear at 3-9
weeks of age. The most common Clinical signs caused by N. caninum in
symptom is paralysis of the hind legs, other domestic hosts are rare and they
often with spastic character include abortions in sheep, goats and
(arthrogryposis) and gradual muscle South American camelids. The infection
atrophy and stiffness. Usually the with N. hughesi in horses is responsible
paralysis is gradual and ascending. for a similar syndrome with the equine
Forelimbs may be also affected but less protozoal myeloencephalitis produced by
severely. S. neurona. Neospora hughesi is not
pathogenic for dogs.
Other clinical symptoms in puppies
include: joint deformations, cervical Pathology. Lesions caused by N. caninum
weakness, dysphagia (caused by are very important mainly from
megaesophagus). During all this time diagnostic point of view, as the presence
dogs are fully conscious and alert. They of histopathological changes can
can survive in this state for several represent a reliable cause-effect
months until finally death occur. Not all correlation. They are different in each
puppies from the same litter show host type.
clinical signs.
Lesions in aborted fetuses include
In dogs older than six month, clinical serosanguinolent fluid accumulation in
neosporosis can be caused by the the body cavities (figure 2.76).
primary infection or by reactivation of a Sometimes, the fetal tissues are in
chronic infection due to various factors incipient or moderate autolysis (figure
(see pathogenesis). 2.77). Other gross lesions are more
difficult to be detected (pale white foci in
The clinical signs are related to the
the muscles). Histopathology from fetal
multifocal nervous lesions or to
tissues reveals generalized non-
polymyositis. Other clinical signs
suppurative infiltrates. The brain is the
recorded in adult dogs are: coughing,
site of somehow more characteristic
progressive ataxia, dysphagia, cutaneous
lesions. They consist of scattered foci of
ulcers. Dogs with severe multifocal
non-suppurative cellular infiltrates,
central nervous involvement usually die.
sometimes necrotic. Neospora caninum
Clinical biochemistry findings in dogs developmental stages can be visible or
include increased levels of creatine not in these histological sections. Other
kinase and aspartate aminotransferase lesions in aborted bovine fetus include:
(due to severe myositis and hepatitis). epicarditis, myocarditis, myositis,
The cerebrospinal fluid has an increased hepatitis, all focal, with non-suppurative
level of proteins and pleocytosis. cellular infiltrates and even focal
Tachyzoites may be present in the necrosis.
162 | P r o t o z o a
include mainly non-suppurative

encephalomyelitis.
Gross lesions in dogs include: multifocal

areas of necrosis and/or fibrosis with or
without mineralization in the striated
muscles (mainly diaphragm), hepatitis
with hepatomegaly, pneumonia and
discoloration of certain areas of the
central nervous system (visible on gross
tissue sections). Histological sections in
puppies which died of congenital
neosporosis reveal the presence of
lesions and parasitic stages in the
Figure 2.76 Serosanguinolent fluid following organs: muscles, myocardium,
accumulation in the abdominal cavity of retina, nerve roots, thymus, kidney, liver,
an aborted bovine fetus caused by adrenal gland, brain, spinal cord, stomach
Neospora caninum. (Photo Ovidiu Șuteu) wall or dermis. The characteristic lesions
are non-suppurative myeloencephalitis,
myositis, polyradiculoneuritis (mainly in
puppies), lymphonoditis, myositis,
cerebral cortical necrosis etc.
Diagnosis. The most difficult task in

aborting cows is to correlate the
presence of Neospora caninum with the
abortion. Finding antibodies in a cow
which aborted or in the cow population
from a farm with endemic or epidemic
abortions is not enough. Moreover,
finding the parasite in the tissues of an
aborted fetus (by PCR or
immunohistochemistry) is not always
enough.
Figure 2.77 Autolysis of the central
nervous system of an aborted bovine The etiologic confirmation of abortions
fetus caused by Neospora caninum. (Photo must be done in specialized laboratories.
Ovidiu Șuteu) All of them have to be correlated with the
presence of Neospora caninum in
histological lesions from the fetus or from
Lesions in congenital neosporosis of the placenta and with other
calves are more or less similar with epidemiological data, including the age of
lesions from aborted fetuses. They fetus and the immune status of the cow.
The lesions in fetuses aborted because of
163 | P r o t o z o a
Neospora usually have disseminated

inflammatory lesions in most of their
internal organs (brain, heart, kidneys,
liver, lungs, muscles). Additionally, other
abortion causes must be excluded.
Various serologic tests are available for

the detection of anti-Neospora antibodies
(IFAT, ELISA, direct agglutination test,
Western blot). They are widely used for
seroepidemiologic surveys. However,
their use in clinical diagnosis has many
limitations. Most of them are not able to
discern between chronic and acute
infection. Moreover, the antibody titers in Figure 2.79 Cyst of N. caninum in the
seropositive cows are fluctuant. cardiac muscles (IHC) (Photo Ovidiu
Șuteu)
Some seropositive cows may become
seronegative (antibody titers below the
cut-off value). Serologic testing can be Immunohistochemistry (IHC) is a very
used also for fetal samples. Serologic useful tool for differentiating Neospora
testing in calves must be done after the tissue cysts from other protozoal cysts
age of 6 months, to eliminate the (figures 2.78 and 2.79). PCR is also
positivity due to maternally transferred highly sensitive and specific.
antibodies.
Serologic diagnosis using recombinant
proteins from tachyzoites (NcGRA7) and
bradyzoites (NcSAG4) allows
differentiating between chronic and acute
infections. If both proteins yield positive
results, this might be indicative of a
reactivated infection during pregnancy.
The same diagnostic principles as for the

abortion apply for diagnosis of congenital
neosporosis in calves.
Diagnosis in dogs relies greatly on the

correlation of symptoms, clinical
laboratory (blood and CSF) and results of
various serological assays (IF, ELISA,
immunoprecipitation). The definitive
diagnosis can be based on the
Figure 2.78 Cyst of N. caninum in the demonstration of the presence of
brain (IHC) (Photo Ovidiu Șuteu) Neospora caninum in the CSF. However,
164 | P r o t o z o a
this is a difficult task, as the number of 12 hours, for at least 4 weeks) with
tachyzoites is very low. In dead animals, pyrimethamine (1 mg/kg, orally,
the presence of the parasite can be made every 24 hours, for at least 4 weeks);
also in histological sections from brain,
 clindamycin (10 mg/kg, orally, every
heart or muscles.
8 hours, for 4 weeks) in adult dogs;
Differentiation from other cyst-forming
 clindamycin (75-150 mg/dog, orally,
coccidia is based on PCR or
every 12 hour, for 6 months) for 13
immunohistochemistry. Differential
months old puppies with congenital
diagnosis in dogs must be done from
neosporosis;
many diseases which produce similar
symptoms and lesions: infection with  sequential treatment with
Hepatozoon canis and Hepatozoon clindamycin hydrochloride,
americanum¸ leishmaniosis, trimethoprim-sulfadiazine and
sarcocystosis, clostridial myositis, pyrimethamine
leptospirosis, ehrlichiosis, trichinellosis,
Treatment of dogs does not always result
trypanosomosis etc.
in the complete recovery or in the full
Serological tests in horses and possibly elimination of the parasite. However,
also in other animals can be difficult to clinical signs may improve. Sometimes
interpret because of suspected cross- the treatment must be done for very long
reaction between antibodies against N. time (up to 18 months) until
caninum and N. hughesi. improvement is seen.
For the isolation of the Neospora caninum Control. It is essential mainly in farms. In
in the lab and for experimental trials, uninfected bovine herds, preventing the
laboratory animals such as mice, gerbils introduction of neosporosis is the main
and fat-tailed dunnarts are widely used. assignment. Newly introduced cows must
be purchased from Neospora-free farms
Treatment is not routinely done in
and they should be serologically tested
bovine neosporosis. Experimental
before.
administration of toltrazuril to calves can
delay the tachyzoite multiplication and Prevention of horizontal transmission is
spread. There is no data on the effect of achieved by restricting the access of
toltrazuril on bradyzoites. freely moving dogs in cattle farms. If they
are present, their direct access to the
The treatment of canine neosporosis
animals or their food must be avoided.
must be approached in all animals with
This is more difficult (or virtually
clinical signs and with a positive
impossible) if cattle are grazed on
diagnosis of neosporosis. Otherwise, the
pastures where dogs or wild canids have
condition is often fatal. The treatments of
access. Monitoring programs must be
choice in dogs are:
introduced (serological testing of cows,
 a combination of trimethoprim- laboratory examination of each aborted
sulfadiazine (15 mg/kg, orally, every fetus).
165 | P r o t o z o a
In infected herds the primary goals are to 2.4.3.4 Other heteroxenous coccidia
prevent abortions, to prevent spreading parasitic in domestic animals
the disease (both horizontally and
vertically), to avoid introduction of new Except the three major heteroxenous
infected animals and ultimately the coccidia presented before (Sarcocystis,
elimination of infection. Toxoplasma, Neospora), several other
genera have been identified in domestic
Permanent serologic monitoring of the
animals. Their importance is rather for
herd is recommended, and negative
the differential diagnosis than for their
animals must be selected for breeding on
clinical importance.
long term. Animals with high antibody
titers or history of repeated neosporal Genus Hammondia is represented by
abortions must be considered for culling. two species. Both are heteroxenous.
Embryo transfer from seropositive Hammondia hammondi has felids as
donors implanted to seronegative definitive hosts and goats and mice as
recipients produces non-infected natural intermediate hosts. Many others
offspring. mammal species serve as experimental
intermediate hosts. Cats are infected only
Proper disposal of fetal membranes
after eating tissue cysts and develop only
(placenta) and aborted fetuses must be
intestinal infection.
strictly followed.
Cats eliminate unsporulated oocysts,
A killed anti-Neospora caninum vaccine is
morphologically similar to those of
commercially available in United States.
Toxoplasma. Oocysts of Hammondia
The vaccine must be used twice in early
sporulate in the environment.
gestation, mainly in farms where the
Intermediate hosts are infected after
infection is present. Vaccination was
ingesting sporulated oocysts. Sporozoites
shown to reduce the rate of abortions.
invade the mesenteric lymph nodes and
The main disadvantage of the vaccine is
other abdominal organs where
the production of seropositive cows;
tachyzoites develop. Ultimately, they
post-vaccinal seropositivity is not
encyst as bradyzoites in the skeletal
differentiable from the post-infective
muscles. The second species, H. heydorni
seropositivity.
uses dogs as definitive hosts and various
To prevent infection of pet dogs, domestic and wild mammals as
administration of raw meat or organs, intermediate hosts. The life cycle is
mainly of bovine origin must be avoided. similar to H. hammondi. The reports of
In bitches known to be infected with the clinical signs associated with Hammondia
parasite, birth control programs infection are scarce. Mild diarrhea has
(including spaying) are to be considered been occasionally reported in dogs. In
for prevention of vertical transmission. intermediate hosts the symptoms are
There is no vaccine available against also normally absent. In experimentally
canine neosporosis. infected goats, fever has been reported.
166 | P r o t o z o a
Genus Besnoitia includes nine species signs include initial fever, anorexia,
parasitic in a great variety of hosts. The tachycardia and tachypnea,
life cycle is known, although not in great corresponding to the rapid multiplication
details, only for few species. It seems the of tachyzoites in various tissues and
life cycle is more similar to Toxoplasma internal organs. The next stage of the
gondii than to Hammondia, as disease consists in cutaneous signs: skin
extraintestinal development takes place congestions with increased sensitivity in
also in the definitive host. various body areas and anasarca
(generalized edema). In the next stage of
Four of the species have cats as definitive
the disease, the skin becomes
hosts. These species and the respective
sclerodermic, with complete loss of hair,
intermediate hosts for each are: B.
severe lichenification and
wallacei (rodents), B. darlingi (opossums,
hyperpigmentation. Sexual organs are
lizards), B. oryctofelisi (rabbits) and B.
also affected. In this chronic stage, the
neotomofelis (woodrats). After cats ingest
affected areas are full of tissue cysts,
tissue cysts from the connective tissues of
which are large enough to be seen at
intermediate hosts, the bradyzoites
gross necropsy. There is no treatment for
follow enteroepithelial merogony and
besnoitiosis.
gametogony, followed by extraction of
unsporulated oocysts. Part of the
bradyzoites will invade also
extraintestinal sites in the cat host, as 2.4.4 Hepatozoidae
Toxoplasma does.
Introduction. The family has a single
Dogs are not known to harbor any genus, Hepatozoon. The genus includes
species of Besnoitia as definitive hosts. around 300 species parasitic in all groups
The life cycles for the other 5 species of of tetrapod vertebrates.
the genus are not known only from few Ecology and transmission. The variety
studies on the asexual development in of life cycles is very high within genus
the intermediate hosts. Among these five Hepatozoon. The full development and
species, three are parasitic in domestic complete life cycle is not known only for
animals: Besnoitia besnoiti (bovines), B. few species. The life cycle is
bennetti (equids) and B. tarandi heteroxenous, at least for those species
(raindeers). where it is known, but probably for all.
The most important species of veterinary One of the hosts is always a vertebrate
importance is Besnoitia besnoiti, (amphibian, reptile, bird or mammal) and
responsible for the bovine besnoitiosis. the other is always an invertebrate. The
Its life cycle is not fully understood. merogonic and gametogonic
Bovines are intermediate hosts; the developments take place in various
definitive hosts are not known. Not all tissues of the vertebrate host. The
infections in cattle become clinically invertebrate is hosting the sporogonic
evident. If they do, the principal clinical development with the oocyst formation.
167 | P r o t o z o a
More details are given in the section of various leukocytes. The meronts of H.
canine hepatozoonosis. americanum are described as multi-
layered “onion skin” cysts, located
Medical importance. Most species are
between the muscular fibers, having 250–
parasitic in cold-blooded vertebrates
500 micrometer in diameter and
(amphibians and reptiles) where they
containing a central nucleus surrounded
usually cause asymptomatic infection.
by concentric rings of membranes.
The only two species of veterinary
importance are H. canis and H.
americanum.
2.4.4.1 Canine hepatozoonosis
Definition. Hepatozoonosis is a tick-

borne disease of dogs, occurring
worldwide with usually sub-clinical
infection. The data in this chapter is
mostly based on the excellent review of
Baneth (2011).
Etiology. Genus Hepatozoon contains

more than 300 species, parasitic in a
variety of vertebrate hosts. Two species
are responsible for canine
Figure 2.80 Gamont of Hepatozoon canis
hepatozoonosis: H. canis and H.
in a neutrophil of an infected dog. (Photo
americanum.
Barbora Mitková)
Morphology. The complexity of the life
cycle results in a great diversity of
developmental stages. However, two Life cycle. Hepatozoon canis has a
stages are practically important for the heteroxenous life cycle (figure 2.81).
diagnosis of the infection in dogs: the Dogs are the intermediate hosts and
gamonts within the neutrophils (figure certain tick species are the definitive
2.80) and the meronts within the tissues. hosts. Although hepatozoonosis is a tick-
Gamonts of H. canis are typically located borne disease, its transmission from ticks
within the cytoplasm of the circulating to dogs is not via the tick bite. Though,
neutrophils. They have an ellipsoidal the dogs have to ingest infected ticks to
shape and the average size is 4 x 11 µm. acquire the infection with H. canis (figure
The meronts of H. canis found in infected 2.81 - 1). After an infected tick or parts of
tissues contain elongated it are ingested by a dog, the sporozoites
micromerozoites arranged in a circle of H. canis leave the body of the tick,
around a clear central centre forming the penetrate the epithelial lining of the
typical “wheel spoke” aspect. The intestine and invade mononuclear cells
gamonts of H. americanum are located in (figure 2.81 - 2). They are transported by
168 | P r o t o z o a
the blood and lymph to the target tissues canis. The main difference consists in the
and organs: bone marrow, spleen, lymph target tissues, which in the case of H.
nodes, liver, kidneys and lungs. americanum are skeletal and cardiac
Immediately after they reach these muscles. The parasitic stages are
organs, the merogonic development transported to the muscle fibers by
starts, resulting in asexual multiplication macrophages. The merogonic stage
with the formation of merozoites within produces a meront, which finally
tissue meronts. Two types of meronts are becomes a cyst surrounded by
formed: type 1, containing up to four mucopolysaccharide layers. When the
larger merozoites (macromerozoites, cyst ruptures, the free merozoites invade
figure 2.81 - 3) and type 2, containing 20 the surrounding tissues. Merozoites enter
to 30 small merozoites (micromerozoites, into leukocytes where they may undergo
figure 2.81 - 4). It is believed that an additional merogonic multiplication.
macromerozoites are released and are Within the leukocytes, the last
responsible for the production of generations of merozoites become
secondary meronts in the same target gamonts. Ticks feeding on the blood of
tissues. Eventually, the micromerozoites infected dogs take the leukocytes infected
will invade monocytes and neutrophils with gamonts. In the body of the tick,
(figure 2.81 - 5) and become gamonts gamonts continue to develop into
(figure 2.81 - 6). The formation of gametocytes. Gametogony is followed by
gamonts corresponds to the beginning of sexual reproduction with the formation
the next stage of the life cycle, the of the zygote and sporogony with the
gametogony. formation of polysporocystic oocysts in
the tick’s hemocoel.
If blood of parasitemic dogs is ingested
by ticks (figure 2.81 - 7), the gamonts will Transmission of H. americanum to dogs is
be released in the tick’s intestine. If the similar to H. canis, via the ingestion of
tick is a suitable host for H. canis, male infected vector ticks.
and female gamonts will develop into
Several tick species have been shown to
male and female gametes and will
act as suitable definitive hosts for H.
associate (figure 2.81 - 8) for the
canis. The most widely distributed vector
formation of the zygote within the tick’s
is Rhipicephalus sanguineus, but other
gut. The zygote begins the last phase of
ticks species were also shown to transmit
the life cycle, the sporogony with the
the infection under experimental or
ultimate formation of the oocysts in the
natural conditions: Amblyomma ovale in
tick’s hemocoel (figure 2.81 - 9). Each
Brazil and Haemaphysalis longicornis and
oocyst contains hundreds of sporozoites
H. flava in Japan. The only know tick-
which are infective for dogs if ingested.
vector for H. americanum is Amblyomma
The overall duration of the life cycle of H.
maculatum. Transstadial transmission in
canis is almost 3 month.
ticks occurs in both Hepatozoon species.
The life cycle of H. americanum is more or However, there is no evidence for
less similar with the one described for H. transovarial transmission in ticks.
169 | P r o t o z o a
Figure 2.81 Life cycle of Hepatozoon canis. For the meaning of numbers, please refer to
the text.
170 | P r o t o z o a
Transplacental transmission has also in young animals influence the

been demonstrated for H. canis. Naturally pathogenesis of new H. canis infections or
infected pregnant bitches gave birth to favors the reactivation of preexisting
infected puppies. Although not proven, ones. The role of the immune system in
another suspected route of infection for the development of clinical infections has
dogs is via carnivorism by predation on been also demonstrated by the
other infected intermediate hosts. appearance of parasitemia in infected
dogs following immunosuppressive doses
Epidemiology. Natural (autochthonous)
of prednisolone.
infections with H. canis generally overlap
with the distribution of its main vector, In the infection with H. americanum, the
the tick R. sanguineus. Thus, canine main pathogenesis is caused by the
hepatozoonosis with H. canis occurs in merogonic development in the muscular
most tropical and subtropical (including tissues. The release of merozoites from
Mediterranean climate) regions, but the muscular cysts induces an intense
cases are known also from countries with local inflammatory response associated
warmer temperate climate. Nevertheless, with severe musculoskeletal pain.
imported cases have been reported in
Symptoms. Several studies suggest that
many other countries. Although the main
the severity of clinical signs in dogs
vertebrate host is probably the domestic
infected with H. canis is positively
dog, several other wild canids are
correlated with the level of parasitemia.
suspected to act as natural reservoirs.
The most common appearance of H.
The infection with H. canis has been
canis-hepatozoonosis is subclinical or
detected in red foxes (Vulpes vulpes),
mild diseases (moderate fever, lethargy,
crab-eating fox (Cerocyon thous), jackals
muscle pains). These cases are associated
(Canis aureus, C. mesomelas), African wild
with low levels of the parasitemia (1-5%
dogs (Lycaon pictus) and spotted hyenas
neutrophils infected with gamonts). The
(Crocuta crocuta).
severe cases can evolve with life-
Amblyomma maculatum is found along threatening symptoms (extreme lethargy,
the US Gulf Coast and Southern Atlantic, cachexia and anemia) and are usually
hence the distribution of H. americanum associated with high parasitemia levels
infection in dogs is limited to this area. (even 100% of the neutrophils infected
with gamonts). The hematology of these
Pathogenesis. There is an evident
cases reveals anemia, extreme
difference in pathogenicity between H.
neutrophilia (as high as 150,000
canis and H. americanum. The dogs
leukocytes/µl blood). Blood biochemistry
infected with H. canis are usually
findings include hyperproteinemia with
asymptomatic. Severe symptoms are
polyclonal hyperglobulinaemia and
more common in young dogs or are
hypoalbuminaemia, and elevated creatine
frequently associated with concurrent
kinase and alkaline phosphatase
infections. It seems that the immune
activities. Often, symptoms of
suppression induced by other infectious
hepatozoonosis are aggravated by other
agents or the immature immune system
171 | P r o t o z o a
overlapping vector-borne disease: examination of blood smears from dogs

ehrlichiosis (Ehrlichia canis), with clinical infection might reveal the
anaplasmosis (Anaplasma presence of gamonts. They are present in
phagocytophilum), leishmaniosis the cytoplasm of the infected neutrophils.
(Leishmania infantum) and babesiosis Histopathology from target tissues (liver,
(Babesia canis, B. vogeli). Concurrent lymph nodes, spleen etc.) reveals the
infections with parvovirus or Toxoplasma presents of typical meronts with the
gondii have also been reported. “wheel spoke” aspect.
The dogs infected with H. americanum In the case of H. americanum, the

usually show fever, abnormal gait (limb parasitemia is generally lower than in
stiffness, inability to rise), muscular pain dogs infected with H. canis. Therefore, the
and generalized muscular atrophy. Often, usual direct confirmation of the disease is
a mucopurulent ocular discharge is by showing the presence of parasites in
present, as a result of decreased tear muscle biopsies. Additionally,
production caused by with inflammation radiography of long bones showing
of the external ocular muscles. American periostitis is another indication for H.
canine hepatozoonosis evolves as an americanum-hepatozoonosis.
acute infection but can also become
Several serological methods (IFAT,
chronic. In either situation, the muscular
ELISA) are available for the diagnosis of
pain is present and this can be
canine hepatozoonosis. The most
generalized or localized, usually at the
sensitive method for the detection of
level of lumbar and cervical spine. The
Hepatozoon spp. in the blood of dogs is
chronic infections can be complicated by
PCR and quantitative evaluation is
immune-mediated glomerulonephritis
possible by real-time PCR.
and uveitis. Clinical hematology and
blood biochemistry are similar to those Treatment. The treatment of the dogs
described for the infection with H. canis. with clinical infection with H. canis is
done using imidocarb dipropionate, 5-6
Lesions. Following death subsequent to
mg/kg every 14 days until gamonts
severe hepatozoonosis, the meronts of H.
disappear from the blood smears.
canis can be found in various tissues:
However, the absence of gamonts from
liver, lungs, kidneys, spleen, bone
the blood smears is not equal to zero
marrow or lymph nodes. Associated
parasitemia. Studies using more sensitive
lesions include hepatitis, pneumonia and
detection methods (i.e. PCR), showed that
glomerulonephritis. In the case of H.
no treatment can completely eliminate
americanum, the most important lesion is
the infection. As dogs with low
the myositis.
parasitemia usually show no clinical
Diagnosis. Direct detection of H. canis signs, the prognosis of such cases is
gamonts in the neutrophils of infected generally good.
dogs is dependent on the level of
The treatment of dogs infected with H.
parasitemia. As symptomatic dogs
americanum must follow a combination
usually have significant parasitemia,
172 | P r o t o z o a
of oral therapy with trimethoprim- disease. The symptoms are not specific
sulfadiazine (15 mg/kg every 12 h), and highly diverse: weakness, lethargy,
pyrimethamine (0.25 mg/kg every 24 h) anorexia, weight loss, fever,
and clindamycin (10 mg/kg every 8 h) for hypersalivation, mucosal ulcers, enlarged
14 days. lymph nodes, anemia. The disease can be
successfully treated using doxycycline (5
In order to avoid clinical relapses, it is
mg/kg, orally, every 12 hours),
recommended that after relief of acute
oxytetracycline (50 mg/kg, every 12
forms, an anti-coccidial drug to be given
hours) until recovery signs or with a
orally for long term. The treatment
single dose of primaquine (2 mg/kg,
suggested is decoquinate at 15 mg/kg
orally).
mixed in food every 12 h for two years.
Supportive therapy might be considered
for pain relief.
2.4.5 Babesiidae
Control. Although canine hepatozoonosis
is a vector-borne disease, its unusual Introduction. Includes several genera
transmission route makes its prevention parasitic mostly in warm-blooded
different than for the other arthropod- vertebrates.
transmitted disease. It is recommended
to avoid the oral ingestion of ticks by Ecology and transmission. All the
dogs, both from the environment and members of the family undergo the
while grooming. Hence, the use of topical merogonic development only in
and environmental acaricides is erythrocytes with no preliminary
encouraged. No vaccine is currently development in white leukocytes or other
available. types of cells. The transmission of the
species for which the life cycle is known
is by the bite of ticks.
2.4.4.2 Feline hepatozoonosis Medical importance. Species of genus

Babesia are very important veterinary
Feline hepatozoonosis is by far less parasites, causing severe clinical
common than the canine infection. It has diseases, mortality and economic losses.
been reported from several countries in Some species are zoonotic, but clinical
Asia, Africa, North America and Europe. signs in humans are present with few
The species of Hepatozoon responsible exceptions only in splenectomized
for the feline infection are not well people.
defined, nor its life cycle known. The
The diseases caused by Babesiidae and
development of Hepatozoon meronts in
Theileriidae are generically known as
cats takes place in the skeletal muscles
piroplasmosis. As the life cycle and
and the myocardium causing elevated
pathogenesis is different, more accurate
levels of creatine kinase.
designation babesiosis and theileriosis or
Decreased immunity caused by FIV and their plural forms (babesioses,
FeLV favor the development of clinical theilerioses) will be used herein.
173 | P r o t o z o a
2.4.5.1 Babesioses Table 2.41 Named species of Babesia

parasitic in domestic animals (modified and
updated after Schnittger et al. 2012)
Introduction. Babesioses are tick-borne
diseases found in all species of domestic Host Species Distribution
B. bovis Worldwide
mammals and in many wild mammals, B. bigemina Worldwide
with great economic impact but also B. divergens Europe
Cattle
medical and veterinary importance. The B. major Asia, Europe
B. occultans Africa
disease is clinically severe in non- B. ovata Asia
immune hosts, causing anemia, fever, B. bovis America, Asia
Buffalo B. bigemina America, Asia
jaundice, hemoglobinuria and sometimes B. orientalis Asia
death. Horse,
B. caballi
Africa, America,
donkey Asia, Europe
Historical notes. Two distinct Pig B. trautmanni Africa, Europe
Sheep, Asia
geographical areas (Eastern Europe and goat
B. crassa
North America) are particularly B. motasi
Africa, Asia,
Europe
important from historical point of view. Africa, Asia,
B. ovis
At the end of the 19th century (1888), Europe
Dog B. canis Europe
Victor Babeş, a Romanian microbiologist,
B. conradae North America
discovered the agent of the disease in Asia, Africa,
B. gibsoni
cattle. One year later, Theobald Smith, a America, Europe
B. rossi Africa
medical doctor from New York, described B. vogeli Worldwide
the agent of Texas fever in USA and was Cat B. felis Africa
B. presentii Asia
the first to elucidate the tick-borne
nature. It was the first time ever when
arthropods were shown to transmit a Certain species of Babesia have been
disease. Babeș originally named the recorded in several mammal species,
species Hematococcus bovis. Smith and raising the question if they are really host
Killborne named the Texas fever agent specific. For instance, Babesia caballi is
Pyrosoma bigeminum. In 1893, Starcovici commonly found in dogs and Babesia
erects genus Babesia and includes both canis is also present in cats. Molecular
species there. In the years to follow, many surveys have shown also other such
new species have been described from cross-infections, but their clinical and
various domestic and wildlife hosts. epidemiological importance is not yet
fully understood.
Etiology. The taxonomy and species
status of genus Babesia is highly dynamic. Morphology. Among the various
As most species descriptions were based developmental forms of Babesia in the
mostly on morphology of the erythrocytic definitive (ticks) and intermediate
stages and host specificity, the validity of (vertebrate) hosts, the most important
some still needs molecular confirmation. stages from morphologic (diagnostic)
The list of valid Babesia species parasitic point of view are those found in the
in domestic animals is shown in table erythrocytes of the domestic mammals.
2.41. The most common intraerythrocytic
174 | P r o t o z o a
stages are the merozoites. They are

usually found in pairs, forming a typical
“V” shape (figure 2.82). In some of the
species of Babesia, multiple divisions
result in the formation of groups of 4 or 8
intraerythrocytic merozoites.
Based on the size of the intraerythrocytic

stages, the species of Babesia are divided
in two types: small Babesia (1.0-2.5 µm)
and large Babesia (2.5-5.0 µm).
Merozoites of small species usually form
obtuse angles, while the larger ones form
acute angles to each other. Sometimes,
atypical forms (amoeboid, ring-shapes, Figure 2.83 Ring-shaped aspect of
round) can be found in the erythrocytes Babesia canis in an erythrocyte from
(figure 2.83). infected dog. (Photo Andrei D. Mihalca)
In other species of Babesia, 4 or 10

merozoites can be seen inside a single
erythrocyte. Detection of free stages in
the plasma is possible but very rare Life cycle. The life cycle of all species is
event. heteroxenous (figure 2.84). As the sexual
development takes place in ticks, they are
considered definitive hosts. Mammals are
intermediate hosts as they are harboring
the asexual stages.
Mammals acquire the infection after a

bite of an infected tick. Through the
saliva, ticks inject into the blood stream
of the vertebrate the infective sporozoites
(figure 2.84 - 1).
They attach to erythrocytes (figure 2.84 -

2) and by endocytosis they enter inside
them (figure 2.84 - 3). Inside the red
blood cells, sporozoites start to feed,
becoming trophozoites (figure 2.84 - 4)
which subsequently divide by binary
Figure 2.82 “V”-shaped disposition of
fission resulting in the formation of two
merozoites of Babesia canis in an
merozoites in each erythrocyte (figure
erythrocyte from infected dog. (Photo
2.84 - 5).
Andrei D. Mihalca)
175 | P r o t o z o a
Figure 2.84 Life cycle of Babesia spp. For the meaning of numbers and letters, please refer
to the text.
176 | P r o t o z o a
Sometimes, one additional cell division present some brief insights into the tick
results in the formation of four biology and mechanism of vectorial
merozoites in each erythrocyte (figure transmission. Ticks have three feeding
2.84 - 6). Merozoites rupture the infected developmental stages: larvae, nymphs
erythrocytes (figure 2.84 - 7) and invade and adults (male and females). Most ticks
new ones (figure 2.84 - 8), repeating the follow a so-called three host life cycle,
merogony several times until many red meaning that each stage feeds on a
blood cells are destroyed. During the different host. After larvae hatch from the
course of infection, some merozoites are eggs, they attach to a host, feed with
transformed into gamonts while still in blood and detach. After detachment,
the erythrocytes of the intermediate larvae fall-off in the environment where
hosts. When a new tick (figure 2.84 - 9, they undergo the first molting and
10, 11) feeds on the infected blood of the become nymphs. Nymphs search for a
intermediate host, the erythrocytes with new host, they attach to it and feed again.
gamonts reach its intestine. They will After fully engorged they detach, fall into
invade the epithelial cells (figure 2.84 - the environment and molt for the second
12) and start the gametogony process. It time, becoming adults. Part of the
seems that the other stages (i.e. nymphs become males, the others
merozoites, sporozoites, trophozoites) become females. Adult ticks attach to the
ingested by the vector are not able to third host, the feed and reproduce
produce the intestinal infection in the sexually. Fully engorged and fertilized
tick. After gamonts sexually join, the females fall-off the host. After some time
zygote is formed. Each zygote spent in the environment, they lay
differentiates into a mobile oocyst-like thousands of eggs and die. Males usually
structure called kinete (figure 2.84 - 13). do not feed, and they are attached to the
Through the hemolymph, the kinetes will host only for finding the females.
invade all the tick’s tissue, including Considering all these events, it is evident
ovaries (figure 2.84 - 15) and salivary that each stage of the tick feeds only once
glands (figure 2.84 - 14). When reaching and only on one host. The next time it will
the salivary glands, the kinetes start the feed it will be already as another
sporogony with the formation of developmental stage. If a larvae (figure
sporozoites. Kinetes from the ovaries will 2.84 - L) feeds on a host infected with
be responsible for the transovarial Babesia, it will acquire the infection
transmission to the eggs produced by the (figure 2.84 - 9). The next time it will
female tick and eventually part of the feed, it will be as a nymph, on another
next generation larvae will be already host. Hence, the maintenance of the
infected when hatch. The sporozoites infection from a stage to another (figure
from the salivary gland will infect a new 2.84 - 9’) is a sine qua non prerequisite
host when the tick feeds again. for the existence and transmission for
any tick-borne disease. This essential
In order to understand the ecological
event is known as transstadial passage
rationale behind the transmission of
(or less accurately, transstadial
pathogens by ticks, it is essential to
177 | P r o t o z o a
transmission). The same situation it to nymphs and then to adults. So the

happens if a nymph (figure 2.84 - N) next adult generation will be ultimately
feeds on an infected host (figure 2.84 - responsible for infecting a new dog. This
10). It will pass the infection to adults means sometimes even years.
(figure 2.84 - 10’) which will eventually
An interesting mechanism of
infect a new host. In the case the stage
transmission for those species vectored
which is infected is an adult female
by one-host ticks (i.e. all stages feed on
(figure 2.84 - F) (figure 2.84 - 11), for the
the same host individual) is by males
infection to be ecologically continuous,
which move from an animal to the other.
the female must be able to pass the
acquired pathogen to the offspring One more essential factor in the
(figure 2.84 - 11’). This is possible in transmission mechanism of tick-borne
certain tick-borne pathogens (but not in disease is the infectivity of the tick saliva
all) because of the presence of anatomical in the first hours or days after
structures which connect the digestive attachment. It was said before that
tube of the tick with the ovaries. This Babesia moves from the intestine of the
feature is known as transovarial tick to the salivary glands where
transmission. Not all species of Babesia sporozoites will be formed. This in-tick
are able to pass by this transovarial migration takes place for most of the tick-
route. It seems that B. felis from cats or B. borne pathogens only after the ticks
microti from rodents are such species. attaches to a host which is suitable for the
pathogen’s development. Factors from
Given the relatively strict host specificity
the vertebrate’s blood will activate the
of Babesia, one more extremely
migration of the pathogens to the salivary
important barrier is not only the
gland and eventually its transmission to
alternation of ecological hosts but also
the host. This key aspect is essential from
the host species. Not all the three hosts
practical point of view. If a tick dies
from a complete life cycle of a tick are
because of an antiparasitic treatment or it
belonging to the same species. For
is mechanically removed from the host
instance in the case of Dermacentor
before the salivary migration occurred,
reticulatus the larvae and nymphs feed
the risk for pathogen transmission is
usually on micromammals and only adult
limited.
ticks use dogs. It is known that D.
reticulatus is the vector of Babesia canis. The vectors for Babesia species of
If Babesia canis infects only dogs, it is domestic animals are always hard-ticks
evident that the only stages which (Ixodidae). Not all tick species transmit
acquire the infection from dogs are all Babesia species. The spectrum of
adults. It logically means that infected vectors for each Babesia species is shown
adults females pass the infection to the in table 2.42.
eggs. Infected larvae which hatch will A possible but rather unusual route of
feed on small mammals, possibly not transmission for Babesia is the vertical
infecting them. However, the larvae transmission in vertebrates, from an
maintain the infection in their body, pass
178 | P r o t o z o a
infected mother to the fetus. shown in table 2.41. Certain species are
Transplacental transmission has been distributed worldwide (of course except
reported in humans, cattle, horses and the polar regions), some others are more
dogs. Transmission through infected or less limited. As domestic animals are
needles or blood transfusion is also everywhere where people are present,
possible. the spatial distribution of Babesia is
largely influenced by the degree of
specificity to the tick-host and the
Table 2.42 Tick vectors for selected Babesia distribution of those ticks.
species of domestic animals
As with most other vector-borne
Babesia Tick vector
species parasites, the occurrence of Babesia is
Rhipicephalus microplus, R. influenced by the ecology of the vectors.
annulatus, R. decoloratus, R.
B. bigemina
geigyi, R. evertsi, Transmission to the vertebrate host is
Haemaphysalis punctata seasonal and correlated with the ticks’
Rhipicephalus microplus, R.
B. bovis
annulatus, R. geigyi dynamics. The outbreaks of acute
Rhipicephalus evertsi, R. bursa, babesiosis typically take place during the
R. sanguineus, Dermacentor
albipictus, D. variabilis, D.
warm seasons.
nitens, D. marginatus, D.
B. caballi
reticulatus, D. silvarum, The newly introduced animals are more
Hyalomma anatolicum, H. susceptible to acute infection. Long-term
dromedary, H. marginatum, H.
scupense, H. truncatum parasite-host associations result in
B. canis
Dermacentor reticulatus, acquired resistance, but with the
Rhipicephalus sanguineus (?)
B. conradae Rhipicephalus sanguineus (?)
presence of parasites in the blood of
B. crassa Unknown clinically healthy animals. This results in
B. divergens Ixodes ricinus, I. persulcatus
a permanent infection source for ticks
B. felis Unknown
B. gibsoni Haemaphysalis longicornis and through them to Babesia-free
Haemaphysalis punctata, H. individuals. The local breeds are more
B. major
longicornis
Haemaphysalis punctata, resistant than imported breeds. Bos
Rhipicephalus bursa, H. indicus breeds are more unlikely to
B. motasi
qinghaiensis (?), Amblyomma
variegatum (?) develop clinical babesiosis.
Hyalomma marginatum, H.
B. occultans rufipes, H. anatolicum, H. The concept of endemic stability is very
truncatum important in the epidemiology of
Rhipicephalus
B. orientalis babesiosis, mainly in large animal
haemaphysaloides
B. ovata Haemaphysalis longicornis communities as livestock (cattle, small
Rhipicephalus bursa, R.
B. ovis
sanguineus (?), R. turanicus (?) ruminants). The endemic stability means
B. presentii Unknown that the pathogen is present in the host
B. rossi Haemaphysalis elliptica
B. trautmanni Rhipicephalus turanicus
population but the clinical disease occurs
B. vogeli Rhipicephalus sanguineus rarely.
Although the disease can be transmitted

Epidemiology. The geographical by a single infected tick, the prevalence of
distribution of various Babesia species is
179 | P r o t o z o a
infection in the tick population is usually Other mechanisms are also involved in
very low. the destruction of infected erythrocytes.
They become osmotically fragile.
The susceptibility to develop clinical
Moreover, during penetration by
babesiosis is higher in adult animals than
sporozoites or merozoites, direct injury
in young ones. This rather unusual
of the cellular membrane can result in
situation is possibly related to immune
mechanical destruction.
factors, most probably to the acquired
transplacental or colostral passive The altered erythrocyte metabolisms and
immunity. membranary processes slow down their
circulation speed in capillaries and favors
Babesia, as most vector-borne parasites
sludging. The most intense erythrocyte
spends all their life inside a host. No
sludging occurs in the central nervous
exogenous stages exist. Therefore, we
system and in the lungs.
cannot discuss about the environmental
resistance of Babesia. Babesia can survive The excessive production of cytokines
in ticks for several years, until the life and other pharmacologically active
cycle of that individual tick ends. compounds cause vasodilatation,
hypotension, increased capillary
Pathogenesis and immunology. Most of
permeability and endothelial damage.
the pathogenesis of babesiosis is related
These are ultimately responsible for the
to the altered immune response of the
disseminated intravascular coagulation,
hosts. This is the reason why the sections
which is usually lethal. The increased
are discussed together.
capillary permeability together with the
The most important pathogenetic resulting edema are responsible for the
mechanism is related to the destruction severe respiratory distress in certain
of erythrocytes. Two mechanisms are species.
involved in this process: immune-
The erythrocyte depletion causes tissular
mediated erythrolysis and non-immune
hypoxia and subsequent failure of various
erythrolysis.
internal organs, including kidneys. As a
After the erythrocytes are infected they result of hypoxia, there is an over
display on their outer surface modified production of lactic acid, resulting in
antigenic structures. Therefore, they metabolic acidosis. Hyperventilation, as a
target the synthesis of opsonizing result of anemia is also considered to be a
antibodies and as a consequence, the compensatory attempt to fight acidosis.
infected erythrocytes are destroyed by Overall, certain species of Babesia are
the mononuclear-phagocyte system. Even responsible for the systemic
uninfected erythrocytes can be the target inflammatory response syndrome which
of autoimmunity, as soluble parasitic results in multiple organ failure: acute
antigens adhere to their surface. renal failure (typically in dogs),
hepatopathy or pulmonary edema.
180 | P r o t o z o a
Massive destruction of erythrocytes is monocytes, macrophages and

followed by hemoglobinuria and neutrophils.
jaundice. However, these seem to be the
The role of the specific immunity is
feature of moderately pathogenic species.
related to the production of antibodies.
Interestingly, the level of parasitemia is They will mediate the cytotoxic killing of
not correlated with the severity of clinical parasites during re-infections.
signs. In cattle infected with B. bovis and
Clinical signs. Most infections are at a
with severe acute signs, the parasitemia
very low level and they are clinically
is normally less than 1%, while
asymptomatic. Clinical signs usually
subclinical or moderate cases with B.
occur in individuals which have never
bigemina are associated with 10-30%
been in contact with the pathogen (see
infected erythrocytes. This could be
immunology). The clinical infection has
explained also by the higher rate of
been documented in most domestic
erythrocytic destruction in the case of
species, in humans as well as in wildlife.
more pathogenic species, resulting in
Because of the associated mortality,
false “low” intensity, as most of the
babesioses of livestock are economically
infected erythrocytes could have been
important. Although the clinical course
already destroyed.
and symptoms vary in each host species
The low infective doses in immune and also between Babesia species, there
animals are responsible for life-long is a general picture which can be
resistance. This non-sterile immunity, considered.
also known as premunition is the most
In all species, the infection with Babesia
prominent immunologic feature in
can be acute, sub-acute or chronic.
persistent, subclinical Babesia infection.
Both components of the immune system Common features of acute babesiosis
are important in the anti-Babesia include fever, anemia, jaundice and
resistance. The innate immunity is the hemoglobinuria. The general status of the
first line defining the host specificity of animals with acute signs can be severely
Babesia species. Experimental altered, with malaise, lethargy,
splenectomy allows the infection of tachypnea, muscle tremors, anorexia and
otherwise resistant host species. The weight loss. An alternation of diarrhea
involvement of innate immunity has been with constipation can be present. The
suspected to be responsible for the duration of the acute form is usually
resistance of young animals to infection. around one week.
One key circumstantial proof for such a Sub-acute and chronic babesioses are
hypothesis is the resistance to infection similar but less severe that acute forms.
of calves born from non-immune Hyperacute forms are reported, but
mothers. However, the colostrally passed rarely. They usually consist in sudden
antibodies also play a role. The most death, within few hours from the onset of
important components of the innate symptoms.
immunity active against Babesia are
181 | P r o t o z o a
As there are certain specific features for associated with a great diversity of
various Babesia species-host species clinical signs: anorexia, lethargy, fever,
associations, the most common of them weakness, weight loss, hemolytic anemia,
will be discussed. icterus, splenomegaly, lymphadenopathy,
vomiting, ascites, diarrhea, buccal ulcers,
In bovines the most pathogenic species is
seizures, ataxia, paresis etc.
B. bovis. Other species (B. bigemina, B.
divergens) are moderately pathogenic In cats the published reports are few. The
while others (B. occultans, B. major) are main sign of the infection with B. felis is
most often non-pathogenic. Babesiosis fever associated with depression, loss of
produced by B. bovis (incubation period appetite, weight loss, weakness,
10-12 days) is characterized by high tachycardia, tachypnea, vomiting, and
fever, ataxia, incoordination, anorexia, diarrhea. Jaundice is uncommon.
hemoglobinuria, nervous signs,
Pathology. Gross pathology of babesiosis
circulatory shock and death. The
is as diverse as the clinical picture is, both
infections with B. divergens or B.
reflecting its complex pathophysiology.
bigemina (incubation period 4-5 days)
produce fever, hemoglobinuria and In cattle infected with B. bovis, the acute
anemia, but nervous signs are absent. lesions include: generalized congestion of
abdominal organs (soft and pulpy spleen,
In sheep and goats, the most pathogenic
hepatomegaly, congested kidneys),
species are B. motasi and B. ovis. It is
generalized anemia and jaundice,
responsible for fever, anorexia,
presence of dark-red urine in the urinary
listlessness, anemia, jaundice.
bladder, distended gall-bladder with
Hemoglobinuria is not constant.
thick and granular content or pulmonary
Acute cases caused by B. caballi in horses edema.
(incubation period 10-30 days) are
The lesions in dogs which died of acute
associated with high fever, dyspnea,
babesiosis (usually caused by small
mucosal congestion, edemas, and anemia.
Babesia) consist of staining of tissues
The icterus and hemoglobinuria may be
with hemoglobin, hepatomegaly,
present, but are less severe that in the
splenomegaly, lymphadenopathy,
infection with Theileria equi.
nephrosis, signs of disseminated
The clinical course in dogs is often very intravascular coagulation. Histologic
severe, but symptoms greatly vary. They findings are consistent with the
depend on various factors, one of them pathophysiology: capillary congestion,
being the species. Certain Babesia species thrombosis in various organs, erythroid
(i.e. B. vogeli, B. gibsoni) have lower hyperplasia in the bone marrow and
pathogenicity and they typically produce vasculitis.
mild or subclinical infection. Others (B.
The lesions in other host species are
canis, B. rossi, B. conradae) are
similar with those described in cattle and
responsible for acute forms, with more
dogs.
severe outcome. The acute form in dogs is
182 | P r o t o z o a
Diagnosis. The clinical signs and lesions Real Time PCR or Loop Mediated
in babesiosis are characteristic but not Isothermal Amplification (LAMP).
pathognomonic. Hence, the diagnosis
Treatment. The efficacy of various drugs
must always be confirmed in the
is different against the various species of
laboratory. The most reliable methods
Babesia. Usually, small Babesia species
are the microscopic detection methods
are more resistant than large Babesia
when the stages of the parasite are seen
species. Two drugs are currently widely
directly by the observer.
used for the treatment of babesiosis in
Detection of the parasite is possible in animals: imidocarb and diminazene
blood smears, when the characteristic aceturate. Treatment does not always
parasitic forms are seen inside the eliminate the infection but it can
erythrocytes. From dead animals, other significantly reduce the clinical impact. In
cytological examination can be severe cases, supportive therapy is
performed if blood is not available required. It is forbidden to use the
anymore (i.e. brain smears, blood from treatment together with anti-Babesia
internal organs). Although the method is vaccination, as the drugs kill the vaccinal
highly specific, its sensitivity is reduced, strain and interfere with a proper
as usually during the chronic phase the installation of immunity.
parasitemia is relatively low, under the
In cattle, diminazene aceturate is
detection threshold. Another
effective at 3.5 mg/kg, intramuscularly, 1-
disadvantage is the relatively long time
2 administrations. The injection protects
necessary for the thorough examination
the cows against reinfection with B. bovis
of a blood smear. Specific identification is
and B. bigemina for 2-4 weeks. Imidocarb
not always possible, mainly in hosts
at 1.2 mg/kg, single dose, given
where more Babesia species are known.
subcutaneously is also effective. Higher
Various immunological methods are doses (3 mg/kg) have even protective
available for the detection of anti-Babesia effect for 1-2 months.
antibodies in the sera of infected animals:
In dogs infected with large piroplasms
the Indirect Fluorescent Antibody Test
(i.e. Babesia canis), the treatment of
(IFAT), ELISA, Immunochromatography
choice is imidocarb (5-6 mg/kg,
Test (ICT). The disadvantage of
intramuscularly, single dose and then
serological methods consist in failure to
repeated in two to three weeks).
detect acute infection (the antibodies are
Imidocarb is not effective against the
not yet produced) and difficulty in
infection with small Babesia (i.e. B.
interpreting the seropositivity (post-
gibsoni).
vaccinal versus post-infective).
Diminazene aceturate has been used in
The most sensitive and specific methods
the past for the treatment of B. gibsoni
are those targeting the parasite’s DNA.
infection, but currently, the most effective
The most widely used is the PCR, but also
treatment is considered to be the
Reverse Line Blot Hybridization (RLB),
183 | P r o t o z o a
combination between atovaquone and 2.4.6 Theileriidae

azithromycin.
Introduction. All Theileriidae are tick-
In cats infected with small Babesia the
borne intracellular parasites of wild and
only effective treatment is with
domestic animals with significant
primaquine phosphate (0.5-1.0 mg/kg
economic importance. Two genera are
intramuscularly, orally or intravenously,
particularly important in domestic
single dose or daily for 3 consecutive
animals: Theileria and Cytauxzoon.
days). Diminazene aceturate (3.5 mg/kg,
intramuscularly, single dose) is effective Morphology. The morphological
against large Babesia of cats. There are no appearance of Theileria is more
reliable clinical studies to show the heterogeneous than Babesia. Intracellular
efficacy of imidocarb in cats. stages in the mammalian host includes
round, ovoid, rod-like or irregular forms.
Diminazene aceturate is recommended
also for sheep, goats, swine and equines. Ecology and transmission. The biology
The dose is between 3.5-5 mg/kg, of Theileriidae is comparable to
intramuscularly, twice at 24 hours Babesiidae, but with two main
interval. differences. In the vertebrate host,
species of Theileria undergo the first
Control. There are several approaches in
multiplication in white blood cells and
preventing and controlling babesiosis in
only later in the course of infection they
domestic animals. One of the most
are able to infect the erythrocytes. In the
successful approaches is the control of
tick host, there is no transovarial
vectors. Long-term strategic programs to
transmission.
reduce the tick parasitism in livestock
result in great improvements. Medical importance. Theilerioses are
important diseases of cattle, sheep, goats
This can be achieved by the use of
and horses in regions with tropical
acaricide drugs. They are expensive and
climate, mainly in Africa but also in
very toxic to the environment so their
warmer regions of Asia and Europe. They
large scale use is often limited. Selecting
are not zoonotic. Recently, the infection
resistant breeds is another option. Bos
with Theileriidae gained importance also
indicus breeds are more resistant than
in dogs and cats.
Bos taurus breeds. The areas with
endemic babesiosis foci should be
populated with breeds known to have
natural resistance. 2.4.6.1 Theilerioses
The most modern approach for Introduction. Species of genus Theileria

controlling babesiosis is the use of are responsible for several nominal
immunoprophylaxis. Commercial diseases mainly in cattle, small
vaccines are available for bovines and ruminants, horses and dogs from tropical
dogs. countries (table 2.43).
184 | P r o t o z o a
Historical notes. The first to observe Etiology. The species of Theileria

Theileria parasites in the blood of cattle parasitic in domestic animals are shown
was Robert Koch. In 1897, he found rod- in table 2.44. Certain species of Theileria
like parasites inside the red blood cells of have been divided into subspecies, but
cows from the current Tanzania. He their taxonomic status is still debated.
considered them to be morphs of Babesia Moreover, these subspecies are
bigemina. In 1901, when Australian cows serologically and morphologically
were introduced to Zimbabwe, many died indistinguishable.
of babesiosis. The surviving cows were
The main difference between them is in
moved to another location. Three weeks
the epidemiological features and
later they died of another, more acute
geographical distribution. However, as
and unknown diseases. Again, Koch
they are commonly used in various
realized it is a different disease than
textbooks, they will be briefly mentioned
babesiosis, Theiler described in 1904 the
herein. Theileria parva has been divided
new agent as Piroplasma parvum. In the
into three subspecies: T. parva parva (the
same year, Dschunkowsky and Luhs
typical agent of East Coast Fever), T.
described the second species, Piroplasma
parva lawrencei (causing the Corridor
annulatum in Transcaucasia. Genus
disease) and T. parva bovis (only mildly
Theileria was erected in 1907 by
pathogenic).
Bettencourt, Franca & Borges.
Table 2.43 Species of Theileria and Cytauxzoon parasitic in domestic animals
Host Species Vector genus Disease Distribution

Mediterranean Coast Europe, Africa, Asia
T. annulata Hyalomma
Fever
T. buffeli Haemaphysalis Benign theileriosis Worldwide
T. mutans Amblyomma Benign theileriosis Africa
East Coast Fever, Africa
T. parva Rhipicephalus
Cattle Corridor Disease
Oriental theileriosis Asia, Europe, Australia,
T. sergenti Haemaphysalis
Africa
T. sinensis Haemaphysalis Benign theileriosis Asia
T. taurotragi Rhipicephalus Benign theileriosis Africa
T. velifera Amblyomma Benign theileriosis Africa
T. lestoquardi (syn. T. Ovine and caprine Europe, Asia, Africa
Hyalomma
hirci) theileriosis
T. luwenshuni Haemaphysalis Ovine theileriosis Asia
Sheep,
Rhipicephalus Benign theileriosis Africa, Europe
Goats T. ovis
Hyalomma
T. separata Rhipicephalus Benign theileriosis Africa
T. uilenbergi Haemaphysalis Ovine theileriosis Asia
Dermacentor, Equine theileriosis Worldwide
Horses T. equi Hyalomma,
Rhipicephalus
Dogs T. annae Ixodes Canine theileriosis Europe, America
Dermacentor, Cytauxzoonosis America
Cats C. felis
Amblyomma
185 | P r o t o z o a
Morphology. From diagnostic point of macromerozoites (2-2.5 µm) and

view, the stages in the mammalian host microschizonts with 80-90
are important. In the white blood cells, micromerozoites (0.7-1 µm). After the
the schizonts of T. parva appear as merozoites rupture the lymphocytes,
circular or irregularly shaped structures, they can follow two ways. They can either
also known as Koch’s blue bodies. They infect other lymphocytes and maintain
measure between 2 and 12 µm (average 8 the lymphocytic infection or penetrate
µm). The macroschizonts have around 8 into erythrocytes, where they usually
nuclei and the microschizonts have 50- remain until engorgement by vector ticks.
120 nuclei. In the tick’s gut, they undergo
gametogony and sexual reproduction,
In the red blood cells, the merozoites are
resulting in the formation of the zygote
usually single (there is no
which ultimately becomes motile and
intraerythrocytic division), they have
bears the name of kinete. They remain in
rod-shape and measure 1.5 x 0.5-1.0 µm.
this stage in the intestinal cells of the
Sometimes, other forms can be seen in
ticks until they molt. After the
the erythrocytes: round, oval, ring etc.
subsequent stages (nymphs or adults)
The morphology of other species is more
start to feed on the next host, kinetes
or less similar. The main differences
invade the salivary glands of the ticks and
consist in morphometric values.
produce thousands of sporozoites.
Life cycle. As a model of life cycle for Sporozoites from the salivary gland will
Theileria, the development of T. parva infect a new host. There is no transovarial
will be described in the following transmission in Theileria.
paragraphs. In other species, there are
The life cycle in genus Cytauxzoon is
small differences in the intensity and
similar to genus Theileria.
ration of multiplication in erythrocytes
and lymphocytes. For instance, if in T. Transplacental transmission from
parva there is no intraerythrocytic infected mother to offspring is suspected
division, in T. mutans, the predominant for certain species, including T. annae in
multiplication takes place in the red dogs.
blood cells.
Epidemiology. The spread and
Transmission of the infection to the distribution of the vector is responsible
mammalian host is by the bite of nymph for the distribution of the diseases.
and adult ticks. As the infection is not Although some species of Theileria have a
transmitted by vertical (transovarial) more broad distribution, with different
route, larvae are not infective. After the vectors in each area they occur, they are
sporozoites are injected into the blood causing endemic diseases only on few
stream, they infect the lymphocytes regions. For instance, T. parva causing the
where they start the merogonic East Coast Fever is distributed in South,
development producing merozoites. Two East and Central Africa. The group of T.
types of schizonts (meronts) are known: parva causing the corridor disease is
macroschizonts, containing around 90 endemic to East and Central Africa, as the
186 | P r o t o z o a
main reservoir is the African buffalo. changes in the structure of the

Theileria annulata is responsible for the membranary proteins of the erythrocyte.
Mediterranean Coast Fever and its
Like in the case of babesiosis, the severity
distribution ranges from Northern Africa
of disease is not correlated with the
(Morocco) to Middle East and Southern
intensity of parasitemia.
Russia.
Immunology. The primo-infection is
The host specificity of Theileria is an
always severe. If animals survive they are
important epidemiological feature. As for
usually resistant to clinical infection. The
instance species parasitic in cattle infect
infection with one species does not
also buffaloes or various wild ruminants,
confer cross immunity against the
the diversity of reservoir hosts creates
infection with another species.
permanent risks of outbreaks. Often, the
pathogenicity in wild ruminants is almost The main immunological mechanism
absent, but when the infection occurs in involves cellular immunity. In the
domestic cattle it has devastating impact. infection with T. parva, the bovine major
histocompatibility complex is mediating
The mortality is also variable. Theileria
the immune response through cytotoxic T
lestoquardi causes between 50 and 100%
lymphocytes. The infection with T.
mortality in sheep and goats. When East
annulata activates the release of
Coast Fever infects previously non-
cytokines by CD4+ T cells. They produce
exposed groups, the mortality can reach
IFN-γ which triggers the production of α
90% or more of the animals.
tumor necrosis factor and nitric oxide by
Young animals are more resistant than non-infected macrophages. These active
adults. Local breeds from endemic areas compounds will destroy the infected
are usually resistant to the infection. cells. The extracellular merozoites are
killed by antibodies produced by B
Pathogenesis. The pathogenicity is
lymphocytes.
different from Theileria species to
Theileria species and even within the Like in babesiosis, the altered immune
same species, between hosts. response is ultimately responsible for the
pathogenesis of the diseases. The
In cattle, the infection of lymphocytes
increased production of cytokines results
with T. parva induces blastogenesis
in increased vascular fragility and
resulting in an increased production of
permeability.
lymphoblasts which invade various
tissues (“leukemia”-like infection). The Clinical signs. Despite the great species
pathogenetic effect is dominated by the diversity, the disease has several
massive alteration of the structure and common clinical features. Usually the
functions of the lymphoid tissue and by adult animals are more susceptible and
the subsequent anemia caused by signs of disease are more severe. The
erythrolysis. The oxidative stress has presence of fever and generalized
been incriminated as the main lymphadenopathy are characteristic.
mechanism of erythrolysis. These induce
187 | P r o t o z o a
The East Coast Fever is characterized by cattle. Symptoms include high fever,
very high mortality in susceptible cattle listlessness, frothy nasal discharge,
populations. Incubation is 1-4 weeks. The jaundice and enlargement of superficial
main clinical signs include: high fever, lymph nodes.
lymphadenopathy, severe dyspnea,
Equine theileriosis produced by T. equi is
tachycardia, and extreme weight loss. The
a severe disease. Infected horses have
fever is high persists until recovery or
high fever, listlessness, hyperlacrimation,
death. Infected animals have aural and
palpebral edema, severe anemia,
palpebral edema and hyperlacrimation.
hemoglobinuria and icterus (signs typical
The severe respiratory distress and the
to babesiosis).
excessive frothy nasal discharge are
indicative of the severe pulmonary Canine theileriosis produced by T. annae
edema which usually precedes death. is a severe disease causing acute fever,
Some animals show hemorrhagic weakness, lethargy, tachypnea,
diarrhea. The clinical hematology tachycardia, anemia and hemoglobinuria.
findings include leucopenia, Clinical hematology reveals regenerative
anemia, reticulocytosis, and
The clinical signs and course of the
thrombocytopenia.
Corridor Disease are similar to the East
Coast Fever but outbreaks are associated Feline cytauxzoonosis is characterized
with the presence of wild buffaloes. by fever, acute onset of anorexia and
lethargy. Following these acute signs,
The Mediterranean Coast Fever has a
increased the cats show increased
much lower mortality rate and occurs
vocalization, weakness, jaundice,
after 1-4 weeks of incubation with fever,
dyspnea, seizures, delayed capillary refill
depression, hyperlacrimation, superficial
time, lymphadenopathy. The outcome of
lymph node swelling, nasal discharge and
the disease is often death, preceded by
weight loss. Except these signs which are
deep coma.
similar but slightly less severe than in the
case of African theileriosis, the infection Pathology. The lesions of animals which
with T. annulata produces also anemia died of theilerioses consist in severe
with hemoglobinuria. pulmonary edema, generalized
lymphadenopathy with enlarged lymph
Benign bovine theilerioses (produced by
nodes and multifocal lymphoid
T. buffeli, T. mutans, T. sinensis, T.
hyperplasia in various parenchymatous
taurotragi and T. velifera) and Oriental
organs (i.e. kidneys, brain). The spleen is
theileriosis (T. sergenti) are either
enlarged and congested. In species
subacute or chronic and if symptoms are
producing marked anemia, the tissues are
present they are typically mild. Death is
icteric and the urinary bladder may
uncommon.
contain hemoglobinuric urine.
Ovine and caprine theileriosis produced
Diagnosis. Acute clinical signs
by T. lestoquardi is a severe disease,
insusceptible animals correlated with the
clinically similar to East Coast Fever of
lesions and the history of the local
188 | P r o t o z o a
endemicity are good diagnosis indicators. mg/kg, daily for 2-5 days). Imidocarb or
The confirmation of the diagnosis is diminazene diaceturate (see babesiosis)
based on demonstration of the Theileria is also effective in horses.
in various samples. The presence of
Dogs infected with T. annae can be
schizonts (meronts) in the infected white
treated with limited success with
blood cells or merozoites in the
babesicidal drugs. Feline cytauxzoonosis
erythrocytes can be observed under the
is treated with a combination of
microscope in blood smears or lymph
atovaquone (15 mg/kg, orally, every 8
node biopsies.
hours) and azithromycin (10 mg/kg,
The most widely used serological test for orally, every 24 hours) for 10 days.
screening of animals, mainly in the
Control. The most efficient and widely
international trade is indirect fluorescent
used method employed for controlling
antibody test.
theileriosis is the control of ticks using
Other serological methods (i.e. ELISA) are acaricides. Factors contributing to an
also used. Molecular methods are highly unsuccessful control include acaricide
sensitive but not implemented in the resistance of ticks, improper use of
routine surveys. acaricide drugs (cheap, poor quality
products, underdosing) or illegal animal
Treatment. Most of the drugs are
movements. Chemoprophylaxis with
improving the clinical presentation but
theilericidal drugs is an option for
are not eliminating the infection.
animals newly introduced to an endemic
The treatment of infected cattle is area.
recommended only during the very early
Prevention by immune prophylaxis is
phase of the clinical diseases. Two
possible in cattle. Live vaccines have been
molecules are widely used: parvaquone
developed for T. parva and T. annulata.
and its derivative buparvaquone.
Parvaquone is used as single dose (20

mg/kg, intramuscularly) in cattle infected
2.5 Ciliophora
with T. annulata or at 10 mg/kg,
intramuscularly, twice at 48 hours Phylum Ciliophora includes very diverse
interval against the infection with T. groups of highly mobile protozoans
parva and T. mutans. Buparvaquone (2.5 known generically as ciliates. Their
mg/kg, single dose, intramuscularly) is defining feature is the presence of hair-
effective against bovine theilerioses. like movement organelles, known as cilia
In cattle but also other species, various (singular cilium). Most species are free-
other drugs are used with variable living, and they usually inhabit aquatic
efficacy. In equids infected with T. equi, environments, both marine and
chlortetracycline hydrochloride and freshwater. The majority of them are
oxytetracycline hydrochloride are predators of smaller microorganisms (i.e.
effective when given intravenously (5.5 bacteria). Other species are symbiotic
and they are associated with a huge
189 | P r o t o z o a
variety of hosts within most animal phyla, There are two types of reproduction in
both invertebrates and vertebrates. ciliates. The asexual reproduction is by
Certain groups inhabit the digestive binary fission. The sexual reproduction is
system of their host where they are a very interesting process and it takes
mutualists, commensals and few species place by conjugation. During conjugation,
parasitic. Others are living on the two cells which are of complementary
tegumentary surface of aquatic animals, mating type, are fertilizing each other.
mostly fish as commensals or parasites.
Two genera are of veterinary importance,
Their medical importance is mainly
both included in Class Litostomatea:
known in aquaculture, as they produce
Neobalantidium and Buxtonella.
outbreaks in farmed fish (e.g. Ichthyo-
phthirius, Trichodina, Chilodonella). In 2.5.1 Ciliates of domestic animals
domestic animals very few species are
known to be potentially pathogenic, and Ciliates are the least represented
the most prominent example is protozoans in the veterinary
Neobalantidium coli. parasitology. They are usually
All species are unicellular and they bear opportunistic pathogens, and the clinical
on their surface variable number of cilia. infections are sporadic. Two diseases will
Their arrangement and patterns are be discussed: balantidiosis of swine and
important in classification. The ingestion buxtonellosis of cattle.
of nutrients is through a small opening in
the cell, known as cytopharynx,
surrounded by a group of cilia. Waste 2.5.1.1 Balantidiosis
material is eliminated from the cell
through another opening, known as Introduction. Balantidiosis is a
cytoproct (or “cellular anus”). The worldwide distributed parasitic disease
internal structure of ciliates is also very of the lower intestinal tract of pigs and
characteristic. They have two nuclei, one humans, with usual subclinical course but
larger (macronucleus) and one smaller problematic in immunocompromised
(micronucleus). The macronucleus is the patients.
true-nucleus and it is controlling the Historical notes. In 1857, Malmstein
metabolic activity of the cell. The role of described a new species of ciliates from
micronucleus is in the sexual the feces of dysenteric patients. He
reproduction. Like all eukaryotic cell, named it Paramecium coli. One year later,
ciliates have all the typical cell organelles Claparède and Lachmann erected the
(mitochondria, Golgi body etc.). genus Balantidium for a newly described
The life cycle of all parasitic ciliates is species, B. entozoon from frogs. In 1858,
homoxenous, and transmission is directly Stein moved Paramecium coli into genus
by contact (in species parasitic on the Balantidium. However, due to evident
skin of fish) or via ingestion of cysts (in phylogenetic differences, in 2013,
species parasitic in the digestive tube). Pomajbíková et al., erected the new genus
190 | P r o t o z o a
Neobalantidium and placed within it The newly formed cysts are passed via
Paramecium coli. the feces.
Etiology. The species responsible for the Epidemiology. The disease is virtually
infection of pigs is Neobalantidium coli. It present wherever pigs are present.
is not clear yet if all Balantidium-like Neobalantidium coli is found in more than
ciliates described from pigs, primates and half of the adult pigs. In young pigs the
camels are conspecific with N. coli. prevalence is lower. In some pig
However, until new data is available, we populations the prevalence can be 100%.
list N. coli as a zoonotic agent.
In humans, the disease is sporadic and
Morphology. According to the the geographic areas with high
description by Pomajbíková et al. (2013), prevalences include Latin America,
trophozoite is elongated, rounded at the Philippines, Indonesia, Papua New
posterior end and narrow at the anterior Guinea and Middle East. Pigs-to-humans
end. The size of the trophozoite is 30-300 and humans-to-humans cycle are
x 30-100 µm. The surface is covered by described. The occurrence of the disease
cilia, arranged in longitudinal rows. The in humans is influenced by several
cytostome-cytopharyngeal complex is factors. The close contact between
located at the apical end and surrounded humans and pigs together with improper
by longer cilia. The cysts (40-60 µm) are waste management seem to be such
spherical or ovoidal s one hypobiotic factors.
trophozoite.
Survival of cysts is longer in warm and
Life cycle. Neobalantidium coli inhabits humid climate. This is why the
the cecum and colon of its hosts. It is not prevalence of human disease is higher in
clear if interspecific transmission is humid tropical areas.
possible. The life cycle is direct
Pathogenesis. Neobalantidium coli is
(homoxenous) (figure 2.85)
typically a commensal of the large
The organisms are passed in feces as intestine. It typically feeds through the
cysts. Cysts are ingested via cytopharynx with debris and other
contaminated food or water by a new particles from the intestinal content
host (figure 2.87 - 1). In the intestine of without any pathogenic effect. Under
the new host, trophozoites excyst and certain condition (decrease of immunity,
grow. They inhabit the surface of the intestinal dysmicrobism) it becomes
mucosa where they feed through their pathogenic by producing proteolytic
cytopharynx with various particles. They enzymes which destroy the intestinal
multiply asexually by binary fission epithelium resulting in acute diarrhea.
(figure 2.87 - 2) or sexually, by Persistent mucosal damage may result in
conjugation (figure 2.87 - 3). When the humans in the production of ulcers. Deep
intestinal content begins dehydration ulcers can be complicated by potential
prior to fecal transmission, N. coli starts fatal intestinal perforations.
the encystment process (figure 2.87 - 4).
191 | P r o t o z o a
Figure 2.85 Life cycle of Neobalantidium coli. For the meaning of numbers, please refer to
the text.
In pigs, they can invade lesions produced Immunology. The role of immunity is not
by other pathogenic organisms. clear. Indirect evidences however suggest
Production of hyaluronidase by N. coli the role of the immune system in
aggravates the ulcers. maintaining the infection asymptomatic.
In immunocompromised patients,
Neobalantidium coli can produce a
192 | P r o t o z o a
systemic disease, infecting the lungs, sulcata. The signs may include mild
lymph nodes. diarrhea.
Clinical signs. The vast majority of Identification of “Balantidium”-like cysts

infected pigs have no clinical signs. Under in the feces of cows is indication of
certain conditions, some pigs will show Buxtonella sulcata.
moderate to severe acute diarrhea.
Pathology. In non-clinical infections,

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1 INTRODUCTION TO PARASITOLOGY ..................................................................................... 1

para (beside) and sitos (grain, food). If we

When attempting to define parasitology Based on most of these definitions, many

Table 1.2 Animal phyla with parasitic 1.2 Parasitism as an interspecific

Figure 1.2 One of the most common

With the view of all above, parasitism

females (80 mm in length). It is highly With high probability, most mutualistic

Ecology of the host itself greatly

If we consider parasitology a branch of Another question is if and how parasites

1.4 A brief history of parasitology

History of medical sciences is a

Early records. Since humans became Figure 1.4 Galen of Pergamum.

the sexual reproduction of A. monograph on parasitic organisms

Emergence of parasitology as a science

Figure 1.6 Original drawing from Redi’s

Figure 1.5 Francesco Redi. (reproduced

published in 1787 his "Versuch einer parasitologists arose in the scientific

As mentioned above, basically all

The end of the nineteenth century

Figure 1.8 Cover of the first edition of

Figure 1.10 Cover of the first edition of

The first journal entirely devoted to

Modern parasitology. Definitely, the

brain, muscles, tendons, heart, blood

(2) Size of parasites

 Microparasites are those not visible

(4) Number of hosts required for the

 Homoxenous (Greek: homos =

Asexual reproduction is also known in ecological or trophic. For examples,

Reservoir hosts are those organisms

Vector hosts are defined as organisms

Dead-end hosts are usually intermediate

1.7 Life cycle of parasites In homoxenous life cycles parasites

 the adverse environmental factors;

 the ecological requirements for host-

Despite all odds, an impressive number of

1.7.1 Types of parasitic life cycles

As shown above (Chapter 1.5), there are

possible due to autoinfection of the

 The third possibility for homoxenous

transmission and with no stages in

 In other groups of diheteroxenous

Ruminant definitive hosts are known to occur in the cestode

Figure 1.23 Triheteroxenous life-cycle (E

host. By parthenogenesis, parasitic complex developmental changes,

arthropods however, lack environmental Transmission strategies are extremely

One of the most crucial milestones in the

Parasites can use passive dispersion

situations include direct transmission and complex. Many parasites are

Figure 1.25 Sarcoptic mange in a camel.

mammals, host specificity is low as (7) Host range depends on immune

(4) Host range depends on the stages Life-cycle of parasites is usually an

host-related factor which influences mostly related to immunity is a key factor

The mechanism by which parasites are

larval cestodes) located in retarded growth. With effects similar to

anatomical barriers, the innate immune hypereosinophilia, increased

Except these intimate mechanisms, there taxonomic position of each parasite. So

kingdom includes several classes, one occurrences are abbreviated (i.e. H.

Table 1.4 Main taxa of parasites