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MODULE-1: PROTOZOA - INTRODUCTION

Learning objectives
At the end of this module, the learners are expected to
have a good understanding of protozoa of veterinary
importance, their structure, locomotion, nutrition and
reproduction.
WHAT IS PROTOZOA?

• Protozoa form a subkingdom of the kingdom protista.

• They are unicellular in size and some are visible to
naked eye.
• The term protozoa is coined by Gold Fuss.
• The structure of protozoa are referred to as
organelles(differentiated portions of cell) which
perform various activities required for metabolism as
in metazoa.
• Difference between protozoa and rickettisia is :
protozoa are eukaryotic, possess a cell wall and
organelle for performing different metabolic
activities whereas rickettisia are prokaryotic like
bacteria and devoid of well developed cell wall
ORGANELLE

Nucleus
• It is true nucleus enclosed in a membrane as seen in
eukaryotes where as primitive nucleus is seen in
prokaryotes like bacteria where nucleus
is unseparated by a membrane.
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• Normally protozoa contain only one nucleus

(uninucleate) sometimes two (binucleate) or more
(multinucleate).
Vesicular Nucleus
• Other than ciliates, the nucleus is vesicular in
protozoa . Vesicular nucleus has nucleoplasm and
nuclear membrane which binds nucleoplasm
chromatin (Feulgen + i.e has DNA) intranuclear body
which is more or less central in the nucleoplasm.
Compact Nucleus
• Compact nucleus contains large amount of chromatin
and small amount of nucleoplasm.
• In cliates: Two types of nuclei found
o Micronucleus: Relatively small, diploid, divide

mitotically during fission. Controls reproductive

function of the organism.
o Macronucleus: Relatively large and divides

amitotically during fission – polyploidy –

controls vegetative function of the organism.
TYPES OF VESICULAR NUCLEUS

There are two types of vesicular nuclei

• In one type the intranuclear body is endosome
(karyosome) with is devoid of DNA , hence feulgen
negative.
• The chromatin which forms the chromosomes lies
between the nuclear membrane and endosome
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o Eg. Trypanasomes, parasitic amoebae.

• In another type of vesicular nucleus the intra body is
nucleolus which is feulgen positive. (DNA precursor)
one or more nucleoli are present.
• Chromatin is present throughout the nucleus.
o Eg. Apicomplexa.

ORGANS OF LOCOMOTION

Flagella (Click here to view video)

• Flagella are whip - like organelle composed of central
axoneme and outer sheath which arise from
kinetosome (or) blepharoplast in the cytoplasm.
• The flagellum may be directed anteriorly or
posteriorly and may be attached to the side of the
body along its whole length by a delicate undulating
membrane and free flagellum also extended if more
than one is present, they perform similar function.
• Eg: Mastigophora: Flagellate stage of sarcodina,
apicomplexa.
• Electron microscopic studies indicate that axoneme is
composed of 2 central filaments surrounded by 9
peripheral filaments (9+2 structure).
Cilia (Click here to view video)
• Eyelash - like organelle, fine short flagellum like
structure arising from kinetosome embedded in the
pellicle or ectoplasm function:
o ingestion of food.

o tactile.

• Cilia are found in ciliphora

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Pseudopodia (Click here to view video)

• Pseudopodia are temporary locomotor organelle that
can be formed and retracted as needed.
• e.g. Amoebae.
Four type of Pseudopods
• Lobopod dense outer layer and more fluid inner zone
e.g. amoebae
• Filopod slender hyaline pseudopod that tapers from
its base to its pointed tip,tend to anastamose and may
fuse locally to produce thin cytoplasm.
• Myxopod (Rhizopod or reticulopod) pseudopods
branch and anastomose to trap food and for
locomotion.
• Axopod projection from the body – no branching (or)
anastomosing.
Gildings: (Click here to view video)
• The body glides smoothly along with changes in shape
(or) size appreciable under light microscope.
However, exact mode of locomotion is still not clear.
• E.g. Toxoplasma, Sarcocystis, coccidian merozoites,
and gregarines.
CYTOPLASM

• This is the extra nuclear part of the cell.

• Consists of outer dense hyaline homogenous layer
ectoplasm and inner more voluminous fluids or
granular endoplasm.
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• They have carbohydrates, protein, lipids, salts, metals

and non-metals.
ECTOPLASM

• It gives the shape – outer most thick layer is the

ectoplast (or) limiting membrane (sarcodine).
• If it is a membrane it is known as pellicle, If it is a
layer – it is called periplast.
Function of Ectoplasm
• Protection, locomotion and adhesion are some of the
functions.
ENDOPLASM

• It is granular because of the inclusion.

• It contains vacuoles – food vacuoles masses of
glycogen, fat globules, proteins chromatoid bodies
granular (type --- Golgi centrosome).
• Mitochondria chromatophores, basal fibrils (costa,
pelta, axostyle)
Function of endoplasm
• Nutrition and reproduction.

MODULE-2: METABOLISM IN PROTOZOA

Types of nutrition
• Autotrophic Nutrition
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o Type in which organism is able to live entirely on

inorganic compounds, it synthesises proteins,
carbohydrates, lipids from inorganic precursor -
occurs in phytoflagellates
• Holophytic Nutrition
o Carbohydrates as syntherised by means of

chlorophyll contained in chromatophores which

vary is size shape, and number – characterstic of
phytoflagellates
• Holozoic Nutrition
o Particular food material (preformed food

material including host tissue) are ingested

through a temporary or permanent mouth.
o Temporary mouth is formed by amoeba when

they engulf food (pseudopodia).

o Permanent mouth is a cytosome seen in ciliates.

o It is simple or leads to cytopharynx.

o Cytostome is lined by cilia which aid in the

ingestion of food.
o The area around the cytostome forms a peristome

or mouth. On entry, food vacuoles are made in

the cytoplasm where it is digested.
o Undigested materials are extruded out though a

temporary opening (or) a permanent opening

“cytopyge” (cell anus).
• Pinocytosis
o Many protozoa ingest nutritious material in

solution by a process known as pinocytosis

(pinching - off vacuoles of fluid through a
temporary opening in the wall).
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o In some protozoa, microscopic micro pores (also

called micropyle or cytosome) seen under
microscope and used for ingestion fluids (or)
solids.
o E.g. Eimeria sp, Plasmodium.

• Saprozoic Nutrition
o Nutrition being absorbed through body wall.

o By simple osmosis.

EXCRETION

• Through body surface /wall.

• Cytopyge (or) cell anus – In ciliates, these are seen in
opposite poles where cytostome is present.
• Contractile vacuoles simple (or) associated with
feeder canals or vacuoles. They are more important as
osmoregulating organelles that are found in fresh
water protozoa.
NERVOUS SYSTEM

• Sliver line system seen by silver impregnation study

cultures
• Photo receptors are photosensitive – pigment spot or
also known as melanosoma
• Sensory vacuoles
• Organelles such as
o Collars

o Stalus

o Suckers

o Polar filament (sporozoa)

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MODULE-3: REPRODUCTION IN PROTOZOA

Asexual reproduction
• Binary fission
• Schizogony
• See gamont and agamont
• Budding
BINARY FISSION

• It is a common method of reproduction

• Two individual daughter cells are formed with
cytoplasm division following nuclear fission. Parent
cell gives rise to two nearly halved daughter cells
• In flagellates, kinetosome goes to one half as in
flagellate and while the other may develop one for
itself.
• It may be longitudinal as in flagellates and transverse
, as in ciliates
• Vesicular nucleus and micronuclei of ciliates divide
mitotically and macronucleus divide amitotically.

SCHIZOGONY

• Schizogony found in Apicomplexa. In this, the nucleus

divides several times before cytoplasm divides.
• The dividing cell is known
as meront (or) schizont (or) segmentor (or) aga
mont.
• The daughter cells are known
as merozoites (or) schizozoites.
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GAMONT AND AGAMONT

• Agamont is a schizont in which merozoites repeat

schizogony
• Gamont is a schizont in which merozoites become
gametocytes initiating sexual phase.
BUDDING
• Here two (or) many daughter forms are produced
from “Parent Cell”.
• In this, a small daughter individual separates from the
side of the mother and grows to full size.
• Division may be apparently amitotic.
• Division may be internal (or) external and number of
buds may vary with species.
TYPES OF BUDDING

• Endodyogeny: It is a type of internal budding in

which two daughter cells are formed with in mother
and breaks out and destroying it
e.g. Toxoplasma, Sarcocystis
• Endopolygeny: If more than 2 daughter cells are
produced by internal budding the process is known as
endopolygeny.
• Ectopolygeny: If more than 2 daughter cells as
produced by external budding , the process is known
as ectopolygeny.
SEXUAL REPRODUCTION

Types of sexual reproduction

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• Conjugation
• Syngamy
CONJUGATION

• This is seen in ciliates.

• Two individuals come together temporarily and fuse
along.
• Part of their micro nuclei divide a number of times
and one of the haploid pronuclear passes from each
conjugant into the another.
• The conjugants then separate and nuclear
reorganization takes place.
SYNGAMY

• It is a process of fusion of two gametes to form a

zygote. If the gametes are same in size they are called
as isogametes and if they are dissimilar, they are
called as anisogametes.
• The smaller gamete is usually called a
microgamete(microgametocyte) which divides
mitotically. Nucleus divides into a number of bits each
surrounded by cytoplasmic fragment forming
microgametes. They are actively motile by means of
flagella.
• The gametes are produced by a special cell called
gamonts; the microgamont (or) microgametocyte and
macrogamont (or) macrogametocyte. The process of
gamete formation is known as gamogony or
gametogony.
Macrogametocyte
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• The large one is a macrogamete. Contains large

amount of cytoplasm with compact nucleus of more
food reserve; they divide by meiosis into a single
macrogamont which is non-motile and ovum like.
• Isogamy :It is a process of fusion of two identical
gametes.
• Anisogamy or heterogamy: Gametes of different size
fuse resulting into a zygote.
SPOROGONY

• Zygote may be divided to form a number of

sporozoites. The process is known as Sporogony.
• Oocyst - Zygote with in a cyst. If they are not expelled,
they develop into sporoblast – if it is in a cyst like
wall, it is called as sporocyst.
• In some, sporoblast has no cyst hence come out start
moving it is called sporokinete.
• The sporoblast becomes sporozoites and become
infective to host.
CYST
• Some protozoa form resistant cysts called as spores. A
cyst results from the formation by the protozoan of a
heavy wall around itself.
• The term pseudocyst is used when the wall is formed
by the host. A spore is produced within the organism
by the formation of a heavy wall around one or more
individuals.
• Each spore or cyst may contain one or more
sporozoites; the vegetative motile stage of a protozoan
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is known as trophozoites which feeds and grows until

division commences.
ENCYSTMENT

• The majority of the parasitic protozoa form cysts at

some period of their existence. The cyst is a resistant
form and they can survive outside the body of the
host. These cysts may be formed at various stages of
development.
Cyst following syngamy
• The internal sporozoa, zygote typically secrete a
resistant envelop to become oocyst. In some sporozoa,
zygote is formed in insect vector which may develop
into a true oocyst in mammalian host or it may, as
seen in some, produce motile ookinete.
• Cyst independent of syngamy:
o Majority of the flagellates appear to be capable of

secreting a nesting wall around them but no

development occurs within the cyst.
o On the other hand, when amoeba encysts

multiplication of nucleus occurs with in cyst.

• Cyst may also be found in the tissue of the host in
such cases and the wall is usually formed by reaction
of the host.
• Eg. Meischer’s tubules in Sarcocystis.

MODULE-4: ORDER-
KINETOPLASTIDA; FAMILY-
TRYPANOSOMATIDAE;
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• Members are all parasitic. They are found in blood,

plasma, lymph and tissue fluids of mammals and
birds, hence called as haemoflagellates.
• They have a characteristic leaf- like body with a single
flagellum attaching to the body by the undulating
membrane. Disease caused is known as
trypanosomosis.
• In man, trypanosomes cause African sleeping sickness
and Chagas' disease. In domestic animals, this disease
is known as surra which means rotten. They are
transmitted cyclically and mechanically by
haematophagous flies.
• It affects a wide range of hosts and commonly seen in
tropical countries like India, South Africa and the
UAE.
MORPHOLOGY- TRYPANOSOMES

• They are fusiform (or) spindle shaped with a vesicular

nucleus and kinetoplast located posterior to nucleus.
• Axoneme arises from kinetosome of basal granule
attached to the body by undulating membrane and is
continuous as free flagellum.
• Movement may be active or sluggish.
• Trypanosomes vary in shape
o short and stout stumpy forms

o long and slender forms ,and

o intermediary forms. Such trypanosomes with

varying shape are called polymorphic

trypanosomes are polymorphic trypanosomes.
o Some may be uniform in size – monomorphic

tryps.
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BIOLOGY OF TRYPANOSOMES

• Multiplication is by longitudinal binary fission.

Division starts form kinetoplast followed by nucleus
and cytoplasm.
• They are transmitted by blood sucking flies in which
development stages occur (cyclical transmission).
• Some of the trypanosomes are transmitted
mechanically in which the infective stages are alive for
a few minutes and they have to be transferrec to a new
host for successful transmission.e.g. Trypanosoma
evansi by Tabanus sp
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• Cyclical development occurs in the vector and may be

in anterior station (salivaria) or in posterior station
(stercoraria).
o In the anterior station development, infection

is transmitted by inoculation by arthropod

vectors when they suck blood from the host.
eg. Trypanosoma vivax
o In the posterior station develpoment ,the

metacyclic trypomastigotes accumulated in the

hind gut are passed in the faeces of the
arthropods. Infection of vertebrate host occur by
contamination of skin or skin wound.
e.g. Trypanosoma cruzi
• Any trypanosomes can be transmitted mechanically
without cyclical changes experimentally this can be
done by syringe passage.
• In nature this is accomplished by blood sucking
insects like Tabanus, Stomoxys, Hippobosca sp., etc.
which feed several times on different animals before
repletion.

DEVELOPMENTAL STAGES- TRYPANOSOMES

• Amastigote (Leishmania like bodies)

o The body is rounded.

o Flagellum is absent or represented by short

fibrils.
o Kinetoplast is present and seen in vertebrates.

• Promastigote (Leptomonad)
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o Kinetoplast and axoneme are at anterior tip of the

body with no undulating membrane.
o It is mostly seen in invertebrates or cultures.

• Epimastigote (Crithidial)
o Kinetoplast with axoneme is anterior to nucleus.

o Undulating membrane is short.

o This stage is seen in vertebrates but principally a

stage in arthropod.
• Trypomastigote (Trypanosomes)
o This is the form seen normally in blood films of

infected animals.
o It is blade like form, kinetoplast posterior to

nucleus and near to posterior extremity.

o Undulating membrane is well developed.

o Free flagellum is often present.

o Found in vertebrate host and also in arthropods.

o It is the infective stage for the invertebrate host.

PATHOGENESIS- TRYPANOSOMES
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• Mainly anemia (Hemolytic Anemia).

o This may be due to immunological mechanism

resulting in haemolysis and erythrophagocytosis.

o Trypanosome antigen attaches to RBCs and

increases erythrophagocytosis.
o Anaemia may result due to reduction in half - life

of circulating cells.
o Due to immune mechanism - enhanced

haemolysis occurs; a hemolytic factor produced

resulting in direct hemolysis of RBC.
o Anemia is also associated with disorders of

clotting like thrombocytopenia and disseminated

intravascular clotting ( DIC).
o Damages to blood forming organs by
trypanosomes.
• Hypoglycemia
o Trypanosome absorbs glucose in blood leading to
increased production of lactic acid. This leads to
less intake of O2 by RBCs resulting in asphyxia.
and acidosis.
• Serum potassium level is increased due to destruction
of blood cells. Calcium and phosphorous ratio is
disturbed.
• The lysed trypanosomes release endotoxin resulting
in toxemia and death.
• Due to the anaemia, mucous membrane is pale.
• Some of the clinical signs are
o Petechial hemorrhages and emaciation.

o Enlargement of spleen, lymph gland and liver.

o Congestion of mucosa of intestine, stomach,

kidney and bone marrow

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o Oedema of dependant parts is common. Animal

will be unable to get up.
o Keratitis and conjunctivitis.
o Nervous symptoms.
▪ CSF section of the brain will show

perivascular cuffing, infiltration meningitis

and encephalitis.
o Lethargy.

MODULE-5: GENUS-TRYPANOSOMA; SPECIES-

TRYPANOSOMA EVANSI;

• Learning objective
• This module deals with the structure, mechanism of
transmission, pathogenesis, diagnosis and control of
trypanosomes affecting domestic animals.
TRYPANOSOMA EVANSI

• It is the first trypanosome shown to be pathogenic to

mammals identified by Griffith Evans a British Vet in
India.

HOST- TRYPANOSOMA EVANSI

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• Natural hosts
o Camel, horse, donkey, mule, ox, goat, pig, dog,

water buffalo, elephant , mongoose , deer and

other wild animals like fox, hyena and tiger.
• Experimental hosts
o Many laboratory animals including mouse , rat,
rabbit, guinea pig and chicken.
LOCATION - TRYPANOSOMA EVANSI

• Blood and lymph. The disease is called

trypanosomosis.
• Name of the disease is different in different countries-
most widely used is surra.
• Classical disease entity in Indian sub-continent and
occurs in horses and is known as surra.
• It is a Hindi word meaning rotten (or) putrified.
• Disease in camel is called Gufar; murrina – in
panama; dorrengadera in Veninzula.
• T.equinum now regarded as dyskinetoplastic strain
of T. evansi, causes mal de caderes in horses in South
America.
PREVALENCE - TRYPANOSOMA EVANSI

• Common in Northern Africa, Asia, Northern and

South America
STRUCTURE - TRYPANOSOMA EVANSI
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• Mean length varies considerably in different hosts and

geographic strains.
• Typically they are 15-34 µm long with a mean of 24
µm.
• Most ones are slender (or) intermediate in shape. But
stumpy forms also occur.
• Sporadic strains without a kinetoplast(
dyskinetoplastic) and visible with light
microscope may arise occasionally and
spontaneously or post-treatment with certain dyes
(e.g. Acriflavin) and drugs such diminazene
aceturate.
CAMEL TRYPANOSOMOSIS

Camel trypanosomosis also known as surra, is a

disease of camels caused by Trypanosoma evansi. The
disease is the most important single cause of economic
losses in camel rearing areas, causing morbidity up to
30.0% and mortality about 3.0%. Severe outbreaks
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occurred in different parts of the world where several

thousand animals died in the 1970s and, of late, in 1994
and 1995 which have been well documented.These
epidemics pose a major constraint to camel productivity
given their importance as a source of meat, milk
production, transportation and draught power, as well as
by-products (wool, hair, skin and hides). In addition, they
also provide foreign currency to their owners from their
export
Etiology
• Trypanosoma evansi is a species belonging to the
subgenus Trypanozoon and is the causative agent of
camel trypanosomosis.
The vector
• Trypanosoma evansi lacks the genes necessary for
mitochondrial development and is therefore , unable
to undergo growth and differentiation in the insect
vector. It is speculated that the widespread occurrence
of Trypanosoma evansi is largely due to its being
spread mechanically by the bites of haematophagous
flies, e.g. Tabanus. Stable flies (Stomoxys) have also
been incriminated, but based on experimental
transmission between horses, guinea pigs and dogs,
they do not appear to be important vectors . More
than 20 different species of Tabanus have been shown
experimentally to transmit Trypanosoma evansi .The
prevalence of some Tabanus spp. all the year round
ensures that transmission of the parasite occurs
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wherever reservoir hosts, vectors and susceptible

hosts co-exist. Although the mode of mechanical
transmission is well established, its dynamics are not
well understood.
Distribution
• Surra is widespread in different parts of the world and
poses a major constraint to camel productivity.
Available information on the prevalence of surra
caused by Trypanosoma evansi in many countries of
the world as reported are Nigeria, Mauritania, Niger,
Kenya, Ethiopia, Jordan, India, Sudan, Iran and
South America
Pathology and pathogenesis
• Anaemia: It is a major component of the pathology
of surra and of African trypanosomosis generally.
Anaemia in Trypanosoma evansi infections of camels
is reportedly macrocytic and hypochromic In the early
phases of infection the anaemia is haemolytic and
haemophagocytic. Several theories have been
proposed, viz, immune complexes, expanded
mononuclear phagocytic system per se , haemolytic
factor produced by the trypanosome, fever and
disseminated intravascular coagulation for the
haemolytic anaemia
• Anoxia : An increase in cardiac output due to
increase in stroke volume and heart rate and a
decrease in circulation time are obvious
manifestations. The central nervous system is
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reported to be most susceptible to anoxia with

consequent development of cerebral anoxia. The
marked depression observed in camel trypanosomosis
is a mental state and is a manifestation of depression
of cerebral cortical function in various degrees. Other
nervous signs reported, such as circling movement,
incoordination and dullness, appear to be the results
of brain tissue disturbance or damage by the
parasites.
• Tissue damage : The atypical lesions of multiple
necrotic foci found in the liver and spleen, as well as
generalized lymphoid tissue hyperplasia in camels
suffering from surra on post mortem, could be
attributed to pathological events that occur in the
tissues of animals infected with Trypanosoma
evansi. The degenerative changes thus observed could
be due to tissue anoxia, possibly caused by anaemia,
which results in a fall in tissue pH and vascular
damage. Other mechanisms may also be
involved. Trypanosoma evansi has a known
preference for connective tissues of a host, where they
disrupt the collagen bundles and destroy the
fibroblasts which produce and maintain the collagen .
This disruption of host connective tissues, along with
the vascular damage attributable to brucei group
trypanosomes release large quantities of cytoplasmic
and mitochondrial enzymes into the serum, thereby
causing further tissue damage. The appearance of
trypanosomes coincides within the host bloodstream
is characterized by a sharp and as yet unexplained rise
in sorbitol dehydrogenase (SDH) activity. Later in the
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infection a large increase in serum levels of glutamic

oxaloacetic transaminase (GOT), now known as
aspartate alanine transferase (AST) and a smaller rise
in glutamic pyruvic transaminase (GPT), now known
as alanine amine transferase (ALT) are reported. The
rise in AST level can be attributed partly to cellular
damage caused by the trypanosomes lysis, while the
increase in ALT probably results from host
destruction of trypanosomes. AST is found mostly in
cell organelles and rises when there is a great damage
to the heart, kidney, skeletal muscles and liver. ALT is
a specific liver enzyme found in the cell cytoplasm and
its rise is associated with cell membrane damage. The
reported increases in these enzymes, especially AST,
is not surprising as it is indicative of organ damage
and supports the post mortem reports of necrotic foci
in the liver and spleen of camels suffering from surra.
• Fever : This is characterized by high temperature
due to the effects of toxic metabolites produced by the
dead trypanosomes.
• Oedema: This is reported in the dependant parts of
the body during the chronic stage and this is due to a
significant decrease in the albumin levels, resulting in
alterations in osmotic pressure of the blood. This
leads to excessive accumulation of fluid in tissue
spaces caused by a disturbance in the mechanism of
fluid interchange between capillaries, the tissue
spaces and the lymphatic vessels. All this possibly
indicates great liver damage.
• The haemorrhage and serous exudates that
occurr are due to haemolysis involving the expanded
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mononuclear phagocytic system. while the frequent

abortions reported may be attributed to endocrine
dysfunction
Clinical manifestations
• In camels, the disease is manifested by elevation of
body temperature. Infected animals show progressive
anaemia, marked depression, dullness, loss of
condition, and often rapid death. Anaemia is a major
clinical finding in camel trypanosomosis. Some
camels develop oedema in their dependent parts of
the body, urticarial plaques and petechial
haemorrhages in serous membranes. Death finally
occurs if untreated. However, some may harbour
trypanosomes for 2-3 years thus constituting
reservoirs of infection to susceptible camels and hosts.
Other well documented field reports are death,
abortion, weight loss, reduced draught power and
nervous signs like circling movement and trembling,
unusual aggressiveness, running aimlessly and
sudden collapse in severely stressed and over -
worked animals. At post mortem, necrotic foci in the
liver and spleen as well as generalised lymphoid tissue
hyperplaisia are common in camels suffering from
surra.
Diagnosis
• There are no pathognomonic signs of surra and so
laboratory diagnosis has to be carried out to confirm
the condition. Parasitological diagnosis is mainly
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carried out by the direct microscopic examination of

blood or buffy coats and/or sub-inoculation of camel
blood into rodents such as mice or rats. However, the
test has a poor sensitivity, often less than 50%.
Serological techniques, e.g. immunfluorescent
antibody test (IFAT), enzyme - linked immunosorbent
assay (ELISA) and the card agglutination test for
trypanosomosis (CATT), although sensitive, cannot
distinguish current from cured infections
• Recent tests, e.g. latex agglutination test (LAT) or
Surratex based on trypanosome- antigen detection in
blood or serum, are more reliable and have shown a
high correlation with patent or sub-patent disease in
camels
Treatment, prevention and control
• Treatment with trypanocidal drugs is the usual
method of control of Trypanosoma evansi and
quinapyramine has been used in camels, and only
recently melarsomine (cymelarsen) was introduced
for the treatment of surra in camels because of the
problem of drug resistance
• Another drug, Trypan, which is a formulation
containing diminazene-di-aceturate
(diamidinophenyltriazene diaceturate tetrahydrate),
phenazone and procaine hydrochloride is effective
against T. evansi infections
• With regard to prevention, it has been confirmed that
a single injection of 15 ml of Trypan affords an animal
protection against a new re-infestation over a period
of three months . Trypan can be used for curative and
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preventive treatment. On the whole, control of surra

requires treatment of infected animals with effective
drugs and reducing blood sucking flies by regular
insecticide treatment.
DOGS

• Disease is acute (or) fatal.

• Death in 2-4 weeks.
• Oedema is marked.
• The classical signs are corneal opacity, oedema of
larynx resulting in voice changes and similar to that
occur in rabies.
CATTLE OR WATER BUFFALOES

• These two animals are the main reservoirs of

infection to equines. Infection is sub- clinical, mild
and inapparent.
• Occasional outbreaks of acute disease are reported
from many places. This may be due to lowered
resistance in carrier animals following debilitating
intercurrent diseases like rinderpest (or) FMD ,etc.,
stress after FMD vaccination and over work in
draught animals.
• Introduction of new strain of parasite into newer
areas may result in acute form of the disease. It
appears as epizootic of variable severity. This can be
highly fatal.
• Clinical signs are
o High fever 41 C
0
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o Intense excitement alternative to those of severe

depression (coma)
o Animals move aimlessly in circles frequently
falling down, show colic, grinding of teeth, eyes
staring wide open , breathing hard and noisy
o Goring against wall apparent blindness stamping
of feet following groaning, micturition, profused
salivation, twitching of muscles followed by
partial loss of senses and prostration
o Parasitaemia due to factors unknown becomes
too high; blood smears are seen with large
number of parasites which occlude cerebral
capillaries.
o Death may occur in 18 hr to 3 days.
o Sudden death may be mistaken for poisoning or
snake bite or anthrax.
o In per acute cases death occurs in 2-3 hours. The
nervous form of the disease show symptoms as
above.
o Sub acute and chronic
▪ The animals look dull, sleepy

▪ lacrimation of eye, progressive emaciation

rapid pulse
▪ Intermittent fever, oedema of leg, diarrhoea

and death
▪ Corneal opacity – twitching of muscles below

eye
▪ Sub normal temp

ELEPHANTS
• The disease is known as thut.
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• The course of the disease is similar to that of camel.

• There is severe emaciation and marked muscular
lesion, fever, lustesless, oedema of dependent parts,
etc.
DEATH IN SURRA

• To sum - up, death in surra is mainly due to

o High fever, toxaemia

o Anaemia – PCV is less than 25 and 30 and

decreased haemoglobin
o damage of bone narrow due to trypano toxin
o Increase in erythrocyte sedimentation rate

o Hypoglycemia – reduction of blood glucose level

by 30%
o Exhaustion of glycogen reserves
o Failure of liver cells to compensate the loss in
glycogen reserve

MODULE-6: DIAGNOSIS - TRYPANOSOMA

EVANSI
• Clinical diagnosis can be done with history and
clinical signs as described.
Laboratory diagnosis
• Direct examination or wet film examination
o It is a quick method of detecting the organism by

studying their movement and relative size (click

here). Species of trypanosomes involved can be
guessed but it is to be confirmed by staining
• Peripheral blood smear examination
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o Thick and thin blood smears at the height of

temperature is more desirable.
o Parasitaemia is common in equines and canines

but not readily seen in cattle, buffalo & camel.

o Smears are stained with any of the Romanowsky

stains
• Lymph node biopsy smears
o Inject sterile normal saline into lymph node

preferably prescapular lymph node with the help

of a tuberculin syringe, massage and then
aspirate.
o It is risky to the operator

• Buffy coat smear

o The suspected blood is spun and the buffy coat is

examined for the presence of trypanosomes

• Biological test or animal inoculation test
o The suspected blood is injected intra peritoneally

into susceptible laboratory animals like white

rat, white mice, guinea pigs, rabbits .etc.,
o Cryptic (or) sub- clinical trypanosomes in blood

will multiply in these animals and cause death of

these laboratory animals- Mouse: 48-72 hours;
guinea pigs- 7 days; rabbits-60 days.
• Culture RPMI-1640,CAM
• Indirect test or Non-specific test to measure alteration
of serum proteins
o Mercuric chloride test

▪ Reliable for surra in camels only.

▪ This is done by adding one drop of suspected

serum into 1: 20,000 solution of mercuric

chloride.
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A white precipitate is formed. In infected

▪

camels , this test gives positive results in 2-3

weeks post infection
o Stilbamidine test

▪ Useful in bovine surra.

▪ 0.5 – 2.5 ml of freshly prepared 10 %

stilbamidine solution is taken in

agglutinating tubes and one drop of
inactivated serum is added.
▪ In positive cases, coagulation occurs on the

surface,begins to settle down in half a minute

and dissolves in 5-10 minutes.
o Formal get test

▪ Useful in camel surra.

▪ Two to four drops of formalin (40%) is added

to 1ml of suspected serum and allowed it to

stand .
▪ In positive cases, gel formation occurs in 2-3

hrs.
o Nitric acid test

▪ One ml of 1.7 % nitric acid test is added to

one drop of suspected serum.

▪ In positive cases, white floccules are seen.

• Examination of other fluids

o Cerebrospinal fluid will be examined in nervous

form for the presence of trypanosomes but it is

not important in veterinary practice.
o Aqueous humor will be examined in case of

blindness and in corneal opacity.

• Serological test
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o Some of the serological tests standardised are

indirect haemagglutination, gel Diffusion,
enzyme linked immunosorbant assay,
complement fixation test and flourescent
antibody test.
• Molecular test polymerase chain reaction (PCR)
and PCR- restricted fragment length
polymorphism (PCR-RFLP) are available for
diagnosis and to know strain variation.
IMMUNITY - Trypanosoma evansi

• The organism is notorious for the antigenic variation

phenomenon as trypanosomes constantly change
their antigenic character because of periodical change
of its surface coa also known as variable surface
glycoprotein(VSG).
• Since antigenic character of strain keeps on changing
the prospects of producing a vaccine against
trypanosomes is bleak.
TREATMENT - Trypanosoma evansi
• Tartar emetic 1.5 to 2 mg/kg in 10% saline as 2%
solution to be given by slow I/V administration.Death
may occur due to occlusion of dead parasites. Care
must be taken not to spill over sub-cutis, otherwise
cellulitis will result
• Suramin (Antrypol) 12 mg/kg as 10% solution I/V
injection
• Quinapyramines used as curative and prophylactic.
o Antrycide methyl sulphate
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It is soluble in water.
▪

▪ It is curative at the dose rate of 3 mg /kg

given as 10% solution by S/C route.

o Antrycide chloride

▪ It is insoluble in water and produces depot

under skin. This serves as prophylactic.

o Antrycide prosalt

▪ It is combination of both the above salts in

the ratio of 3:2 given at the dose rate of 7.4

mg/kg to be repeated after 8 weeks in fly -
borne areas.
▪ It is available by trade name Tribexin,

Triquin and the dose is 1.3 ml/kg maximum

of 10 ml.
• Diminazine(Berenil)
o It is given at @ 8-16 mg/kg B.W by deep I/M

route.
o This drug is well tolerated by cattle, less tolerated

by equines, camel and in dogs, general reaction

occurs.
CONTROL - TRYPANOSOMA EVANSI

• Surra is seasonal synchronizing with breeding of

tabanid flies. So control of tabanids and bush clearing
for malaria control have indirectly contributed much
to decrease the incidence of tryps.
• Chemotherapy of ailing and susceptible animal.
• Destruction of reservoir host (or) game animals.
• Chemoprophylaxis in horse 2-4 months with
Antrycide prosalt at 5 mg /kg.
• Breeding trypanotolerant breeds like – N’dama cattle.
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• Quarantine measures.
TRYPANOSOMA THEILERI

Synonym: T. himalayanum, Occult Trypanosome

• This occult or cryptic trypanosome cannot be usually

detected in bloodstream.
• Largest of the trypanosome.
• It is distributed worldwide occurring in cattle,
domestic and wild bovidae, antelopes and buffaloes.
• It is probably quite common but is rarely found in
blood smears.
• Usually it occurs in latent form. i.e., organism
occurring in lymph nodes.
• Organism is demonstrable only when blood is
cultured. So the trypanosome is called occult (or)
cryptic trypanosome.
• It exhibits rather rigid host restriction and does not
infect other mammals, especially laboratory rodents.
MORPHOLOGY - Trypanosoma theileri
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• It is large in size, ordinarily 60-70 µm long.( 15-34 µm

in T. evansi) Sometimes it is up to 120 µm and smaller
ones of 25 µm are occasionally found. Posterior end is
long and pointed.
• The kinetoplast is large sized and lies some distance
from the posterior and undulating membrane well
developed free flagellum well defined.
• Both trypomastigote and epimastigote may occur in
blood. Body is somewhat curved and is drawn to fine
point at posterior end. Important character in this
trypanosome is the possession of well marked
myonemes.
LIFE CYCLE - Trypanosoma theileri

• Life cycle is indirect.

• Multiplication occurs by binary fission in the
epimastigote form in the lymph nodes and in various
internal organs.
• Transmission is by cyclical transmission by tabanid
fly.
• Trypanosomes under go development in the hind gut
(posterior station) of the tabanid flies
like Tabanus and Haematopota (here the infective
metacyclic trypomasitgotes are found).
• Cattle are infected by contamination of the mucous
membrane with fly faeces containing the small
metacyclic trypomastigotes (Stercoraria).
• Intra uterine infection also occurs (organisms are
seen in the stomach of aborted).
PATHOGENESIS - Trypanosoma theileri
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• Usually considered non-pathogenic.

• But under condition of stress, splenectomy,
vaccination especially rinderpest, parasitaemia occur
resulting in serious symptoms and even death.
• Trypanosoma theileri is incriminated as the cause of
death in the cattle following rinderpest vaccination.
• Incubation period is 4-6 days.
• This infection is associated with nervous form like
turning sickness in Uganda.
• In such cases, organisms are found in the brain.
• The infection is associated with abortion and
depressed milk production in cows.
• Occasionally, it appears in peracute form due to
swarming infection leading to death as seen
in anthrax.
DIAGNOSIS - TRYPANOSOMA THEILERI

• As it is rarely seen in blood smear, diagnosis depends

on cultivation in a variety of media like NNN medium
(Novy, Macneel, Nicolle).
• The suspected blood is incubated at 27° C ,only
epimastigote form (or) crithidial form develops and if
incubated at 37°C, both trypomastigote and
epimastigotes are seen.
TREATMENT AND CONTROL - TRYPANOSOMA
THEILERI

• Treatment given for T.evansi can be tried and control

is by elimination of vectors.
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MODULE-7: AFRICAN ANIMAL

TRYPANOSOMOSIS

• African animal trypanosomosis (AAT) is a disease

complex caused by tsetse-fly
transmitted Trypanosoma congolense, T. vivax, or T.
brucei brucei, or simultaneous infection with one or
more of these trypanosomes. African animal
trypanosomosis is most important in cattle but can
cause serious losses in pigs, camels, goats, and sheep.
Infection of cattle by one or more of the three African
animal trypanosomes results in subacute, acute, or
chronic disease characterized by intermittent fever,
anaemia, occasional diarrhoea, and rapid loss of
condition and often terminates in death. In southern
Africa the disease is widely known as nagana, which is
derived from a Zulu term meaning "to be in low or
depressed spirits"— a very apt description of the
disease.
• African animal trypanosomosis is caused by protozoa
in the family Trypanosomatidae
genus Trypanosoma. T. congolense resides in the
subgenus Nannomonas , a group of small
trypanosomes with medium-sized marginal
kinetoplasts, no free flagella, and poorly developed
undulating membranes. In east Africa, T.
congolense is considered to be the single most
important cause of AAT. This trypanosome is also a
major cause of the disease in cattle in west Africa.
Sheep, goats, horses, and pigs may also be seriously
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affected. In domestic dogs,chronic infection often

results in a carrier state.
• T. vivax is a member of the subgenus Duttonella, a
group of trypanosomes with large terminal
kinetoplasts, distinct free flagella, and inconspicuous
undulating membranes. T. vivax is a large (18-26 μm
long) monomorphic organism that is very active in
wet-mount blood smears. Cattle, sheep, and goats are
primarily affected. Although this organism is
considered to be less pathogenic for cattle than T.
congolense , it is nevertheless the most important
cause of AAT in west African cattle. This trypanosome
readily persists in areas free of tsetse flies (for
example, in Central and South America and in the
Caribbean), where it is transmitted mechanically by
biting flies or contaminated needles, syringes, and
surgical instruments.
• T. brucei brucei resides in the
subgenus Trypanozoon. T. b. brucei is an extremely
polymorphic typanosome occurring as short, stumpy
organisms without flagella, long slender organisms
with distinct flagella, and intermediate forms that are
usually flagellated. Horses, dogs, cats, camels and pigs
are very susceptible to T.b. brucei infection. Infection
of cattle, sheep, goats and sometimes pigs results in
mild or chronic infection. This last observation,
although widely accepted, has been called into
question by Moulton and Sollod (13), who cite
evidence that this organism is widespread in east and
west Africa and that it can cause serious disease and
high mortality in cattle, sheep, and goats.
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Host Range
• Cattle, sheep, goats, pigs, horses, camels, dogs, cats,
and monkeys are susceptible to AAT and may suffer
syndromes ranging from subclinical mild or chronic
infection to acute fatal disease. Rats, mice, guinea
pigs, and rabbits are useful laboratory animals. More
than 30 species of wild animals can be infected with
pathogenic trypanosomes, and many of these remain
carriers of the organisms. Ruminants are widely
known to be active reservoirs of the trypanosomes.
Wild equidae, lions, leopards, and wild pigs are all
susceptible and can also serve as carriers of
trypanosomes.
Transmission
• In Africa, the primary vector for T. congolense, T.
vivax, and T. b. brucei is the tsetse fly. These
trypanosomes replicate in the tsetse fly and are
transmitted through tsetse fly saliva when the fly
feeds on an animal. The three main species of tsetse
flies for transmission of trypanosomes are Glossina
morsitans, which favours the open woodland of the
savanna; G. palpalis, which prefers the shaded habitat
immediately adjacent to rivers and lakes; and G.
fusca, which favours the high, dense forest areas.
Trypanosomosis is also mechanically transmitted by
tsetse and other biting flies through the transfer of
blood from one animal to another. The most
important mechanical vectors are flies of the
genus Tabanus, but Haematopota, Liperosia,
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Stomoxys, and Chrysops flies have also been

implicated. In Africa, both T. vivax and T. b.
brucei have spread beyond the "tsetse fly belts" (20),
where transmission is principally by tabanid and
hippoboscid flies. The vector for T. vivax in the
Western Hemisphere remains unknown, but several
species of hematophagous (especially tabanid and
hippoboscid) flies are believed to serve as mechanical
vectors.
Pathogenesis
• Initial replication of trypanosomes is at the site of
inoculation in the skin; this causes a swelling and a
sore (chancre). Trypanosomes then spread to the
lymph nodes and blood and continue to
replicate. Thus, there is a persistent infection that
results in a continuing cycle of trypanosome
replication, antibody production,immune complex
development, and changing of surface-coat
glycoproteins.Immunologic lesions are significant in
trypanosomosis, and it has been suggested that many
of the lesions (e.g., anaemia and glomerulonephritis)
in these diseases may be the result of the deposition of
immune complexes that interfere with, or prevent,
normal organ function. The most significant and
complicating factor in the pathogenesis of
trypanosomosis is the profound immunosuppression
that occurs following infection by these parasites. This
marked immunosuppression lowers the host's
resistance to other infections and thus results in
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secondary disease, which greatly complicates both the

clinical and pathological features of trypanosomiasis.
Clinical Signs
• Because simultaneous infections with more than one
trypanosome species are very common (18), and
simultaneous infection with trypanosomes and other
haemoparasites, the cardinal clinical signs observed in
AAT is anaemia. Within a week of infection with the
hematic trypanosomes
(Babesia spp., Theileria spp., Anaplasma spp.,
and Ehrlichia spp.) frequently occurs, it is difficult to
conclude which clinical signs are attributable to a
given parasite. Few adequately controlled studies have
been made, and thus a "typical" clinical response to
each trypanosome is difficult to reconstruct. What
follows is a summation of the syndromes observed in
field and experimental cases of trypanosomosis
caused by each of the three African animal
trypanosomes.T.congolense and T. vivax) there is
usually a pronounced decrease in packed cell volume,
haemoglobin, red blood cell, and white blood cell
levels, and within 2 months these may drop to below
50 percent of their preinfection values. Also invariably
present are intermittent fever, oedema and loss of
condition. Abortion may be seen, and infertility of
males and females may be a sequel. The severity of the
clinical response is dependent on the species and the
breed of affected animal and the dose and virulence of
the infecting trypanosome. Stress, such as poor
nutrition or concurrent disease, plays a prominent
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role in the disease process, and under experimental

conditions, where stress may be markedly reduced, it
is difficult to elicit clinical disease It is a haematic
trypanosome found only in the blood vessels of the
animals it infects. It does not localize and multiply
outside blood vessels. Infection with T.
congolense may result in peracute, acute, or chronic
disease in cattle, sheep, goats, horses, and camels.
Pigs often develop a milder disease; chronic disease
is common in dogs.
• The incubation period is followed by intermittent
febrile episodes, depression, lethargy, weakness, loss
of condition, anaemia, salivation, lacrimation, and
nasal discharge. As the disease progresses, loss of
condition and hair colour changes from black to
metallic brown are seen. The back is often arched and
the abdomen "tucked up." Accelerated pulse and
jugular pulsation occur and breathing is difficult.
Anaemia is a prominent sign. Early in the infection,
the organisms are readily demonstrable in blood
smears, but, as the disease progresses to its acute and
chronic forms, organisms are most readily
demonstrated in lymph node smears.T. vivax has a
variable incubation period, and, although it is
considered to be less virulent for cattle than T.
congolense, mortality rates of over 50 percent can
occur.There seems to be a marked variation in the
virulence of different strains of T.vivax, but it remains
the most important cause of trypanosomosis of
cattle,sheep, and goats in west Africa. It causes mild
disease in horses and chronic disease in dogs. T.
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vivax is often difficult to find in blood smears and can

also be demonstrated in lymph node smears.T. brucei
brucei has a relatively short incubation period and
causes severe to fatal infection in horses, camels,
dogs, and cats. It usually causes mild, chronic, or
subclinical disease in cattle, sheep, goats, and pigs.
• A febrile response occurs in the horse 4-14 days after
infection. This is followed by recurrent febrile
reactions. The heartbeat and respiration may be
accelerated, and loss of condition and weakness are
seen, whereas the appetite remains good. Progressive
anaemia and icterus, and oedema of the ventral
regions, especially the male genitalia, are
characteristic. The organisms are not always easily
perceived in blood smears and are best demonstrated
in tissue smears or sections, (e.g., lymph nodes).
Infected animals die in a few weeks or several months,
depending on the virulence of the strain of T. b.
brucei.The marked immunosuppression resulting
from trypanosome infection lowers the host's
resistance to other infections and causes in secondary
disease, which greatly complicates both the clinical
and pathological features of trypanosomosis.
Diagnosis
• Trypanosomosis should be suspected when an animal
in an endemic area is anaemic and in poor condition.
Confirmation depends on the demonstration of the
organism in blood or lymph node smears.In the early
phases of infection, especially with T. vivax and T.
congolense, the parasite can readily be observed by
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microscopic examination of a wet-mount of blood

slides. Thick blood films and stained with Giemsa are
also a good technique but in thin fixed blood films,
which are favoured for species identification,the
parasites may be hard to demonstrate. When
parasitemia is low, smears of buffy coat (obtained by
microhaematocrit centrifugation) can be useful for
demonstration of the parasites. Because T.
congolense tends to associate with the erythrocytes, it
is essential that buffy coat and adjacent erythrocytes
be included in the smear to ensure demonstration of
the parasite. Stained lymph node smears are a very
good method for diagnosis, especially for T.
vivax and T. b. brucei.
• In chronic T. congolense infection, the parasites
localize in the microcirculation of the lymph nodes
and in other capillary beds, allowing diagnosis by
examination of lymph node smears or smears made
with blood collected from the ear.
• Early in infection, blood smears are optimal for the
demonstration of T. congolense.These conventional
techniques of microscopic examination for the
presence of trypanosomes are still widely used, but
newer and far more sensitive methods are beginning
to supplant them. The antigen-detecting enzyme-
linked immunosorbent assay is extremely sensitive for
the detection of trypanosomosis in cattle and goats
and species-specific DNA probes have been shown to
detect simultaneous infection of cattle with T. vivax,
T. b. brucei, and T. congolense when conventional
methods revealed only single infections.
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Treatment
• Antrycide prosalt are still used and give effective
protection against infection in horses, camels, and
cattle for up to 3 months. The drug pyrithidium
bromide (Prothidium and AD2801) is useful in the
prophylaxis of T. vivax and T.congolense infections in
cattle, sheep, and goats and can give protection for up
to 6 months. The most widely used newer
chemoprophylactic drug (and also the least expensive)
is the isometamidium chloride . This drug, in use for
over 20 years and sold under the trade names
Samorin, Trypamidium, and M&B 4180A, is excellent
for the prophylaxis of all three African animal
trypanosomes, and gives protection for 3-6 months.
The development of resistance to this drug has been
reported in both east and west Africa. Homidium
bromide has also been found to be an effective
chemophrophylactic drug in Kenya, and the newly
introduced arsenical Cymelarsan is effective in
treatment of T. b. brucei infection.
• Fly eradication and drug prophylaxis are the only
effective trypanosomosis control methods now
available. Several approaches to fly control have been
used with varying degrees of success.Discriminative
bush clearing, extensively used in early tsetse fly
eradication campaigns, has been locally useful
because it eliminates the breeding places of the tsetse.
But, to be completely effective, bush clearing requires
ecologically unacceptable destruction of vast areas of
bush and forest. It is still a useful procedure when
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used locally in conjunction with other control

methods. Game elimination, and thus elimination of
the main source of bloodmeals for the tsetse, was used
in early eradication campaigns.
• A very widely used chemotherapeutic drug is
diminazine aceturate (Berenil), which is effective
against all the three African animal trypanosomes.
The isometamidium drugs are also excellent
chemotherapeutic agents as, are the quaternary
ammonium trypanocides, Antrycide, Ethidium and
Prothidium. Although extensively used in
trypanosomosis control, chemoprophylaxis is an
expensive, time-consuming, and thus unsatisfactory
long-term solution to the problem of African animal
trypanosomosis.
SLEEPING SICKNESS - MAN

• Sleeping sickness is a tsetse fly transmitted disease

seen in Africa and often results in swelling of the
brain.
Causes
• Sleeping sickness is caused by Trypanosoma brucei
rhodesiense and Trypanosomoa brucei gambiense.
The more severe form of the illness is caused by T.
rhodesiense. Tsetse flies carry the infection. When an
infected fly bites man, the infection spreads through
blood. The disease is endemic in Africa. The disease is
very rare in the United States, and is only found in
travelers who have visited or lived in Africa.
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Symptoms
General symptoms include:
• Anxiety
• Drowsiness during the day
• Fever
• Headache
• Insomnia at night
• Mood changes
• Sleepiness (may be uncontrollable)
• Sweating
• Swollen lymph nodes all over the body
• Swollen, red, painful nodule at site of fly bite
• Weakness
Examination and Tests
Physical examination may show signs of inflammation of
the brain and its covering, the meninges
(meningoencephalitis).
Tests include the following
• Blood smear
• Cerebrospinal fluid tests
• Complete blood count (CBC)
• Lymph node aspiration
Most antibody and antigen tests are not reliable as they
cannot differentiate between the current and past
infection. Specific IgM levels in the cerebrospinal fluid are
indicative.
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Treatment
Medications used to treat this disorder include:
• Eflornithine (for T. gambiense only)
• Melarsoprol
• Pentamidine
• Suramin (Antrypol)
• Some patients may receive combination therapy
Prognosis
• Without treatment, death may occur within 6 months
from cardiac failure or from T. rhodesiense infection
itself. T. gambiense infection causes the classic
"sleeping sickness" disease and gets worse more
quickly, often over a few weeks. Both diseases should
be treated immediately.
Possible Complications
• Complications include injury related to falling asleep
while driving or performing other activities, and
progressive damage to the nervous system. Sleep
becomes uncontrollable as the disease gets worse, and
eventually leads to coma. Inflammation of the heart
(myocarditis) may also develop.
Prevention
• Pentamidine injections protect against T. gambiense,
but not against T. rhodesiense. Because it is a toxic
drug, the use of this drug for prevention is not
recommended.
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• Insect control measures can help prevent the spread

of sleeping sickness in high-risk areas.
CHAGA'S DISEASE

• Chagas' disease (also called American

trypanosomosis) is caused by Trypanosoma cruzi.
This protozoan parasite is transmitted to humans and
other mammals by triatomine bugs, Triatoma,
Rhodnius, and Panstrongylus genera.
TRANSMISSION

• In Chagas-endemic areas, the main mode of

transmission is through an insect vector .A triatomine
bug becomes infected with T. cruzi by feeding on the
blood of an infected person or animal. During the day,
triatomines hide in crevices in the walls and roofs.The
bugs emerge at night, when the inhabitants are
sleeping. Because they tend to feed on people’s faces,
triatomine bugs are also known as “kissing
bugs”.After they bite and ingest blood, they defecate
on the person. Triatomines pass trypomastigotes
of T.cruzi parasites in feces left near the site of the
bite wound. Scratching the site of the bite causes the
trypomastigotes to enter the host through the wound,
or through intact mucous membranes , such as the
conjunctiva. Once inside the host, the trypomastigotes
invade cells, where they differentiate into intracellular
amastigotes. The amastigotes multiply by binary
fission and differentiate into trypomastigotes, which
are then released into the bloodstream. This cycle is
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repeated in each newly infected cell. Replication

resumes only when the parasites enter another cell or
are ingested by another vector.
• Dense vegetation and urban habitats are not ideal for
the establishment of the human transmission cycle.
However, in regions where the sylvatic habitat and its
fauna are thinned by economic exploitation and
human habitation, such as in newly deforested areas,a
human transmission cycle may develop as the insects
search for new food sources. T. cruzi can also be
transmitted through blood transfusions . Other modes
of transmission include organ transplantation,
through breast milk , and by accidental laboratory
exposure. Chagas' disease can also be spread
congenitally through the placenta. In 1991, farm
workers in the state of Paraíba, Brazil, were infected
by eating contaminated food. A 2007 outbreak in103
Venezuelan school children was attributed to
contaminated guava juice.
EPIDEMIOLOGY
• Chagas disease affects 8 to 10 million people living in
endemic Latin American countries, with an additional
300,000–400,000 living in non-endemic countries,
including Spain and the United States. An estimated
41,200 new cases occur annually in endemic
countries, and 14,400 infants are born with congenital
Chagas disease annually. About 20,000 deaths are
attributed to it each year. The disease is present in 18
countries on the American continents, ranging from
the southern United States to northern Argentina.
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Although Triatominae bugs feed on them, birds

appear to be immune to infection and therefore are
not considered to be a T. cruzi reservoir.
• The primary wildlife reservoirs for Trypanosoma
cruzi in the United States include opossums,
raccoons, armadillos, squirrels, woodrats and mice
• Screening of donated blood, blood components, and
solid organ donors, as well as donors of cells, tissues
and cell and tissue products for T. cruzi is mandated
in all Chagas endemic countries and has been
implemented.
CLINICAL SIGNS

• The acute phase , with high parasitaemia, commonly

lasts around two months. Most ofthe cases are a- or
oligosymptomatic, but depending on the inoculation
site,the first sign can be a skin chancre (chagoma) or
unilateral purplish orbitaloedema (Romaña sign) with
local lymphoadenopathies and fever over
severalweeks. That can be accompanied, among
others, by headache, pallor, myalgia,dyspnoea,
oedema in inferior limbs or face, abdominal pain,
cough,hepatomegaly, rash, painful nodules,
splenomegaly, generalized oedema,diarrhoea,
multiple lymphoadenopathies, myocarditis (chest
pain, heart failure)and more rarely
meningoencephalitis (seizures, paralysis). Morbidity
can be higher in children under five, elderly,
immunocompromised or in cases with possible high
parasite inoculum, such as seen in oral outbreaks. In
AIDS themeningoencephalitis is the more frequent
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manifestation (differential diagnosis with

toxoplasmosis).
• The chronic phase, with parasites hidden in target
tissues - especially heart and digestive smooth muscle,
hasdifferent possible clinical forms: a) asymptomatic
(indeterminate form), more frequent, typically in the
beginning of the chronic phase and lasting all life in
most of the patients; b) cardiac form, till 30% of the
patients, with conduction disorders, arrhythmia,
cardiomyopathy, heart failure and secondary
thromboembolism; c) digestive lesions
(megaoesophagus and megacolon) or mixed forms
(cardiac plus digestive), till 10% of the patients, just
seen south tothe Amazon basin.
LABORATORY DIAGNOSIS

• A blood wet smear or a blood concentration technique

such as microhaematocrit or Strout technique, must
be used. Stained preparations detect parasites when
parasitaemia is high (acute phase). In the chronic
phase, serologic tests should be used. A conventional
or recombinant enzyme-linked immunosorbent assay
(ELISA), indirect hemagglutination assay, indirect
immunofluorescence assay and western blot assay are
used. Especially for research purposes, haemoculture,
xenodiagnosis (faeces examination of uninfected
triatomine bug fed with the patient's blood) and
polymerase chain reaction (PCR) are also used.
TREATMENT
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• The etiological treatment is urgently indicated in the

acute phase and reactivation (immunosuppression).
At that moment parasitological cure rates are almost
100% and they decrease with longer duration of the
infection/disease. At younger age the prevalence of
side-effects is also lower. The etiological treatment is
indicated, as well, in congenital infection and early
chronic phase. In adults, especially those with
indeterminate form, etiological treatment should be
offered, but balancing potential benefits(to prevent or
delay the development of the Chagas disease) against
a long treatment schedule together with frequent side-
effects.
• The two available drugs are benzimidazole and
nifurtimox. Main contra-indications are pregnancy
and renal or hepatic failure. The side effects especially
with nifurtimox are psychiatric or neuronal disorders
(such as seizures) temporary side effects in many
patients including skin disorders, brain toxicity, and
digestive system irritation.
PREVENTION

There is not any available vaccine. A number of potential

vaccines are currently being tested. Vaccination
with Trypanosoma rangeli has produced positive results
in animal models.More recently, the potential of DNA
vaccines for immunotherapy of acute and chronic Chagas'
disease is being tested by several research groups.
Vector control
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• A yeast trap can be used for monitoring infestations of

certain species of triatomine bugs
• Promising results were reported with the treatment
of vector habitats with the fungus Beauveria
bassiana .
• Targeting the symbionts of triatominae through
paratransgenesis can be done
House improvement (such as plastered walls, cement
floors, corrugated-iron roofs) and personal preventive
measures(such as bed nets) and good hygiene practices in
food preparation, the transmission control through blood
transfusion and organ transplantation are important
Secondary prevention is important in congenital
transmission - diagnosis of infected pregnant women and
detection of possible newborn infection with
parasitological or serological tests after eight months of
age (with no longer existing maternal antibodies);
Laboratory accident prevention using safety standard
protocols (laboratory coat, gloves, face mask, cap,
glasses),especially when dealing with trypomastigotes are
essential

MODULE-8: GENUS-LEISHMANIA

Learning objective
In this module, the importance of Leishmania as a
zoonotic parasite, transmission, damages caused to
visceral organs by the multiplication of the parasite,
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diagnosis, complications in man, treatment and control

will be highlighted.
GENUS: LEISHMANIA

• World Health Organization (WHO)

declared leishmaniosis as one of the six important
infectious diseases of man.
• Members are primary parasites of mammals. It causes
disease in man, dogs, rodent, guinea pigs.
• It occurs in about 50 countries and there are about
400, 000 new human cases of leishmaniosis each
year.
• Leishmania sp is heteroxenous transmitted by sand
fly, Phlebotomus sp.
• It is found as amastigotes inside the mononuclear
phagocytic cells of various visceral organs (like
Kuppfer cells of liver, microglial cells of brain, etc) of
the vertebrate host and as promastigotes in the
intestine of sand fly and culture.
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VECTORS - LEISHMANIA

• Phlebotomus
argentipes and Lutzomyia sp. Phlebotomus
argentipes is common in Assam, West Bengal, Bihar,
Chennai , Kerala and Eastern parts of U.P.
STRUCTURE - LEISHMANIA

Amastigote stage
• It is structurally similar and they are small, spherical
or ovoid measuring 2.5-5 x 1.5 – 2 µ.
• The organism has oval nucleus which appears red,
bluish cytoplasm, kinetoplast, and tracer internal
fibrils.
• These are called as LD (Leishman - Donovan ) bodies.
• This is seen in MPS of vertebrate host.
• In the invertebrate host, promastigote form occurs
with flagellum and undulating membrane.
• One species and subspecies of Leishmania are
differentiated by a combination of clinical,
pathological, serological, biochemical, geographical
difference.
• Leishmaniosis occurs in different forms
o Visceral leishmaniosis (or) 'kala azar", "dum dum

fever", death sickness (or) tropical splenomegaly,

black fever - L. donovani complex. It is the most
serious form and potentially fatal if untreated.
o Cutaneous leishmaniosis or oriental sore (or)

"Delhi boil" (or) "Jericho boil" -

L.tropica complex. It is the most common form
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which causes a sore at the bite site, which heals in

a few months to a year, leaving an unpleasant
looking scar. This form can progress to any of the
other three forms.
o Diffuse cutaneous leishmaniois – this form
produces widespread skin lesions which resemble
leprosy and is particularly difficult to treat.
o Mucocutaneous lesihmaniosis -
(Espundia) L.braziliense complex.It commences
with skin ulcers which spread causing tissue
damage to (particularly) the nose and mouth

DEVELOPMENT IN THE INSECT- Leishmania

• Development takes place to promastigote from

amastigote. This takes about 3 days after blood meal.
• The promastigote migrates forward and blocks the
food channel when the fly attempts to feed, the plug of
organism is first injected into the mammalian host,
before the fly takes a blood meal.
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• Infection also occurs when infected sand flies are

crushed on the skin.
• Mechanical transmission by biting flies and needle
passage are possible.
• In India, mostly disease transmission is by crushing of
the vector flies on the body of the host.
VERTEBRATE HOST- LEISHMANIA
• Leishmania is found in macrophages and other cells
of reticulo- endothelial cells in skin, spleen, liver, bone
narrow lymph node, mucosa, etc.
• It may be found in the large mononuclear cells of
blood. It multiplies by binary fission in the amastigote
form.
• The parasitized macrophages spread the infection by
metastasis through bloodstream and set up visceral
leishmaniosis.
• After the development of amastigotes they are seen
free in lumen , then attach to mucosa in foregut and
hind gut of sand flies before inoculation into the
hosts.

CULTIVATION - LEISHMANIA

• Cultivation in NNN medium.

• Promastigotes develop in cultures.
PATHOGENESIS- Leishmania

• Kala azar is an important fatal disease of man in

India. In 1981, seven lakhs cases have been reported
from India. If untreated, 90% die and 15% if treated.
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Incubation period is 10 days to several months.

Clinical signs include irregular fever for months.
• Hypertrophy of spleen and liver with mortality 75-
90% (or) more in adults than infants splenomegaly
and hepatomegaly.
• They destroy the macrophage by their proliferation
(once in every 24 hours) parasites are seen for long
time in lymph nodes. It is called as reticulo -
endotheliosis.
• There is double rise in temperature within 24 hours.
• Anaemia, symptoms of malaise, head ache, occasional
abdominal pain, dysentery (or) diarrhoea are
common.
• Haemorrhages in mucous membrane of mouth and
nostrils.
• Skin darkens and hair tends to be brittle. Enlarged
spleen may occupy the entire abdomen.
• The characteristic feature of the disease essentially is
the reticulo endotheliosis, where the macrophages,
myelocytes and polymorphonuclear cells of bone
narrow are filled with parasites.
• The lymph nodes are usually enlarged. In
dogs, L.donovoni may cause either visceral or
cutaneous leishmaniosis but cutaneous forms are
more common.
• It is usually chronic, with low mortality and
sometimes acute highly fatal type occurs. Anaemia
and diarrhoea are terminal signs.
POST KALA AZAR DERMAL LEISHMANOID
(PKADL)
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• Some patients [about 10%] develop lesion up to 5 year

after apparently recovered from Leishmania infection.
• There is desquamation of skin, cutaneous ulcers,
especially in lips and eyelids called as post kala azar
dermal leishmanoid [PKADL].
• It consists of papules or macular yellowish
discoloration of the lesion on the face and other parts
of the body sometimes including mouth. The papules
are full of dividing amastigote.
• They are an important source for sand fly infection
particularly in India where the disease is not a
zoonosis.

MODULE-9: GENUS-LEISHMANIA
• Learning objective
• In this module, we will continue to know the
diagnosis, treatment and control of visceral
leishmaniosis and introduction to cutaneous
leishmaniosis.
DIAGNOSIS- LEISHMANIA

• Peripheral blood smear (or) thick blood smear.

• Culture of blood in NNN medium, chick embryo yolk.
• Biopsy from sternal (or) iliac lymph node
• Crest puncture for taking bone marrow or spleen
biopsy.
• Indirect method:
o Blood picture acute: Mild leucopaenia, slight

anaemia Chronic: Progressive hyper chromic

anaemia
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o Serological test Indirect haemagglutination,

indirect fluorescent antibody, complement
fixation test
TREATMENT- LEISHMANIA

• Pentavalent [pentostan] antimony compounds or

trivalent.
• Sodium stibogluconate by i/m route .- Drug of
choice.
• Pentamidine isothionate.
• Urea stibamidines toxic in canine infection-
Treatment is less effective.
CONTROL- LEISHMANIA

• Sand fly control with chlorinated hydrocarbons,

organo phosphorus chloride spray at breeding places.
• Insect repellants.
• Removal of decaying vegetation.
• Mosquito nets. Region where "kala azar" is zoonosis,
treat dogs.
• Destruction of stray dogs to remove reservoir hosts.
CUTANEOUS LEISHMANIASIS

• Synonym:
o Oriental sore, Aleppo button, Delhi boil, Jericho

boil and Old world cutaneous leishmaniosis.

• It is caused by L.tropica complex.
HOST- CUTANEOUS LEISHMANIASIS
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• Man, dog and rodents are the susceptible hosts.

• Gerbils act as reservoir host.
VECTOR- CUTANEOUS LEISHMANIOSIS

• Phlebotomus sergenti in India

DISTRIBUTION- CUTANEOUS LEISHMANIOSIS

• Pakistan, central and northern parts of India,

northern parts of USSR, Jordan, Iran, Iraq, America,
etc;
• In India, dry type of the disease is reported in Central
and Northern parts of India especially Delhi.
• Dry oriental sore is prevalent in hot dry climate.
CLINICAL PICTURE- CUTANEOUS
LEISHMANIOSIS

• This varies from locality to locality.

• In dry cutaneous form, incubation period varies from
few days to several months.
• Ulcers/ sores of classical type are found on the
exposed parts of the body.
• At first, they resemble the mosquito bite.
• Reddish papule persists with vesicle, grows slowly and
becomes covered with thick brown skin.
• Itching occurs.
• After some month (or) longer, connective tissue is
formed.
• A permanent scar is left.
• Lesions may coalesce to form large ulcer.
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• In USSR, moist type of cutaneous leishmaniosis is

encountered.
DIAGNOSIS- CUTANEOUS LEISHMANIOSIS

• Microscopic examination of material from edge of the

lesion
• Biopsy from proximal lymph node
• Culture in NNN medium
• Agar gel precipitation test, complement fixation test,
intra dermal test.
TREATMENT AND CONTROL- CUTANEOUS
LEISHMANIASIS

• As that of visceral leishmaniosis, metronidazole can

also be given.
• Control is as that of visceral leishmaniosis

MODULE-10: ORDER-
TRYCHOMONODIDA; FAMILY-
TRYCHOMONODIDAE;
• Learning objective
• The protozoa Tritrichomonas foetus causes severe
economic loss in dairy industry as it causes abortion
in cattle. The bulls become sterile and cows will give
rise to stillbirths.
GENUS - TRITRICHOMONAS FOETUS

• Synonym: T.foetus. T.bovis. T.genitalis T.vitulae,

T.mazzanni
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HOST - TRITRICHOMONAS FOETUS

• Ox, Zebu, possibly pig and horse.

DISTRIBUTION - TRITRICHOMONAS FOETUS

• World wide.
• Prevalence in the US is probably third to brucellosis
and leptospirosis as a cause of abortion in cattle.
• It has been reported from West Bengal, Bihar,
Rajasthan , Jammu and Orissa in India.
MORPHOLOGY- TRITRICHOMONAS

• The body is spindle to pear shaped, 10-25 X 3-15µ in

size. They are actively motile.
• The parasite has three anterior flagella of equal
length. The posterior flagellum which trails as a free
flagellum is as long as anterior flagella.
• The undulating membrane extends almost the full
length of the body and there is an accessory filament.
Costa is prominent.
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• The axostyle is thick hyaline with a capitulum (slightly

enlarged anterior end) and chromatin ring at its point
of emergence from the position end.
• The para basal body is sausage shaped and ring
shaped. Parasite’s anterior end is rounded and
posterior end is pointed. There is no pelta .
• The organism has single nucleus. It multiplies by
longitudinal binary fission.

TRANSMISSION - Tritrichomonas foetus

• Naturally by coitus.
• By improper artificial insemination with dirty gun and
contaminated sheath- rare-iatrogenic.
• Examination with contaminated vaginal speculum.
SITE OF PREDILECTION - TRITRICHOMONAS
FOETUS

• Bull -Preputial cavity.

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• Cow -Throughout the genital tract, abomasum of

foetus, uterus and intermittently the vagina.
• Incubation period is variable about 15 days.
PATHOGENESIS-COW- TRITRICHOMONAS
FOETUS

• The organism inhabits the preputial cavity of the bull

and transmission to the cow occurs during coitus or
natural service.
• Trichomonads reach the uterus via cervix to produce a
low grade endometritis.
• After infection, organisms multiply in vagina causing
vaginitis, then invade uterus, oedema of endometrium
and intermittent vaginal discharge. [Organisms are
found in the amniotic and allantoic fluid]
Subsequently, cows appear to self cure and in most
cases appear to develop a sterile immunity.
After foetus development
• The organism may invade the foetus, cause placentitis
with detachment of placenta and death of foetus.
• Early abortion at 1-16 weeks after successful breeding
is very characteristic of this infection.
• Early embryonic death and abortion:
o If the infection occurs in 1-2 weeks after breeding,

foetus with all membrane passes out.

Pyometra and sterility
• If the infection occurs 8-16 weeks, foetus with all
membrane may not be completely eliminated.
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• Corpus luteum and cervical seal of pregnancy is

retained leading to maceration of foetus, chronic
catarrhal or chronic purulent endometritis usually
ending in permanent sterility.
Sequelae of the infection
• If placenta and foetal membrane are expelled
completely, spontaneous recovery follows. This is
most common.
• The animal will be anoestrous.
• Persistent uterine discharge occurs especially when
animal lies down. At times cervix is closed, with
persistent corpus luteum, closed pyometra results.
• Late abortion after 6 months is rare.
• Uterus is filled with large volume of thin greenish
white odourless material with swarms of
trichomonads in it.
• Due to anoestrous, owner may think that the animal is
pregnant.
• In long standing cases, the trichomonads may
disappear from the uterine fluid.
• Normal gestation and calving may occur in infected
animal but it is rare.
• Cows may remain carrier for a year. Persistence of
infection or pre patent infection is rare.
BULL- TRITRICHOMONAS FOETUS

• Bulls, once infected, remain carriers . The male

reproductive organs like testes, epididymis and
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seminal vesicles are involved. Spontaneous recovery

is rare.
• The infection shall be regarded as a permanent source
of infection. Infected bulls suffer from swelling of
prepuce and remain permanently infective unless
treated.
• No gross lesions are noticed in bull. And the infection
does not affect vitality of sperm and fertility of bull.
• Clinical signs in bulls include painful micturition,
disinclination to serve, reddish nodule on mucosa,
and mucopurulent discharge.
DIAGNOSIS - TRITRICHOMONAS FOETUS

• Herd history- failure to conceive even after repeated

breeding.
• Examination of preputial washing [rarely in semen],
vaginal, mucopurulent discharge from uterus, vagina.
Uterine discharge from aborted animal (or) 2-3 days
before next oestrous period collected and examined.
• Contents from aborted foetus, stomach , abomasum,
placenta, amniotic or allantoic fluids following
abortion
• Culture in CPLM (cysteine- peptone liver extract
maltose serum) BGPS (beef extract glucose, peptone
serum) (or) Diamond’s media, kidney tissue
monolayer, chorio-allantoic membrane of chicken
embryo.
• Serological test, cervical mucus agglutination
test, intra dermal test
• Conduct several examinations before the animal is
declared as positive or negative. A bull can be
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considered negative if it is negative for organisms in at

least six examinations done at weekly intervals and he
is bred to two (or) more virgin heifers and they also
remain negative.
• A cow can be considered negative after at least three
negative examinations and she has two normal
oestrous periods and subsequently conceives and
bears a normal calf. She should be bred by AI to avoid
infecting the bull.
TREATMENT - TRITRICHOMONAS FOETUS

• Ordinarily trichomonosis is self- limiting in cows,

hence treatment is unnecessary. No satisfactory
treatment is known.
• Breeding rest is important followed by artificial
insemination to avoid infecting a clean bull.
• Treatment of bull is not advocated as it is tedious and
time consuming unless bull is valuable.
• Slaughter is the best option.
Some of the treatment options for valuable bulls are
• Trypan blue or acriflavin in an ointment base can be
applied on the penis and prepuce and 30 ml. of the
solution is also injected into prepuce
• Diminazene 100 – 150ml of 1% solution injected into
prepuce for 5 days
• Dimetronidazole - 50 mg /kg for 5 days orally,
single i/v dose of 50 mg/ kg (or) i/v injection 10
mg/kg daily for 5 days. Similar dose for cows can be
tried.
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CONTROL - TRITRICHOMONAS FOETUS

• Proper herd management.

• Slaughter of infected bull.
• Adopt strict A.I after breeding.
• Strict sterile vaginal examination.
• Examination of bulls before service.
• Use of communal bulls is discouraged.
• Use of clean bulls for artificial insemination.
• They should be examined for T. foetus before
purchase and the herd from which they originated
should be studied at the same time.
• In addition, they should be examined at weekly
intervals while in use.
• Freezing of semen with glycerol appears to be toxic to
trichomonads at refrigeration temperature not in
incubation temperature (37o C).
IMMUNITY - TRITRICHOMONAS FOETUS

• Cows or heifers that recover from infection are usually

relatively immune although re- infection can occur
due to a different serologic strain of T. foetus.
• There is little evidence of bulls becoming immune to
infection and organism persists for life in them.
TRICHOMONAS GALLIINAE

• The protozoan Trichomonas gallinae is a

cosmopolitan parasite of pigeons and doves. Other
birds such as domestic and wild turkeys, chickens,
raptors (hawks, golden eagle, etc.) may also become
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infected. The disease in pigeons is commonly called

"canker". A similar condition in falcons is called
"frounce.In 2005, Trichomonas gallinae was first
recognized as a cause of disease in British finches,
with Greenfinch and Chaffinch most affected,
although a range of garden birds have been found to
be susceptible to the parasite. Recent studies have
shown that up to a third of adult wood pigeons in
Spain may carry the disease.

Life cycle
• T. gallinae is generally found in the oral-nasal cavity
or anterior end of the digestive and respiratory tracts.
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The trichomonads multiply rapidly by simple division

(binary fission), but do not form a resistant cyst. They
therefore, die quickly when passed out of the host.
Transmission
Transmission of the parasite from one bird to another
occurs in one of three ways:
1. Infected parent feeding young
2. Contaminated drinking water
3. Infected bird is a prey meal for another bird (raptors
most commonly)
Pathology
• Avian trichomonosis is principally a disease of young
birds. T. gallinae varies greatly in its virulence. The
severity of the disease depends on the susceptibility of
the bird and on the pathogenic potential of the strain
of the parasite. Adult birds that recover from the
infection may still carry the parasite, but are resistant
to reinfection. These birds do not show obvious signs
of infection. Interestingly, infection and mortality
rates are not closely linked. The disease varies from a
mild condition to a rapidly fatal one with death in 4–
18 days post infection.
• In young birds, the early lesions appear as small white
to yellowish areas in the mouth cavity, especially the
soft palate. The lesions consist of inflammation and
ulceration of the mucosal surface. The lesions increase
in size and number and extend to the oesophagus,
crop and proventriculus. The lesions may develop into
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large, firm necrotic masses that may block the lumen.

Occasionally, the disease may spread by penetrating
the underlying tissues to involve the liver and other
organs.
• The early lesions in the mouth are small, yellowish,
circumscribed plaques on the mucosa. More velogenic
strains can cause caseated abscessation of the
oropharynx. Eventually these space occupying lesions
obstruct the oesophagus and trachea resulting in
emaciation and asphyxiation.
• Although lesions are usually seen in the mouth and
oropharynx in raptors, it can also affect other mucus
membranes. According to a report,an owl having eye
lesions from oral infection spreading into the
nasolacrimal duct. Bony involvement can occur after
soft tissue destruction. The organism does not survive
posterior to the proventriculus, except in pigeons.
Unlike other birds infected with T. gallinae, pigeons
are susceptible to secondary organ invasion by
virulent strains of the parasite. The visceral form of
the disease involves the liver and gastrointestinal
tract, causing organ dysfunction.
Symptoms
• In acute cases, there may be little indication that the
bird is infected, and death may occur quite suddenly.
In other cases, infected pigeon squabs may stop
feeding, lose weight, look ruffled and dull, and be
unable to stand or maintain their balance. Erosion of
the papillae on the palatal flaps is a good sign of
infection. Birds may have difficulty swallowing and
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breathing due to the cheese- like deposits in the

mouth lining and down the oesophagus and trachea.
• Diarrhoea may also occur. Death may occur within
three weeks of infection. Greenish fluid or cheesy
material may accumulate in the mouth and crop, and
this material may exude from the beak. A pendulous
crop may develop in turkey poults and chickens.
Diagnosis
• Diagnosis can be accomplished by clinical signs and
direct exam or culture. Clinical signs of trichomonosis
include pronounced swallowing motions, excessive
salivation and caseous-diphtheritic membranes of the
mouth, crop and pharynx. Characteristic yellowish-
white nodules in the oral cavity, oesophagus and crop
strongly suggest trichomonosis. The infection is
confirmed by finding the organism during
microscopic examination of the greenish fluids,
cheesy material or the lesion.
Treatment
• Antiprotozoal medications, such
as dimetridazole and metronidazole, are commonly
used to treat birds infected with T. gallinae.
Treatment usually is successful after 1–2 days. A new
culture system called InPouch has practical
advantages over the usual in vitro system. If a bird is
dyspneic or cannot swallow food, oral plaques can be
removed with thumb forceps.
Prevention
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• Trichomonosis can be controlled in a flock by culling

or treating carrier birds. Food and water sources, as
well as bird baths, should be cleaned regularly and
protected from contamination by wild pigeons and
other birds.
• Generally parasitic trichomonads cannot survive
drying out. Cleaning feeders and bird baths and
leaving them dry for a week may help in decreasing
spread of disease although natural infections probably
occur in the wider environment. Some related
trichomonads form cysts resistant to drying.
• Bird diseases such as trichomonosis rarely, if ever,
affect people; but it is sensible to take care when
handling bird feeders by good hand washing after
tending the feeders, or wearing suitable disposable
gloves. From the sources used, there have been no
reports of Trichomonas gallinae infecting humans

MODULE-11: FAMILY-
MONOCERCOMONADIDAE

• Learning objective
• Histomonosis is an important protozoan disease
caused by Histomonas meleagridis. This protozoan is
much known in turkey rearing areas where the young
one of turkeys ,poults die in large number so that it is
very difficult to rear turkey and poultry together in
mixed farming concept
HOST- HISTOMONAS MELEAGRIDIS
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• Turkey, chicken, Japanese quail – pea fowls, guinea

fowl and various other gallinaceous birds.
LOCATION - HISTOMONAS MELEAGRIDIS

• Caecum and liver.

DISTRIBUTION - HISTOMONAS MELEAGRIDIS

• It is worldwide in distribution.
• It is the most important disease of turkey causing
heavy loss.
• Prevalence is common in chicken although incidence
of disease in them is low.
MORPHOLOGY - HISTOMONAS MELEAGRIDIS

• It is pleomorphic in appearance.
• The morphological appearance depends on location
and stage of disease; the forms in the tissue have no
flagellum although the granule is found near the
nucleus.
• Four forms have been described:
o Invasive forms: These are found in early caecal

and liver lesion and are at the periphery of old

lesion. They are extracellular, 8-17 mm long and
actively amoeboid.
o Vegetative forms: These are found near the

centre of the slightly older lesions. They are less

active. They are found often packed together and
cause disruption of tissue. They are large sized
(12-21 x 12-15µm).
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o Resistant forms: They are enclosed in a dense

membrane but it is not a true cyst measuring 4-11
µm in diameter. They are extra cellular but may
be engulfed by phagocytes (or) giant cells.
o Flagellar forms: It is present in lumen of caecum

and cultures. They are amoeboid, 5-30 µm in

diameter.
• Cytoplasm may contain bacteria and other food
particles. Occasionally food particles include RBC.
• There is single vesicular nucleus with dense
karyosome. Near the nucleus is a basal granule (or)
kinetosome from which flagellum arises.
• The flagellum is typically simple and short but as
many as four are reported.
• Flagella produce jerky oscillary movement resembling
that of trichomonads. No undulating membrane is
seen.
LIFE CYCLE - HISTOMONAS MELEAGRIDIS

• Reproduction is by binary fission and there is no

evidence of sexual cycle.
• The naked trophozoites are delicate and do not
survive more than a few hours when passed in faeces.
• Turkeys can be infected by ingesting trophozoites and
this mode of infection plays a part in transmitting the
parasite once disease has appeared in a flock.
• However, large numbers of the parasites must be
ingested. Protozoa of caecal origin are about 100
times as effective in producing histomonosis in
turkeys as those of liver origin and pre-treatment with
bile renders the latter non-infective.
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MODE OF INFECTION - HISTOMONAS

MELEAGRIDIS

• The most important mode of transmission is in the

eggs of caecal worm Heterakis gallinarum.
• Its discovery by Smith and Graybilll (1920) was a
milestone in the history of parasites.
• Protozoa first invade the germinal zone of the
nematode ovary where they multiply extra cellular
and penetrate the developing oocysts.
• They feed and divide both here and in the newly
formed eggs becoming gradually smaller.
• Earth worms can transmit both Heterakis sp.
and Histomonas sp. and are probably important for
the long time survival of the Histomonas in soil.
EPIDEMIOLOGY - HISTOMONAS MELEAGRIDIS

• Chicken are reservoir hosts for turkeys. So this

accounts for the fact that it is almost impossible to
raise turkeys successfully on the same farm with
chicken.
• Infective Heterakis eggs can survive for 1-2 years (or)
even longer.
• Earth worms can harbour infected Heterakis larvae
for a long time and act as a source of infection to
birds.

MODULE-12: HISTOMONOSIS IN BIRDS

Turkeys - Histomonas Melegridis

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• Disease is called as histomonosis, black head

infection, entero- hepatitis (or) typhlo- hepatitis.
• It affects turkeys of all age groups.
• Poults of 3-12 weeks are severely affected.
• Mortality is 100%. The birds die with 2-3 days after
showing first signs of disease. Poults less than three
weeks are refractory.
• Adult birds suffer mostly a chronic disease.
• Recovery may take place.
• Mortality is low and decreases with age.
CHICKEN - HISTOMONAS MELEAGRIDIS

• They are less susceptible and show no signs of disease

but serious outbreaks are reported in very young
birds.
OTHER BIRDS - HISTOMONAS MELEAGRIDIS

• Japanese quail is not a suitable host but can be

infected.
• The disease is occasional in pea fowl.
• Histomonads are released in caecum from the larva
of Heterakis gallinarum.
• They enter (or) invade wall and multiply in one or
both caeca causing small raised pinpoint ulcers with
numerous organisms.
• Ulcers become enlarged and involved the whole caecal
mucosa. Caecum contains a hard caseous adherent
coat.
• There is enlargement of caecum with haemorrhage.
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• Organisms invade deeper into mucosa and gain entry

into bloodstream.
• Later they reach liver through bloodstream.
• Incubation period is 15-21 days.
LIVER - HISTOMONAS MELEAGRIDIS

• There is focal necrosis which increases by peripheral

extension to produce a characteristic circular
depressed lesion (saucer shaped lesions).
• Lesions are yellow to yellowish green area of necrosis
with grayish peripheral region with radiating streaks
of necrosis.
• The size of lesion may be one cm or more. Such
lesions are formed in deeper tissues of liver/ these
lesions are not encapsulated but merge with healthy
tissue.
• Kidney and lung are occasionally affected.
Histopathological examination reveals presence of
parasites.

CLINICAL SIGNS - HISTOMONAS MELEAGRIDIS

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• There is droopiness among birds. Birds appear

drowsy with ruffled feathers, drooping wing and tail.
• Typical signs include sulphur yellow coloured
droppings.
• Head may or may not be darkened, cyanosis of comb
and wattle, hence the name black head.
• Similar conditions may occur in other diseases of
birds.
• Parasites disappear from tissues and the repair takes
place. There may be extensive scar tissue.
IMMUNITY -HISTOMONAS MELEAGRIDIS

• Birds which recover are immune to reinfection.

• Susceptibility decreases with age.
• Rectal inoculation of the culture stimulates immunity.
DIAGNOSIS - HISTOMONAS MELEAGRIDIS

• Clinical signs are not confirmatory.

Post mortem lesions
• Typical lesion in liver are pathogonomonic.
• Demonstration of parasites histopathologically in liver
lesion and caecal lesion.
• Examination of caecal scrapings and liver lesions.
TREATMENT - HISTOMONAS MELEAGRIDIS
• Effective drugs are carbarsone ,nitrarsone (Histostat
50) and furazolidone (NF 180) 0.01-0.02% -as
preventive dose. 0.04% - as curative dose
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• Enhepatin-7 in drinking water 0.05% - as preventive

dose 0.1% - as curative dose.
• Nithiazide (0.02%) is more potent and less toxic.
• Dimetronidazole – 0.0125% in feed ,Ronidazole-
0.0045-0.006% in water for 3 weeks
• Promidazole -0.025% in feed
CONTROL - HISTOMONAS MELEAGRIDIS
• Proper management.
• Never raise turkey and poultry together.
• Young turkeys should be separated from adults.
• Same attendant should not be used for chicken and
turkeys.
• Birds should be reared on sandy soil to prevent the
infection through Heterakis and earthworms.

MODULE-13: SUB-PHYLUM-
SARCODINA; FAMILY-ENDAMOEBIDAE;
Learning objective

Amoebosis, a zooanthroponotic disease, is primarily a disease of

humans, produces dysentry of animals in close proximity to
mankind.

ENTAMOEBA HISTOLYTICA
▪ Sub Phylum: Sarcodina
▪ Order: Amoebida
▪ Family: Endamoebidae
▪ Genus: Entamoeba
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▪ Species: E. histolytica
• Members are parasitic in intestines of vertebrates and
invertebrates.
• Genera are differentiated on basis of nuclear structure.
• This genus contains parasites of domestic animals and man
but only one of these contains pathogenic species.

GENUS: ENTAMOEBA
• They have vesicular nucleus with comparatively small
endosome located at or near its centre with or without
periendosomal granules around the endosome and with a
varying number of granules around periphery of the nucleus.
• Cysts are usually formed.
• Four groups are recognized based on the size, hosts and
pathogenesis.
o Histolytica group
o Coli group
o Bovis group
o Gingivalis group
• It is a typical example of zooanthroponosis.
• The disease is intestinal amoebosis or amoebic dysentery,
hepatic or extra -intestinal amoebosis.
• It is worldwide in distribution.

HOSTS - ENTAMOEBA HISTOLYTICA

• Man and other primates like orangutan, gorilla,

chimpanzee, gibbons, dog, cats, rats, pigs and rarely
cattle.
LOCATION -ENTAMOEBA HISTOLYTICA
• Large intestine especially colon, occasional small intestines
liver, lung, spleen, brain and sometimes in skin.
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PREVALENCE- ENTAMOEBA HISTOLYTICA

• Most as a parasites of man, it is second to Giardia lamblia in
U.S.
• It is more prevalent in tropics and sub- tropics than in cooler
climates and an average of 18% human cases positive by only
1/5 of them show clinical symptoms.

• Large and small trophozoites are present.

• Large trophozoites are 20-30 µm and pathogenic.
• Those of small trophozoites are 12-15 µm.
• They have a thick layer of ectoplasm and granular
endoplasm.
• They move rapidly when warm, usually moving forward in a
straight line with a single clear pseudopod at the anterior
end.
• Trophozoites often ingest RBCs.
• The nucleus is vesicular, has a central endosome and a ring
of peripheral granules with a few scattered chromatin
granules in between.
• Cytoplasm is granular with food vacuoles containing bacteria
and RBCs.

CYST- ENTAMOEBA HISTOLYTICA

• Cysts of large and small races are 10-20 um.
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• They have four nuclei when mature and often contain rod-
like chromatid bodies with rounded ends.
• Diffuse glycogen is present in young cyst and absent in
mature cyst.
• The cyst wall is visible in living specimen but not seen in
stained preparations.
• It is about 0.5 µm thick, initially uninuclear but later four
nucleated.

LIFE CYCLE- ENTAMOEBA HISTOLYTICA

• It is direct (homoxenous).
• Infection is by ingestion of cyst in food and water with faecal
cyst contamination through fly transfer.
• Trophozoites multiply by binary fission.
• Excystation occurs in small intestine and tetra nuclear
metacystic forms come out.
• Following division of nucleus and cytoplasm from this stage,
it undergoes series of nuclear and cytoplasmic division
resulting in production of eight small uninuclear amoebulae
(or) amoebae.
• These pass into large intestine and grow bigger feeding on
bacteria, tissue debris, RBCs, etc.
• These trophozoites remain in lumen and invade tissues,
multiply by binary fission in preparation to encystment.
• They are active with pseudopodia moving and feeding.
• The amoebae divide producing smaller forms, expel food
particles, round up and cease to feed and then encyst to
become uninucleate cyst.
• Following nuclear division, it becomes first binucleate and
then finally quadrinucleate cyst is produced.
• These have chromatoid bodies and glycogen vacuoles.
• They become mature cysts possessing chromatoid bodies (no
glycogen vacuoles).
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• Cysts are passed in faeces in all stage of development but

apparently only quadrinucleate forms which represent
mature stage remain viable and are capable of inducing new
infection.
• It is the most infective stage.
• When ingested by susceptible host metacystic stages emerge
following which eight amoebulae are released.
• In formed stool, especially from chronic infection, cysts are
passed in stool.
• In diarrhoeic stool, i.e. in acute infection, vegetative forms
(trophozoites) are passed especially in flacks of mucus (or)
blood clots.

MODULE-14: ENTAMOEBA HISTOLYTICA

• Learning objective
• The pathogenesis of amoebae in man as well as in animals
are elaborated and a short account of Giardia which is a less
known pathogen in animals is given.

PATHOGENESIS- ENTAMOEBA HISTOLYTICA

• Large forms produce considerable pathogenesis.
• Trophozoites are the invasive stage.
• They invade epithelial cells cause lysis and pressure atrophy.
• The mechanism of invasion is not clearly understood,
penetration of intestinal epithelial cells brought about by
proteolytic enzymes- pepsin and trypsin but not
chymotrypsin in E.histolytica .However these enzymes are
present in non pathogeneic strain also.
• Meerovitch (1977) considered the intial destruction of
mucosal cells results from the action of potent
phosphohydrolases released from an amoebic surface
liposome’s following contact between cells and parasites.
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• It has been found that the intestinal flora like Aerobacter

aerogenus and Escherchia coli aid in establishment and
invasion of tissues.

INTESTINAL AMOEBOSIS
• Following invasion of epithelium amoeba multiply to form
small colonies and then penetrate into deep mucosa, reach
submucosa and even into muscularis where they are spared
laterally.
• They undertermine mucous mem,brane and produce a
pathgnomonic flask shaped ulcers which has a narrow canal
or neck leading to lumen of the bowel and a dilated distal
part in submucosa and eventually to intestinal wall becomes
sagged.
• Principal site of initial lesionis seen in vermiform
appendix and ascending colon.
• These lesions show little cellular reaction whereas
every bacterial invasive process leads to the lytic necrosis. -
lesions may remain confined to mucosa – repair may keep
pace with disappearance of of protozoa resulting in
spontaneous elimination of organisms.

AMOEBIC GRANULOMA
• Amoebae penetrate more deeply into intestinal wall with
invasion of bacteria, hyperaemia, inflammation, neutrophilic
infiltration- ulcers form (amoebae found chiefly at periphery
of ulcers in contact with a healthy tissue and/or ulcers filled
with necrotic tissue (hyaluronidase possibly assists in
pathogenicity of organism) causing peritonitis their in to
perforation extraintestinal - systemic locations.

EXTRA INTESTINAL AMOEBOSIS

Hepatic amoebosis
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• Amoebae may invade other tissue almost all soft tissues, the
commonest location being liver especially right lobe (as it is
close to ascending colon) via lymphogenous (or)
haemotogenous route or by extension.

LYTIC NECROSIS

• Amoeba trapped in thrombi in inter- lobular vein-

lysis of the wall of the vessels - lesions increase in size-
enlarged one (or) two may form hepatic amoebic
abscess.
• Fibrous wall is produced over abscess in chronic
cases.
• Amoebae may also be seen in lungs, brain, spleen and
rarely skin (amoebic cutis). since intestinal and
liver lesions show remarkable absence of cellular
infiltration, it has been suggested to be indicative of
local (or) central immunodepression i.e amoebic
disease must be proceeded by a degree of
immunodepression as immune responses are
important in limiting invasion of amoebae.
• Prepatent period: 1-5 days.
• Incubation period: 4 days – one year.
AMOEBOSIS IN ANIMALS
• Dog, kitten, guinea pig and mice infected experimentally.

Kitten

• Highly susceptible through oral and rectum routes.

• Acute amoebic dysentery with extensive ulceration of bowel
wall.
• No encystment.
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Dogs

• Natural infection recorded – caecum. symptomless course

due to contact with infected human content.

Cattle

• Two reports – one in dysentery another in the lung of young

zebu at slaugher an account of generalized streptothricosis.
• Amoebosis possess considerable biosafety concerns in
laboratories.
• Colonies of chimpanzea.

Rats

• Rat infection reported.

SYMPTOMS- ENTAMOEBA HISTOLYTICA

• Acute, sub acute and chronic common.
• Acute blood mucous.
• Tenderness over colon, liver colic, loose morning stool.
• Mucous coated (or) mucous diarrhoea frequent but recurrent
diarrhoea sometimes with blood dysentery alteration in
bowel movements.
• Loss of weight, fatigue, offensive odour, deep invasive types,
tenesmus, alteration in bowel habits.
• Vague subjective symptoms like loss of weight, fatigue and
fulmunative dysentery.

EPIDEMIOLOGY- ENTAMOEBA HISTOLYTICA

• It is primarily a pathogen of man and primates.
• Man act as R/H host for domestic animal.
• Infection by ingestion of cyst ,trophozoites don’t survive long
outside the host. validity ½ - 2 hrs.
• Hence infection is by ingestion of cysts.
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• Cyst relatively resistant producing –clinical cases.

• 2 weeks in stool at room temperature
• 2 months in refrigerator
• Up to 5 weeks in water at room temperature
• Thermal death point 500 C
• Desiccation: rapidly fatal
• Water chlorination does not affect cyst but can be removed
by sand filtration.
• Cysts transmitted through food, water, raw vegetables
cultivated with night soil sewage, various
flies Musca, Lucilia capable of food or water -borne
transmitted in vomitus.
• Major outbreak of human amoebosis plumbing of drinking
water system may cause contamination of drinking water
with sewage where cross seepage between water and sewage
pipes laid in most ditch prevalent in tropics.
• Poor sanitation and personal hygiene.
• Food handlers may play an important role in transmission of
amoeba even though cysts rarely survive > 101 in hands
except under finger nails –onycophagia – sexual contact is
more common than water contamination in homosexuals.

ENVIRONMENTAL FACTORS - ENTAMOEBA

HISTOLYTICA
• Bacterial flora stabilises intestinal environment for
trophozoites and provides food for them.
• Note: spices, chilly, irritant food and cholesterol rich food
increase amoebosis

DIAGNOSIS - ENTAMOEBA HISTOLYTICA

• Clinical
• History evidence in endemic area
• Symptomatology
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• Other investigation
• Sigmoidoscopy: Appearance of mucosa of large intestine
• Skiagram: hepatic, intestinal pulmonary
• Therapeutic
• Cultural methods; special medium
• Demonstration of presence of parasites:
o Diarrhoeic stool –tropozoites-actively motile. With
addition of drop of iodine , cysts can be seen.
o Haematoxylin stain – fixed in Schaudinn's fixative is
also recommended.
• Coproscopy: stained with Heidenham’s iron haematoxylin-
faecal smears.

Direct Smear Examination

• Trophozoites/ vegetative stage: present in warm saline-

actively motile-pseudopodia-ideal mostly- flakes of mucous
with blood clots
• Cysts: characteristic, in formed stools- to facilitate easy
detection add to sample a drop of iodine solution i.e
saturated iodine with 1% KI.
• Concentration by ZnSo4(other floatation fluids sugars, salt
cause distortion and cysts. FTE sediment(formalin triton
ether) merthiolate iodine formaldehyde concentrate MIFC.
• PVA technique-Marshall.
• Scholten (1972) technique.

Staining Faecal Smears

• Fix in Schaudinn’s solutions stain by Heidenhams iron

hemotoxylin

Culture

• Various media: dibasic coagulated. e.g. slant overlaid with

Locke’s solution.
• Diamond’s medium
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Animal Inoculation

• Kittens, hamsters.

Immunodiagnosis

• Kagar(1980), latex agglutination.

• IHA, AGPT, CIEP, IFAT, ELISA (NII DOT- EIA KIT) widely
used sensitive specific for invasive amoebosis.
• Sensitivity is minimal when the invasion is minimal.

• and others act upon their in lower lumen.

• Metronidazole
o 2-methyl 5- nitromidazole -1 ethane act on both sites.
Parasitological cure implies that the intraluminal
commensal infection has been eliminated.
o Acts by partial reduction of the nitro group to produce a
toxic compound with in the organisms that alkylates
DNA and so blocks nucleic acid synthesis. In short
courses, metrinidazole is safe- nausea, metallic taste in
mouth, dizziness, rashes, weakness and ataxia.
Prolonged courses can cause leucopenia and peripheral
neuropathy. Oncogenic.
o Adults
▪ 800mg t.i.d for 5-8 days in invasive stage.
▪ 400 mg t.i.d for 5-8 days also given may fail to
eliminate intraluminal infection, so clinical elapses
occur.
o Paediatric dose
▪ 35-50mg/kg in 3 divided doses.
• Nitroimidazoloes
o Tinidazole especially in children-50-60mg/kg for 3-5
days.
o Secnidazole 2 g in single dose.
• Emetine Hcl
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o Effective tissue amoebicide potentially toxic deep i/m or

s/c. 1 mg/kg daily maximum 60mg for 10 days, course
should be repeated with in 28 days.
o Local pain, myositis, skin necrosis if injections are too
superficial- autonomic blockade CVS toxicity- emetic
contra indicated in heart disease. Now dehydroemetic
synthetic compound release slightly safe.
• Chloroquine
o Adults: 150 mg 4 times dailly for 2 days followed by 150
mg for 19 days (peadiatric dose 10 mg/ kg daily).
o Best for preventing development of hepatic lesions. No
effect upon intra luminal amoebae or intestinal invasive
amoebiasis.

Antibiotics

• Tetracycline, erythromycin 250 mg / b.i.d for 2-10 days.

• Tetracyclines
o Only for several consequences of its antibacterial
activity upon the amoebic infection.
• Erythromycin
o Direct amoebicidal action – invasive intestinal disease
poor luminal amoebicide.
• Diloxanide Furate
o Dichlora a cetrinilade derivative. Flatulence is the
common side effect.
• Luminal Amoebicide
o Adult: 500mg t.i.d for 10 days.
o Paediatric: 20 mg/kg daily in 3 divided doses.
• 5 Hydroxy Quinalones
o Usual di iodo hydroxyquin (di iodoquin).
o Adult: 650 mg t.i.d for 20 days.
o Paediatric: 30-40 mg/ kg 3 divided doses to a
maximum of 2 g daily for asymptomatic carriers.

Supportive therapy
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• Fluid electrolyte replacement.

• Gut perforation- grave prognosis.
• Hepatic
o 5-8 days- metronidazole.
o Wise to give diloxamid when 8 days.
o Metronidazole given for 5 days is best.
o Emetine both cross blood brain barrier.

Line of treatment

• Specific drug.
• Supportive therapy
o Antizymatics and digestive enzymes.
• With course of anti amoebic drugs, Lactobacillus culture
should be given.

PREVENTION- ENTAMOEBA HISTOLYTICA

• Good sanitation.
• Improved sewage disposal.
• Water supply systems should be built without cross
connections.
• Personal hygiene in food handlers, regular stool
examination.
• Avoid eating raw vegetables or take after special treatment to
render it cyst- free.
• Improved filteration of waste, their chlorination.
• Boil water for 5 minutes.
• Saladvegetables can be soaked in a dilute solutions like
sodium hypo chloride.
• Weak solutions of iodine is a more potent cysticide than
chlorine.
• Soak in vinegar containing 5% acetic acid .
• Repeated mass chemotherapy with metronidazole and
dialoxin in endemic areas.
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• In temperate countries, routine stool examination is

recommended for residing visitors from tropics and new
residents from such countries.

MODULE-15: GIARDOSIS
Introduction

• Giardiosis is an important gastrointestinal disease of man

and animals caused by a microscopic flagellate
protozoan Giardia. The parasite attaches itself to the lining
of the small intestines in humans, where it sabotages the
body's absorption of fats and carbohydrates from digested
foods.
• This disease has worldwide distribution. Earlier more than
50 species of Giardia have been described but only five
species are currently recognized as valid.

SPECIES AND HOST

Species Host(s)
G. duodenalis (Syn. G. Mammals including man,
intestinalis & G. lamblia) animals (domestic & wild)
G. agilis Amphibians (frog)
G. muris Rodents
G. psittaci Birds (budgerigar or
parakeet)
G. ardeae Birds (herons)
• G.duodenalis is a common parasite affecting 40 species of
vertebrates including humans. Many genotypes
of Giardia have been isolated from animals and
environmental samples. Despite its long history, our
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understanding of Giardia taxonomy, pathogenicity and

relationship with its hosts are still poorly understood. Recent
studies have concluded that Giardia should be considered as
a zoonotic parasite. Giardiosis is common in dogs and cats
and infection varies from place to place. Infection is also
prevalent in domestic ruminants. Small rodents, beavers and
other mammals have also been found to be infected with G.
duodenalis

EPIDEMIOLOGY AND TRANSMISSION

Epidemiology

• It is ubiquitous and is the most common pathogenic parasite

of human beings. Higher prevalence is found in children. In
majority of untreated patient’s infection, it is selflimiting.
High environmental faecal contamination, lack of portable
water, inadequate education and housing, overcrowding and
high population density and animal reservoirs of infection
are the possible risk factors for man. The establishment of
cause of disease in animals is very difficult and concurrent
infections are often present.

Genotype and host range of isolates within G.

duodenalis morphological group:

• Genotype / Assemblage Host range

o Zoonotic / A Human & other primates, cat, livestock,
dog & other wildlife
o Zoonotic / B Human & other primates, dog, beavers &
other wildlife
o Dog / C – D Dog
o Livestock / E Cattle, sheep & pig
o Cat / F Cat
o Rat / G Domestic rats
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Cattle are susceptible to infection with zoonotic genotype

of Giardia and calves may be infected with genotype of
Assemblage A which could pose a significant public health risk
directly to handlers and indirectly as an important reservoir from
human waterborne outbreaks of giardosis. The public health
significance of such infections in pets has been the subject of
much debate and is still a question of uncertainty for
veterinarians. In Australia, both zoonotic genotype for
Assemblage A and the ‘dog’ genotype Assemblage D are both
equally common in dogs. In Assam , 20% dogs were found to be
infected with Giardia and all were infected with zoonotic
genotype mostly genotype Assemblage A. This reflects a closer
association between dogs and their owners.

Transmission of Giardia
• Giardia cysts are spread via the faecal-oral route. Cysts may
be ingested with contaminated food or water, or acquired
from unwashed hands. Foodborne transmission of giardosis
are attributed to an infected food handler. Giardia cysts are
able to survive in fresh water, and it is the most common
cause of epidemic water-borne diarrhoeal
disease. Giardia cysts are quite resistant to chlorination,
making water filtration the key to effective water treatment.
Since Giardia cysts can sometimes be isolated from filtered
drinking water, however, boiling water is the best way to kill
chlorine-resistant Giardia cysts.In addition to outbreaks
associated with ingestion of unfiltered or poorly chlorinated
water, Giardia can also be a cause of recreational water
outbreaks of gastroenteritis—swimming pools, water parks,
hot tubs and spas. Cysts in recreational water generally come
from other users versus a primary contaminated water
source.Male homosexual contact has also been implicated as
another transmission factor with oral-anal sexual practices
serving as a route of transmission.
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• Although humans are the main reservoir of the parasite, a

variety of animals carry Giardia species, which can be passed
on to humans. Giardia duodenalis cysts from beavers may
contaminate community water supplies. Although the
possibility of Giardia transmission from dogs to humans
(zoonoses) has historically been a subject of debate, recent
studies have provided strong evidence that this can be
possible.
• High environmental faecal contamination, lack of portable
water, inadequate education and housing, overcrowding and
high population density and animal reservoirs of infection
are the risk factors for man. G. duodenalis is a common
parasite of vertebrate animals apart from humans.
• Giardiosis is common in dogs and cats and infection varies
from place to place. Infection is also prevalent in domestic
ruminants. Small rodents, beavers and other mammals have
also been found to be infected with G. duodenalis.
• Giardia is very common in both beef and dairy cattle
throughout the world and longitudinal studies have
consistently demonstrated prevalence rate of 100%. Cattle
are susceptible to infection with zoonotic genotype
of Giardia and calves may be infected with genotype of
Assemblage A could pose a significant public health risk
directly to handlers and indirectly as an important reservoir
from human water borne outbreaks of giardiosis.

PATHOGENESIS AND CLINICAL SIGNS

Pathogenesis in man

• The pathogenesis of Giardia is not clearly understood and is

highly variable. In majority of untreated patient’s infection it
is self- limiting and symptoms usually disappear in a few
weeks. Giardia may also inhibit the activity of pancreatic
lipase causing fat malabsorption. Overgrowth of bacteria in
small intestine occurs in giardiosis and the associated bile
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salt deconjugation may explain the case of steatorrhoea in

giardiosis.

Clinical signs

o Man
In acute and chronic cases, there may be
▪
diarrhoea, cramps, weight loss, flatulence,
vomiting, abdominal pain, fatigue, foul smelling
stool, mucous in stool, malnutrition syndrome and
failure to thrive.
o Aanimals
▪ In animals, very little attention has been paid to
clinical symptoms of the disease. Adult dogs are
usually asymptomatic carriers. Clinical signs are
considered to be rare in domestic livestock. An
outbreak of giardiosis was observed in a sheep
farm in central Italy. The establishment of cause of
disease in animals is very difficult and concurrent
infections are often present. In young dogs and
cats, the main sign is intermittent or chronic
diarrhoea which may present for several months.
The stool is soft, pale, mucoid and greasy. Though
appetite is not usually impaired, there may be a
reduced growth rate or weight loss. A poor hair
coat is attributed to deficiency of fat soluble
vitamins. Excess faecal fat has been found in
infected cats.

DIAGNOSIS
Trophozoite

• Trophozoites are not usually seen but in severe cases of

diarrhoea, it can be demonstrated.
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• Detection of Giardia infections can be achieved by the zinc

sulphate concentration technique that is commonly regarded
as the best diagnostic method. However, morphological
detection of Giardia cysts in faecal samples by this
procedure is technically difficult and time consuming, and
requires high degree of client compliance. Highly sensitive
and specific enzyme-linked immunosorbent assays (ELISA)
that detect an antigen of Giardia in stool samples or direct
fluorescent antibody tests can also be used for this purpose.
Coproantigen capture ELISA kits and direct fluorescent tests
have been extensively used in veterinary medicine, Recently,
several immunochromatographic antigen detection tests
have been developed to enhance the rapid detection
of Giardia.

• The performance of the

RIDA®Quick Cryptosporidium/Giardia-Combi test (R-
Biopharm AG) as a rapid method for the routine diagnosis of
giardiosis in dogs. Compared to an ELISA coproantigen test
(Prospect® Giardia Microplate Assay), the chromatographic
test had a sensitivity of 83 %, a specificity of 79 %. Although
the chromatographic test is simpler to perform, it can not
replace the Giardia ELISA coproantigen test for rapid
diagnosis of giardiosis in dogs, since its sensitivity and
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specificity appear to be not comparable to those of the ELISA

kit.

TREATMENT
• No drugs are approved for treating giardosis in animals.
Fenbendazole (50 mg/kg/day) effectively
removes Giardia cysts from the faeces of dogs without side
effects, and it is safe for pregnant and lactating animals.
Fenbendazole is not approved in cats, but may reduce
clinical signs and cyst shedding at 50 mg/kg/day per os for
3-5 days.
Albendazole is effective at 25 mg/kg per os b.i.d for 2 days in
dogs and for 5 days in cats, but should not be used in these
animals because it has led to bone marrow suppression and
is not approved for use in these species.
• Giardia- infected calves may be treated with albendazole or
fenbendazole. Oral fenbendazole may also be an option in
large animals and some birds.
• Metronidazole (25 mg/kg, per os b.i.d for 5-7 days) is 65%
effective in eliminating Giardia spp. from infected dogs but
may be associated with acute development of anorexia and
vomiting, which may occasionally progress to pronounced
generalized ataxia and vertical positional nystagmus.
Metronidazole may be administered to cats at 10-25
mg/kg per os b.i.d for 5 days. The comparative efficacy of
albendazole, fenbendazole and metronidiazole revealed that
fenbendazole was most effective for the treatment of canine
giardosis.

PROPHYLAXIS
• A killed vaccine available for dogs and cats reduce clinical
signs and number and duration of cysts into environment.

GIARDIA CANIS
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• Most infections with Giardia are asymptomatic. In the rare

cases in which disease occurs, younger animals are usually
affected, and the usual sign is diarrhoea. The diarrhea may
be acute, intermittent, or chronic. Usually the infected
animals will not loose their appetite, but they may lose
weight. The faeces are often abnormal, being pale, having a
bad odour, and appearing greasy. In the
intestine, Giardia prevents proper absorption of nutrients,
damages the delicate intestinal lining, and interferes with
digestion.

Can Giardia of dogs infect people?

• This is another unknown. There are many species of Giardia,

and experts do not know if these species infect only
specific hosts. Sources of some human infections have
possibly been linked to beavers, other wild animals
and domestic animals.

Treatment

• There are several treatments for giardosis. Fenbendazole

can help control Giardia. It may be used alone or with
metronidazole. Metronidazole can kill some types of bacteria
that could cause diarrhoea. Unfortunately, metronidazole
has some drawbacks. It has been found to be only 60-70%
effective in eliminating Giardia from infected dogs, and
probably is not 100% effective in cats, either. It can be toxic
to the liver in some animals. It is suspected of being a
teratogen so it should not be used in pregnant animals.
Finally, it has a very bitter taste and many animals resent
taking it – especially cats.Quinacrine hydrochloride has been
used in the past, but is not very effective and can cause side
effects such as lethargy, vomiting, anorexia, and fever. These
treatments only remove the cysts from the faeces but do not
kill all the Giardia in the intestine.
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Prevention

• The cysts can live several weeks to months outside the host
in wet and cold environments. So lawns, parks, kennels, and
other areas that may be contaminated with animal faeces can
be a source of infection for pets. Prevention of the spread
of Giardia centres on testing and treating infected animals
and using sanitary measures to reduce or kill the organisms
in the environment. Solutions quaternary ammonium
compounds are effective against Giardia

MODULE-16: COCCIDIA
• Learning objective
• In this module, general description about coccidian parasites
of animals, their life cycle, pathogenesis are discussed.

FAMILY- EIMERIIDAE
• Members of this family are commonly called coccidia.
Organisms are intracellular parasites of the epithelial cells of
intestine.
• They have a single host in which they undergo asexual
(schizogony) and sexual (gametogony) multiplication. Macro
and microgametocytes develop independently the later
producing many gametes.
• The zygotes result from the union of these and a lay an outer
wall by a process of sporogony variable number of spores
(sporocyst) containing one or more sporozoites are formed.

LIFE CYCLE
• Oocyst which contains a zygote is extruded from the host
tissue and passed to the exterior in the faeces. This is the
resistant phase of the life cycle and under favourable
condition, it forms the mature infective oocyst on the ground
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and the infection of the host takes place by the ingestion of

developed sporulated oocyst.
• Oocysts are exposed to gastric juices in stomach and
intestines. Trypsin acts on oocyst and excystation takes place
resulting in the release of sporozoites.
• Liberated sporozoites are sickle shaped and measures 5-
10µx1.5µ. Nucleus is at the centre and cytoplasm granules.

Schizogony

• Sporozoites enter the epithelial cells and become rounded up

and enlarge. They are called as trophozoites. In few hours the
nucleus of trophozoites divides by multiple fission to become
a schizont. This is first generation of schizogony.
• Mature schizont and enlarged host cell rupture releasing I
generation merozoites.
o No of merozoites vary according to the species. I
generation merozoites enter the epithelial cells of the
area and repeat schizogony.
o They form II generation III generation. Due to resistant
of the host or due to some other factor, merozoites
differentiate into gametogonus forms or sexual forms

Sexual or gametogony

• Two kinds of gametocytes are produced.

• In microgametocyte, nucleus undergoes multiple fission and
release large number of microgametes which are slender and
slightly bent and anterior end is pointed with two flagella.
• Some of the merozoites form macrogametocyte and its
nucleus does not divide. Large number of refractile granules
is seen in the macrogametocyte and are known as Plastic
granules. These granules arrange at the periphery of
macrogametocytes.
• Fertilisation of macrogamete by a microgamete results in the
formation of a zygote.
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• Plastic granule unite to form another wall and thus becomes

a oocyst when the cyst wall is complete, the oocyst is
extruded from the tissue and passed to the exterior along
with faeces.

MORPHOLOGY OF THE STAGES OF COCCIDIA

Description of sporulated oocyst of Eimeria

• Oocyst may be spherical or sub- spherical oval or ellipsoidal

and vary in size according to species.
• The sporulated oocyst has a double contoured wall, outer
thicker and inner thinner. Some posses micropyle opening at
the anterior pointed end. Micropyle is covered by polar cap
formed by inner cyst wall.
• Just below the micropyle, retractile granule known as polar
granule is seen. Initially, zygotes fills almost the oocyst cavity
but in few hours outside the host the protoplasm contracts
from the wall of oocyst and becomes a sporont leaving a clear
space between it and wall.
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Sporogony

• Oocyst nucleus divides to form sporoblast which in turn is

covered by a protective covering becoming sporocyst.
• A portion of cytoplasm is left unutilised and known as
oocystic residual body.
• The sporocyst in turn divides to form sporozoites and the
portion of cytoplasm left is known as sporocystic residual
body. At one pole of each sporocyst, a refractile granule
looking like a mucous plug known as stieda body is seen.
• Period taken for the development of oocyst is known as
sporulation time and only sporulated oocyst is able to infect
other hosts. Sporulation time is specific for each species of
coccidia. By mixing the faeces with 2.5% potassium
dichromate solution and keeping it in a thin layer in dish,
sporulation of oocysts can be observed.
• It can be preserved for long time also. Oocysts are viable for
two years under appropriate conditions.
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• Genus Eimeria contains four sporocysts each containing two

sporozoites. Genus Isospora contains two sporocysts each
containing four sporozoites.
• Coccidia are generally specific to the host. Eimeria is more
specific than Isospora.
• Specificity to organ, cells and even the location in cell is
noticed.
• Incubation period is shorter than prepatent period.( time
taken from the ingestion and to release of oocysts) i.e
infection begins even before the oocysts appear in the faeces.

PATHOGENESIS AND SYMPTOMS

• Disease is called as coccidiosis. Extensive destruction of
epithelial cells by schizogony results in enteritis.(3-
dimensional architecture is disturbed) II generation of
merozoites developing in the cells of sub- endothelial layers
destroys those and injures and exposes the capillaries
resulting in haemorrhagic areas.
• In epithelium mucosa becomes swollen and thicker and even
slough off. Leakage of blood through breakage or seepage of
capillaries leads to anaemia.
• Bacterial contamination takes place resulting in the
formation of ulcers. Animals become weak and emaciated.
• Usually young animals suffer most and succumb. There is
marked abdominal pain and strain. In chronic cases,
thickening of mucosa and papilliform growth are noticed.
• Coccidiosis is a self- limiting disease because there are a
definite number of asexual and sexual generations.
• Presence of oocyst marks the end of schizogony and no
further tissue damage occurs. Adult act as carriers
• Coccidial infections are self limiting and asexual
reproduction does not continue indefinitely.
• In the absence of the infection, therefore only one cycle of
development can take place.
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• Under natural condition, repeated infection usually occurs

and the host may develop immunity which inhibits the life
cycle of coccidia. Therefore, only few oocysts may be
developed.

DIAGNOSIS
• Detection of merozoites and oocysts in faeces
• In suspected cases, sacrifice one or two ailing birds and look
for developmental stages

TREATMENT
• Many different anticoccidial drugs are used, these include
sulphonamides, nitrofurans, imidazoles, benzamides. None
of these drugs can cure a case of coccidiosis once clinical
signs of the disease appear.
• They are all prophylactic and act on meronts in higher doses
against gamonts but occasionally against sporozoites, thus
preventing the completion of the life cycle . In nature,
exposure to coccidia is continuous. Hence the anticoccidial
drugs have to be continuously used. Drugs help to stimulate
host defences and production of immunity by not destroying
sporozoites.
• Drug resistance is a problem in the use of chemotherapeutic
agents. So switching of drugs at specific time intervals is
recommended to avoid development of resistance. This is
called shuttle programme.
• Some of the prophylactic drugs are
o Sulpha drug
o Sulphamezathine (Sulphadimidine)
o Sulphaquinoxaline
o Sulphadimidine
o Sulpha guanidine
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• Early administration will prevent much destruction and act

as coccidiostat interfering with the nuclear division of
schizont
o Nitrofurazone
o Furazolidone
o Bifuran
o Nitrophenide
o Nicarbazine
o Mepacrine Hcl
o Amprolium
o Cardinol
o Salinomycin, Monensin, Lasolacid, Narasin, etc., are
ionophores
o Antibiotics like chloramphenicol, erythromycin, and
tetracycline
o Halofuginone hydrochloride

Synergists

o Pyrimethamine
o Diaverdin
o Whytsin
o Spiromycin
• In poultry sulpha drug is given in feed 0.1 to 1% of the drug
in feed for 6 days or 16% solution sulpha mezathine in water
at 0.2% strength.

CONTROL
• Avoid over crowding.
• Deep litter system of poultry Industry is advocated
• Removal of droppings quickly at least before 48hrs after the
passage
• Proper disposal of dropping by mixing it with ammonia and
dumping it
• Provision of clean water and feed
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• Disinfection of coop with 10% ammonia or ethyl bromide.

• Bedding and soil is sterilised with 1.25% with sodium
hypochlorite or 0.5% phenol or cresol
• Fumigation with formaldehyde is useful
• Don’t allow susceptible animals i.e.young animals with
carriers
• Avoid infection by mechanical methods by birds Pecking at
ground Raised wire net can be used as flooring
• Allow them a limited infection to develop immunity and give
sulphamezathine, if symptoms are seen
• Commercial vaccines like coccivac (oocysts attenuated by
serial passage in chicken host) can be given orally.
Supportive therapy with vitamin A and K is given.
• The other vaccines available are Livacox and immucox based
on precocious coccidia lines with abbreviated life cycle.

MODULE-17: EIMERIA OF CATTLE

• Learning objective
• Coccidia affecting ruminants, carnivores and poultry the life
cycles and pathogenesis are dealt here.

INTRODUCTION
Comparatively smaller. Micropyle indistinct in many species.
Oocyst contains four sporocysts each containing two sporozoites.

Important species affecting cattle and buffaloes

• Cattle
o Eimeria alabamensis
o E.auburnensis
o E.bovis
o E.brasiliensis
o E.canadensis
o E.cylindrica
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o E.ellipsoidalis
o E.pellita
o E.subspherica
o E.zuernii
• Buffalo
o Eimeria ankarensis
o E.bareillyi
o E.gokaki
o E.ovoidalis
o E.thianethi

EIMERIA ZUERNII
• This is very common coccidia of cattle and buffalo calves, 4-
18 months are mostly affected . Disease is called Red
dysentery or Winter coccidiosis. Oocysts are spherical or sub
spherical 18x16 µ
• Micropyle is absent. Oocyst wall is thin, transparent with
homogenous polar granule. Oocystic and sporocystic residual
bodies are absent.
• Sporulation time is 48-72 hrs

Location

• Schizogony occurs in lower small intestine and caecum.

• Gametogony is seen in rectum.
• Incubation period is 7-10 days and prepatent period is 19-20
days.
• More than one asexual generation is seen

Pathogenesis

• E.zuernii is an acute infection and most pathogenic coccidia

of cattle
• Bloody diarrhoea in calves.
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• Diarrhoea becomes more severe, bloody fluid, clots of blood,

lipid faeces (steatorrheoa) straining and coughing may cause
the mixture to spurt out to 6-8 ft.
• Dysenteric faeces will be madded in perineum. Anaemia,
weakness, emasciation accompany dysentery. Secondary
infection especially pneumonia are common. This acute
phase lasts for 3-4 days. Calves may recover or die. In
chronic case, the diarrhoea will be seen. Emaciation,
dehydration, weakness, rough coat, drooping of ear, sunken
eyes are the other signs.

Lesion

• Generalised catarrhal enteritis is observed.

• The affected portion is filled with semi- fluid material with
blood.
• Ulcers are seen.

EIMERIA BOVIS

• Host: Cattle and buffalo

Morphology
• Bigger in size than E.zuernii; 28 x 20 µ, oval in shape.
• Micropyle present.
• Oocyst is coloured greenish to yellowish brown.
• Sporocystic residual body is present.
• Sporulation time is 48-72 hrs.
Location
• Small intestine (schizogony) caecum, colon terminal
ileum (gametogony).
• Only single asexual generation takes place.
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• Mature schizont is visible to naked eye as whitish balls

and is useful in the parasite identification.
• The incubation is 18 days and prepatent period is 21
days
Pathogenesis
• Diarrhoea with blood.
• Tenesmus (straining) high temp 1060F, severe
pathologic changes occur in colon and terminal ileum
due to sexual stages.
• Congestion, oedema, thickening of mucosa with
petechiae or diffused haemorrhages sloughing off
mucosa.
• Coccidiosis in cattle infection with single species is
rare.
• Bovine coccidiosis is a disease of young animals (3
weeks to 6 months)
Diagnosis
• History
• Symptoms and lesions
• Scraping from affected intestinal mucosa will reveal
schizonts, merozoites, and developing stages
Treatment
• Sulphamezathine, mepacrine hydrochloride,
amprolium
Prevention
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• Sanitation and Isolation

EIMERIA ARLOINGI
• Host: Goat
• Location: Small intestine

Morphology

• Oocysts are ellipsoidal, 27 X 18µ .

• Micropyle and micropylar cap are present.
• Polar granules and sporocystic residuum are present.
• Sporulation time is 3 days.
• Lambs and kids of 2- 4 months are mostly affected. This is
common in intensive system of rearing
• Incubation period is 13 days
• Prepatent period is 19 days.
• Two generations of schizogony are observed. First generation
schizont is a giant schizont( megaloschizonts)

Pathogenesis and symptoms

• Abdominal pain
• Watery faeces and occasionally blood tinged mucus
• Emaciation
• Lesion small slightly haemorrhagic areas scattered through
out the S.I, thickening and oedema with white opaque
patches made up of groups of heavily parasitized villi. In
chronic cases, papilliform elevation up to a centimetre long
due to proliferation of epithelium of small intestine because
of parasitic infection

Treatment

• Sulphamezathine and amprolium at the dose rate of

100mg/kg b.w
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Control

• Feed trough and water container should be constructed at a

higher level so they are not contaminated by oocysts. Proper
drainage of the feed lot is necessary.

MODULE-18: POULTRY COCCIDIOSIS

• Learning objective
• In this module, the coccidian parasites affecting chicken will
be taught. Chicken coccidiosis is the major economically
important disease that affects poultry industry.

CHICKEN COCCIDIOSIS
Introduction

• Coccidiosis is a realistic problem and one of the most

important diseases of poultry worldwide. It is caused by a
protozoan parasite known as Eimeria that invade the cells of
the poultry intestine. Species of coccidia which commonly
affect poultry are Eimeria tenella, E. acervulina, E. necatrix,
E. maxima , E. brunetti, E.mitis , E.hagani and E.precoax.
The disease is characterised by enteritis, diarrhoea and
mortality. The bird develops reduced ability to absorb
nutrients, which results in weight loss and eventually death.
Sub clinically, it is manifested by poor performance,
impaired feed conversion, poor flock uniformity and poor
growth. Coccidia can also damage the immune system and
leave poultry more vulnerable to pathogens like Clostridium,
Salmonella and E. coli.
• The disease is considered as one of the most severe health
and economical problems in poultry that causes an
enormous loss to poultry producers worldwide. An outbreak
of coccidiosis in a poultry flock has a very high negative and
economical impact on the flock as well as for the poultry
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producer. It is a well-recognised fact that treatment alone

cannot prevent the economical losses. It is well established
within the poultry sector that the only choice is prevention of
the disease. However, an effective and sustainable
prevention and control programme against the disease is not
easy.
• Coccidiosis is particularly difficult to combat because several
different species of Eimeria exist in the field. Poultry may
become infected with different species because the immunity
that develops after infection is specific only to one
species. Eimeria has a very complex life cycle that involves
many developmental stages within the host cells.
Each Eimeria type is able to infect only one host species and
each attacks a different segment of the intestine in their host.
• The disease causes economic losses to the producer in the
form of mortalities, reduced market value of the affected
birds and sometimes culling or delayed slaughter time.
Another predisposing factor is the confined host rearing
conditions, which lead to an increase in the number of
oocysts, which are ingested by poultry via the litter. These
lead to destruction of the integrity of the intestinal mucosa
and interfere with nutrient absorption, ultimately causing
diarrhoea, which in turn causes high medication costs.
Ultimately, all these setbacks lead to huge losses for the
producer.

E.TENELLA
• Very common and most pathogenic species affecting young
birds from 10 day-10 weeks 4-5 weeks chicks are more
susceptible.
• Oocyst is oval measuring 23x19 µ. Oocyst wall is smooth. No
micropyle, sporulation time 18-48 h.
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Lifecycle

• Chicks pick up sporulated oocysts.

• Sporozoites are liberated invade the surface epithelium of

caeca in caecal coccidiosis.
• Trophozoites develop and produce I generation schizonts,
release of I generation merozoites which is 900 in number in
60-72 hrs. These merozoites penetrate other epithelial cells
to become trophozoites
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• Affected epithelial tissue gets detached. These merozoites

migrate to sub- epithelial tissue where mature II generation
schizonts are formed in 96 h.
• Disruption of II generation schizont and overlaying
epithelium release II generation merozoites which is 200-
350 in number into caecal lumen. Damage caused is high.
• All capillaries exposed causing seepage of blood and
haemorrhage is seen before gametogony. Symptoms are seen
in the form of blood tinged droppings.
• No oocyst is seen.
• Incubation period is earlier than prepatent period. III
generation schizont or gametocyte are formed. Following
syngamy, oocyst is formed.
• Prepatent period is about 7 days.

Pathogenesis and symptoms

• In general clinical coccidiosis is produced only when heavy

infections are acquired over a relatively shorter period of
time not exceeding 72 hrs.
• Chicken droop 72 hrs after infection and cease feeding,
huddle to keep warm. By 90th hr blood appears in droppings.
• Intense haemorrhage occurs in 5-.6 days after infection and
by 8-9 day, the bird is either dead or recovered .
• Mortality is highest at 4-6 days sudden death may occur due
to excessive loss or blood. Birds recovering from acute cases
results in chronic illness and persistent caecal core develops
and expelled in 14 days after infection

Diagnosis

• PM examination of representative bird from a flock provides

a good indication of the intensity of the coccidia problem on
the farm including the species involved . Haemorrhagic
lesion in caecum indicates E. tenella.; haemorrhage in
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central part of small intestine is E necatrix and In rectum E.

brunetti
• Oocysts may not be present in earlier stage of infection.
Schizonts and gametocytes are seen in the epithelial cells .
Therefore, it is advised to examine the intestinal scraping for
the developmental stages for early diagnosis of coccidiosis.

E.NECATRIX
• Birds about 10 wks of age are affected. In older birds this is
pathogenic producing more chronic disease than E. tenella.
• Oocyst is similar to E. tenella but smaller 20x17 µ. No
micropyle. Sporulation time is 2 days. Schizogony in small
intestine and gametogony in caecum.
• Prepatent period is 9 days. Incubation 5-7 days
• Principle lesion is seen in the middle 3rd of small intestine
and show well developed round spots( colonies of developing
schizhont)
• Mucoid enteritis with some haemorrhage. Recovered birds
remain emaciated for several months

Treatment and control

• Preventive measures should be taken since once the disease

occurs. The damage to intestinal epithelium cannot be
reversed.

EPIDEMIOLOGY
• It is a disease of young birds while others act as carriers .
• Crowding and lack of sanitation increase the hazard.
• Successive batch of birds placed in contaminated
surrounding suffer more. oocysts are ingested along with
food or water.
• Disease picture depends on the number of oocysts ingested
Repeated small doses results in some degree of immunity.
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TREATMENT
• Sulphanamides
o Sulphamerazine
o Sulphamethazine at 0.1-0.25% in mash
sulphamethazine and
o Sodium Sulpha dimidine at 0.2% in drinking water .
o Sodium Sulphaquinoxaline 0.4% in drinking water
o Shuttle programme 3days of treatment followed by two
days rest and then three days of treatment
o All sulphamides are coccidiostat rather than curative.
None will cure when signs occur. Usually given
continuously in feed to abort the disease
• Nitrofurons
o Nitrofurazone
o Furazolidone
o Bifuron (mixture of both)(0.0055% of N.F and 0.008%
furazolidone)
o This is also an antibacterial agent Furazolidone acts
against salmonella in chicks and also it has effect
against Histomonas meleagridis and Trichomonas
gallinae
• Nicarbazine 0.01-0.0125% in feed
• Pyrimethamine (Daraprim)
o Synergistic drug-combing with sulpha drugs reduce the
quantity of sulpha drugs (chickmash , grower mesh)
• Amprolium 0.0125%
• Glycarbilamide 0.003%
• Unistat 0.1%
• Salinomycin 0.006-0.01%
• Zoalene 0.0025%-0.05%
• Clopidol 0.0125%
• Vitamin K
• Monesin 0.0121%
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• Drug resistant strains of coccidia against sulphanamide ,

nitrofurazone glycarbilamide are reported.

IMMUNITY
• Coccidiosis is a selflimiting disease and the recovered birds
are generally immune
• Recovered birds may be reinfected resulting in mild infection
• Best type of environment to control coccidiosis is to allow
chicks to become infected lightly enough to develop
immunity without suffering from the disease
• Immunity develops against coccidiosis on suppressive
therapy- coccidistats or anticoccidials.

PREVENTION AND CONTROL

• Coccidia oocysts are extremely resistant to environmental
condition, remain in soil for a year or more. Oocysts will not
sporulate in the absence of oxygen.
• Ordinary antiseptic and disinfectant are ineffective.
Ammonia fumigation is of practical value. Methly bromide is
also an effective fumigant.

MODULE-19: GENUS-ISOSPORA
• Oocyst contains two sporocysts each containing four
sporozoites
• Most coccidia of carnivores come under this genus. Oocysts
are comparatively much larger in size and they are not very
pathogenic.
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• In cat, tiger and other felidae large size 43x33µ and no

micropyle is seen.
• Sporulation time is 72 hrs
• Affects small intestine- fairly benign
• Rarely pathogenic in large number
• Catarrhal enteritis in mild cases
• Haemorrhagic enteritis is common in heavy infection

Treatment

• Sulphamethazine
• Combination of sulphanamides
• Mepacrine 0.01 gm /kg body wt for cats

ISOSPOROSIS
Isosporosis is a disease of developed and developing countries,
caused by an apicomplexan protozoan parasite belonging to the
genus Isospora.

Species

The following species of Isospora are recognized in animals and

man.
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• Isospora canis, I. ohioensis, I. burrowsi and I. neorivolta in

dogs
• I. orlovi and I. cameli in camels
• I. rivolta and I. felis in cats
• I. suis in pigs
• I. belli in man.

Transmission and epidemiology

• Infection can occur either by ingestion of infective

(sporulated) oocysts from a contaminated environment or
occasionally from ingestion of infective cyst containing
tissues of paratenic or transport host. Although the direct
form of transmission is most common but many mammals
can serve as paratenic host including rodents, other prey and
uncooked meat from herbivores. Over crowded, unsanitary,
high stress conditions in setting such pet shops, kennels,
pounds, catteries and laboratory colonies, concurrent
disease, malnutrition and immunosuppression are
predisposing factors. Thus, these coccidia are opportunists.
• Infection with a particular species of Isospora confers a
strong and lasting immunity only to that species. Therefore,
pups observed to suffer repeated bouts of isosporosis are
probably experiencing infection with a series of different
species.

Isosporosis

• Porcine neonatal isosporosis has a high morbidity and

usually a low but variable mortality. It causes yellow watery
diarrhoea, dehydration, loss of condition and death, or
stunted growth. Illness usually begins at 7-10 days of age.
Piglets continue to nurse but may vomit clotted milk.
• Isosporosis in dog and cat is a largely a clinical entity and
usually non -fatal. Young animals are usually affected and
having the history of diarrhoea of several days duration and
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the animal is dehydrated. Isosporosis has occasionally been

associated with chronic malabsorption.
• Isosporosis in man is more severely and frequently seen in
immunocompromised patients particularly with AIDS. It
causes fever malaise, cholecystitis, persistent diarrhoea,
weight loss, steatorrhoea and even death.

Diagnosis

• The diagnosis can be made by identification of isosporoid

oocysts in fresh faeces. Identification of oocysts in a healthy
animal with normal faeces indicates a self- limiting
commensal infection and seldom if ever warrants treatment,
although treatment might help to reduce environmental
contamination with oocysts.

Treatment and control

• If clinical signs are attributed with diarrhoea, effective

coccidiostats should be used for treatment, such as
sulfadiamethoxine (50-60mg/kg per day, orally for 10 days),
trimethoprim-sulfa (30mg/kg per day, orally for 10 days),
quinacrine (10mg/kg per day orally for 5 days). Amprolium
is not approved for use in dogs. However, it is given orally as
20% powder in gelatin capsules at a total dose of 100 mg
once daily for small breed pups or 200 mg daily for larger
breed pups for 7 to 12 days.
• Proper sanitation and elimination of overcrowding help to
prevent the spread of infection in kennels and catteries.

CRYPTOSPORIDIOSIS
• Cryptosporidiosis is an emerging zoonotic disease of both
developed and developing countries. Cryptosporidium
muris was first recognised by Tyzzer in 1907 from the
gastrointestinal tract of mouse and in 1912 he identified a
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second species smaller than C. muris and named it

as Cryptosporidium parvum. Since then more than 25
species have been reported from domestic and wild animals,
birds, fish, reptiles and humans. Till 1970, the parasite was
generally considered non- pathogenic. The first report of
human cryptosporidiosis was recorded in a 3 years -old child
in USA during 1976, who suffered from severe diarrhoea for
two weeks. After that a number of cases have been recorded
in immuno-compromised and immuno- competent persons
from all over the world including India. In 1993 more than
400,000 people developed diarrhoea during a water-borne
outbreak in Milwaukee (Wisconsin) and estimated loss of
$64.6 million. It has been estimated that United Kingdom
will make expenditure for £ 23 million /year to meat the
requirements for removal of Cryptosporidium from drinking
water.
• Cryptosporidiosis in recent years has come to national
attention as a potential cause of water-borne disease in
humans, due to contamination of the water supply by
infected animal faeces. However, as well as being a potential
human disease, cryptosporidiosis is also a significant cause
of disease in young farm animals.

SPECIES
• There are at least 20 established Cryptosporidium spp. and
more than 40 unnamed genotypes. C. parvum human
genotype-I has been named as C. hominis, bovine genotype-
II as C. bovis, dog genotype as C. canis, pig genotype as C.
suis and Cryptosporidium deer like genotype as C. ryanae
. Humans are most frequently infected with C.
hominis and C. parvum. Recently, Cryptosporidium cervine
genotype has been named as C. ubiquitum which is
geographically widespread and infectious for a wide range of
mammalian hosts.
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Species Host(s)
C. parvum Rat*, mice*, ruminants*, pig, monkey,
shellfish, man
C. hominis Man*, monkey* shellfish
C. wrairi Guinea pig*
C.meleagridis Turkey*, man, shell fish
C. galli Chicken
C. felis Cat*, man, cattle
C. baileyi Chicken*, turkey, quail, duck
C.muris Rodent*, camel, hamster, squirrel,man
C. andersoni Ruminant*
C. canis Dog*
C. bovis Cattle*
C. suis Pig*
C .xiaoi Sheep*
C. ryanae Cattle*
C. fayeri Red kangaroo*
C. ubiquitum Wild and domesticated ruminants*,
rodents, carnivores and primates
including humans.
* Major hosts and others are minor hosts

TRANSMISSION
• Cryptosporidium infection is directly transmitted by
ingestion of sporulated oocysts through contaminated feed
and water. Cross infection occurs between domestic and
laboratory animals and man. Autoinfection also takes place
due to excystment of thin wall cyst within the gut of the host.
In human beings, infection usually takes place due to direct
contact with infected animals but many cases have been
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reported with contaminated water supplies. Some outbreaks

have also been recorded with treated water supplies that
could be due to small size of the oocysts and their resistance
to chlorination. Swimming pools and water park wave pools
have also been associated with outbreaks of
cryptosporidiosis. Untreated river water, pond water or well
water used for drinking may be sources of infection.

LIFE CYCLE

• Cryptosporidium is a monoxenous parasite and its entire life

cycle completes within a single host. Oocyst( a ) sporulates
within the host and contains four sporozoites. Two types of
oocysts are formed. The thick walled oocysts are passed in
the faeces/stool whereas the thin walled excyst within the gut
and release their sporozoites causing auto infection. After
ingestion of sporulated oocysts and their excystation, the
sporozoites( b ) invade the microvillus brush border of the
enterocytes or other tissues such as the respiratory tract and
the trophozoites ( C ) rapidly differentiate to form schizonts (
D ) with 4-8 merozoites. Two types of schizonts develop. The
type I schizonts ( E ) produce up to eight merozoites that
recycle,producing either more first type schizonts or
generation of second schizonts.The second schizonts ( F )
produce four merozoites that become gametocytes. Upon
fertilization of the macrogamonts( H ) by the micro gametes(
G ) , zygotes are formed( I ). From zygotes, two different
types of oocysts are produced, the thick-walled,( J ) which is
commonly excreted from the host and the thin-walled oocyst
( K ) which is primarily involved in autoinfection. Oocysts are
infective upon excretion, thus permitting direct and
immediate faecal-oral transmission , The extensive recycling
of merozoites from type I schizonts or autoinfection within
the host is responsible for massive infection.
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PATHOGENESIS
• Pathogenesis of cryptosporidiosis varies with immune status
of the host. It has been hypothesized that cells of the
epithelial mucosa release cytokines that activate resident
phagocytes. These activated cells release soluble factors that
increase intestinal secretion of water and chloride and
inhibit absorption. Cell death is a direct result of parasite
invasion, multiplication and extrusion. Cell damage may
occur through T cell-mediated inflammation, producing
villus atrophy and hyperplasia. Diarrhoea in
cryptosporidiosis is due to malabsorption associated with
villus atrophy of an immature population of epithelial cells
on the surface and occupation of a large portion of the
surface area of absorptive cells by the organism. In the
neonate of ruminants Cryptosporidium frequently occur
concurrent with E. coli, rota or corona virus. In the
immunodeficient patients developmental stages are not only
confined to the gastrointestinal tract but have been reported
from lung, pancreas and liver causing respiratory problems,
cholangitis and pancreatitis.

CLINICAL SIGNS

• Cryptosporidiosis is usually seen in calves between

one and two weeks of age. It is very rare in animals
older than a month old, because by this age most
animals may become immune to infection. Clinical
disease occurs in neonates and immunologically
compromised animals. Older animals are less severely
affected. The Pre- patent period varies between 2-12
days depending on host species. Profuse watery
diarrhoea,abdominal tension and inappetance,
resulting in dehydration are symptomatic of clinical
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cryptosporidiosis. In young ruminants (cattle, sheep

and goats) the prepatent period is usually of 2-5 days
and is followed by profuse diarrhoea that may persist
for 7 days. Many infected calves fail to develop
diarrhoea, the reason for this is not known In many
cases, Cryptosporidium is seen with other diseases,
particularly rotavirus infection. In this case disease is
often more severe with more affected calves.
• Infection in dogs,cats, small rodents, rabbits,
hamsters and guinea pigs normally remains
asymptomatic, unless associated with other
infections. In turkey and peacock chicks, upper
respiratory tract infection of Cryptosporidium with
30% morbidity and 20% mortality is on record. In
peacock chicks, the symptoms observed are
depression, gurgling respiration, coughing and
sneezing with a serous ocular discharge.
Last modified: Tuesday, 13 Ma
DIAGNOSIS, TREATMENT AND CONTROL
Diagnosis

• Diagnosis of cryptosporidiosis can be made on the basis of

the identification of Cryptosporidium oocyst in the
faecal/stool sample by conventional and immunodiagnostic
methods. Several techniques have been tried singly or in
combination for the demonstration and identification
of Cryptosporidium with variable results. Oocysts can be
directly visualized under phase contrast microscopy after
concentration of the stool sample.
• Various methods can be used to concentrate oocysts.
Sheather’s sugar/Zinc sulphate(sp. gr. 1.18-1.20) floatation
methods, formalin-ether concentration, and formalin-
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ethylacetate sedimentation are the common methods for

concentration of Cryptosporidium oocysts in the stool.
Sample should be concentrated prior to staining and
centrifugation for 10 minutes at 500× g is recommended.
• Modified Ziehl-Neelson (MZN) staining method is the most
common conventional method for the identification of oocyst
in the faeces. Both hot and cold modified Ziehl-Neelson
(MZN) staining methods work well for the staining of
oocysts. Staining can also be done with carbol fuchsin as an
alternative quick technique. Modified acid –fast staining
may not detect carriers or the patients having mild grade of
infection. The patient should only be declared negative if
samples are found negative even after five to six times
examination.

• Oocysts of many species of Cryptosporidium are nearly

identical in size and shape which create confusion in the
identification. To overcome this problem, PCR– RFLP has
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been used for the detection and differentiation

of Cryptosporidium spp. A multiplex PCR could provide a
means to predict the accurate source of oocyst
contamination and disease causing potential of contaminant
in man and animals. A real-time PCR (qPCR)assay based on
the 18S rRNA gene and utilizing a Scorpion probe has been
developed to detect all human-
pathogenic Cryptosporidium without the usual need for
nested amplification. These Scorpion probe qPCR assays are
simpler to perform than existing nested PCR and RFLP
methods for diagnosis and epidemiological investigation of
cryptosporidiosis.

Treatment

• Many cases will recover without treatment.

• If calves become dehydrated then electrolytes should be
given.
• If disease is severe, halfuginone can be used to reduce
disease severity and prevent spread to other animals.

Control

• To achieve effective control of Cryptosporidium , good

management and hygiene is vital. The major source
of Cryptosporidium is left-over oocysts from previously
infected calves. These oocysts can be killed by freezing and
by composting, but they are very resistant to disinfectants.
Hot washing of surfaces followed by thorough drying is
effective. Most commercial disinfectants are ineffective at
recommended safe concentrations, except for some
ammonia-based disinfectants.

Prevention of disease is, therefore, based on

Animals
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• Regularly changing feed and water troughs

• Preventing faecal contamination of feed and water troughs,
by raising or covering
• Increasing the bedding to reduce contamination
• Cleaning and disinfecting all buildings with products that kill
oocysts.
• Mass medication can be used as a preventive, but it is no
substitute for good management.

Man

Keeping in view of their emerging disease of zoonotic importance,

the following precautions are advocated to
avoid Cryptosporidium infection

• Hands should be properly washed before taking food.

• There should be proper disposal of faecal/ stool and
contaminated materials.
• AIDS patient with CD 4 count below 200/ mm3 should be
given boiled or filtered water.
• Persons at risk (animal handlers, veterinarians and health
care staff) should avoid contact with source of oocysts. Food
particularly of marine origin should be properly cooked
before consumption.
• Leafy salads should be taken after thorough washing.
• Preferably water should not be consumed directly from
lakes, river, stream or spring. Use of filtered water with
appropriate filters (ultra-filtration or reverse osmosis) is
desirable.
• Swallowing of water should be avoided during swimming in
lakes, pools, rivers and sea.

MODULE-20: TOXOPLASMOSIS
• Learning objective
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• Another zoonotic protozoan causing abortion in animals and

man . This is an important zoonotic disease in developed
countries like US where felines are the important pets . This
is different from coccidian parasites of animals in that tissue
cysts which are viable for life long are produced and the life
cycle of this parasite proceeds in a wide host range.

GENUS: TOXOPLASMA
• The genus Toxoplasma has only one recognized
species, Toxoplasma gondii discovered by Nicolle and
Manceaux in 1908 from an African rodent Ctenodactylus
gundi.
• This is a facultative intracellular tissue cyst forming
coccidian with cats and the family of cats as the definitive
hosts and practically all other animals including man as the
intermediate hosts.
• Toxoplasma gondii attacks all warmblooded animals and
infects every nucleated cell. It is not known to produce any
toxin.
• The name Toxoplasma ( Toxon – arc, plasma – life or form)
is derived from the crescent/arc/comma shaped tachyzoite
stage.
• The genus is characterized by asexual reproduction i.e
merogony or schizogony in both the intermediate and
definitive hosts.
• Merogony in the definitive hosts leads to formation of
meronts/schizonts and gamonts and later isosporan type of
oocysts in the intestinal epithelium.
• Sporulation takes place outside the hosts in the environment.
• Merogony in the intermediate hosts leads to the formation of
tissue stages tachyzoites and bradyzoites within the host
cells.

LIFE CYCLE - TOXOPLASMA

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The parasite is transmitted via 3 ways

• Congenital
• Carnivorism, and
• Faecal oral route.
• The resistant oocysts in the cat faeces aid in the
dissemination of the parasite.

There are 3 infective stages of Toxoplasma

• Tachyzoites in the pseudocysts.

• Bradyzoites in the tissue cysts, and
• Sporozoites in the sporulated oocysts.

Tachyzoites

• Refer to the rapidly multiplying sporozoites in the host cells.

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• They enter the host cells either by active penetration or by

phagocytosis.
• Tachyzoites multiply by repeated endodyogeny within the
host cell till it is filled with the crescent shaped zoites,
enclosed in a parasitophorous vacuole.
• This is termed as clone or pseudocyst (as there is no well
defined parasitic membrane surrounding the groups of
zoites.

Bradyzoites

• Refer to the slowly dividing forms in the host cells.

• Thousands of bradyzoites are enclosed in a tissue cyst with a
well defined membrane and is referred to the resting stage of
the parasite in the host cell.
• Tissue cysts are spherical and the shape and size vary with
the chronicity of the infection.
• Persistent tissue cysts are located in the neural and muscular
tissues like the brain, eyes, skeletal and cardiac muscles,
although they can also occur in the visceral organs like the
lungs, liver and kidney.
• Intact tissue cyst will not cause any harm to the host and can
survive for the active life of the hosts.
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Sporozoites

• Are found within the isosporan oocysts infecting the

definitive hosts via contaminated feed/water.
• There are two developmental cycles in the transmission of T.
gondii.
o Entero-Epithelial Cycle
▪ This occurs in the felines, the definitive hosts
leading to asexual reproduction by endodyogeny
and endopolygeny and the formation of
merozoites, gamonts and oocysts in the intestinal
epithelium when they ingest any one of the
infective materials like pseudocysts, tissue cysts
and sporulated oocysts.
▪ A series of asexual generations from type A to E
are produced in the intestines which multiply to
form the gametes and oocysts.
▪ Cats shed oocysts 3 to 5 days, 9 to 11 days and 21 to
24 days after ingestion of tissue cysts, pseudocysts
and oocysts, respectively.
▪ Tissue cysts containing bradyzoites are most
infective to felines.
o Extra -Intestinal Cycle
▪ This occurs in the non- felines i.e. the intermediate
hosts when they ingest sporulated oocysts or
infected meat or via placenta.
▪ Upon ingestion of sporulated oocysts along with
feed or water, the oocysts initiate an enteric
infection releasing the sporozoites which multiply
intracellularly in the in the intestinal epithelium.
▪ They spread to regional lymph nodes and various
organs via circulation tending to form pseudocysts
carrying tachyzoites in the various host cells like
fibroblasts, reticular cells, myocardial cells,
hepatocytes and neurons.
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▪ Accumulation of tachyzoites will eventually

destroy the cells and fresh cells will be infected
further.
▪ The presence of tachyzoites indicates an acute
visceral infection.
▪ If the hosts overcome this acute stage, the
tachyzoites transform to bradyzoites with the
formation of tissue cysts especially in the heart,
eyes and skeletal muscles.
▪ Tissue cysts indicate the chronic stage of the
infection. The cycle is completed when tissue cysts
are ingested by the felines.
▪ During carnivorism, meat with tissue cysts upon
ingestion will be digested by the proteolytic
enzymes releasing the bradyzoites.
▪ They will enter the host cells forming tachyzoites
and eventually encysting in tissues waiting for the
felines to prey upon.
▪ Congenital infection can occur when a previously
non- infected host becomes infected during
pregnancy.
▪ The organism multiplies in the placenta and then
in the foetal tissues also. Although infection can
take place at any time of gestation, the foetus is
seriously affected if the dam is infected during the
first half of gestation.

Click here to view animated life cycle

PATHOGENESIS
• Toxoplasmosis is a mysterious disease in that it ranges from
in apparent infection to acute fatal condition.
• Animals are not equally susceptible.
• Asymptomatic toxoplasmosis in very common and rarely
may exhibit clinical signs in affected animals.
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• Cause of death in a host is attributed to necrosis of the

intestines and mesenteric lymph nodes much before the
other organs are affected. This necrosis is by the intracellular
growth of the organism.
• A host may die of acute toxoplasmosis but more often it
recovers with acquisition of immunity.
• By the 3rd week of infection, tachyzoites disappear from the
visceral organs and localize as cysts in the neural and
muscular tissues causing chronic infection.
• This immunity is strong and persists for the life of the host.
• Sometimes on failure of immunity tachyzoite formation is
revived and the host suffers from the fatal effects once again.
• Encephalitis, pneumonia and eye lesions are the commonly
encountered lesions of chronic toxoplasmosis. In immuno
compromised persons, toxoplasma encephalitis(TE) is
common.
• Although serum antibodies to T. gondii have been
demonstrated in many domestic animals world wide,
isolation of the organism from tissues has been rarely
successful.
• In India, antibodies have been detected in sheep, goat, pig,
cattle, camels, dog, cat and chicken and the organism has
been isolated from pig, sheep, rodents and chicken.

TOXOPLASMOSIS IN CATS
• Clinical entity is a rare occurrence in cats although they form
the main hosts of the organism.
• It is said that 90% of the cats which have already shed
oocysts during a primary infection will not shed any more
oocysts upon re infection unless there is a break in the local
intestinal immunity.
• Cats suffering from a primary infection may exhibit a mild
enteritis, fever, lethargy, pneumonia, retinitis and
encephalitis.
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• Congenital infection is common in cats.

TOXOPLASMOSIS IN DOGS
• Clinical form is fatal.
• It is usually seen along with canine distemper virus which
produces immunosuppression.
• There are three major clinical signs
o Neuromuscular with symptoms of progressive paresis
and paralysis.
o Respiratory with that of dyspnoea and
o Gastrointestinal with that of diarrhoea. The other
important sequelae are pneumonia, myositis and
encephalitis.

TOXOPLASMOSIS IN SHEEP AND GOATS

• Toxoplasma gondii causes abortion, still birth and neonatal
mortality in small ruminants. Toxoplasma gondii is most
pathogenic to sheep and goats.
• Early embryonic death, mummification of foetus,abortion,
still birth and birth of weak lambs and kids are noted.
• White necrotic areas of clusters of tachyzoites will be noted
on the foetal cotyledons.
• Anorexia due to severe damage of cotyledons(placental
necrosis) plays an important role as the cause of death of
foetus.
• Abortion can occur at any stage of gestation and in ewes of
any age that acquire the infection during pregnancy.
• Abortion in subsequent pregnancies is less common.
• Animals that abort return to heat and conceive normally.
• In goats, abortion can occur within 21 days after infection.
• They suffer from fever, anorexia, respiratory distress and die
of enteritis.
• The organisms persist in the edible tissues for long time and
the tissue cysts are found in the thigh muscles, heart, liver,
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kidney, brain and diaphragm with a greater number in the

liver and muscles.

MODULE-21: TOXOPLASMOSIS IN PIGS

• The main source of infection to pigs is from the environment
through ingestion of oocysts.
• New born piglets attain the infection by congenital
transmission and succumb to it very easily.
• Mostly it is sub -clinical infection with pulmonary disorders
and in coordination of movements.
• In pigs, pyrexia, lacrimation, nasal discharge,tachypnoea,
prostration and abortion were noticed. Mortality is more in
young pigs.

TOXOPLASMOSIS IN CATTLE AND HORSES

• These are the most resistant species to T. gondii.
• It is still doubtful if T. gondii is a primary cause of abortion
in cattle.
• Cattle and horses are more resistant to toxoplasmosis than
other species of livestock but young calves developed fatal
bronchopneumonia 20 days post infection.

TOXOPLASMOSIS IN BIRDS
• The organism has been isolated from farm yard chicken,
pigeon, crow, canaries, turkey, quail, etc.
• The disease is chronic resulting in emaciation, pallor,
blindness and nervous signs and death.

TOXOPLASMOSIS IN MAN
There are 2 types of human toxoplasmosis.

• Congenitally acquired, and

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• Post- natally acquired type

Congenitally acquired

• Congenitally acquired occurs when a woman acquires the

infection during any time of pregnancy.Maximum damage is
seen to affect the foetus when it happens during the first
trimester of pregnancy.
• Mode of infection is by ingestion of uncooked or partially
cooked meat especially pork/ pork products containing
tissue cysts. Oocysts defecated by cats around or inside
houses also form source of infection. Babies will be born
dead or alive with extreme symptoms like hydrocephalus,
retino-choroiditis, cerebral calcification and encephalitis.
This is referred to as “ tetrad of signs”.
• The child may live for a few weeks and succumb to the
infection. In some cases babies will be born with no
symptoms at all and will develop signs like learning
disabilities, dyslexia and gradual loss of vision as they grow
older. The common sequel of congenital toxoplasmosis is the
ocular damage involving the posterior chamber of eye.

Post- natally acquired

Post - natally acquired toxoplasmosis occurs when the hosts come

in contact with the infectious material during his/her life.

There are 4 types

o Lymph adenopathy
o Exanthematous
o Cerebral and
o Ophthalmic.
• Lymph adeopathy is the most commonly observed
form. It is associated with enlargement of lymph
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nodes (cervical), fever, fatigue, lassitude, muscle pain,

sore throat, eye lesions etc.
• Heart and organ transplant recipients are also at a greater
risk of contacting toxoplasmosis. Similarly cancer and AIDS
patients are likely to develop the infection as they are
immuno- compromised. Toxoplasma encephalitis (TE)
is the most frequent cause of focal nervous system
disorder complicating AIDS. In immuno-compromised
host, tachyzoites replicate freely in the brain causing lysis of
host cells and resulting in necrotic foci in the brain leading to
TE and other neurological complications. Infection is most
often seen to occur when CD4+ count is less than 0.1x103 .
Seroprevalence of Toxoplasma is highest in France (90%) in
adults since people eat raw meat, followed by U.K. (80%)
and USA (60%) due to high level of contamination of the
environment by oocysts. In India 20% children and 75 to
80% adults have Toxoplasma infection. The highest
seroprevalence (77%) was reported from Kumaon region of
India . The common neurological deficit includes altered
sensorium, cranial nerve palsies, pyramidal tract sign,
movement disorders, neuropsychiatric manifestations and
cerebellar sign. A presentation from South India at
4th International Congress on AIDS reported 10% TE in HIV
patients.
• Pregnant women should be continuously monitored for both
IgM and IgG antibodies during the time of pregnancy to
confirm the risk of transfer to the foetus by serological tests.
ELISA is very popular in this regard (TORCH ELISA).
Infection in the foetus is detected by ultrasound scan,
amniocentesis and PCR.
• Sulphadiazene (100 mg/kg) and pyrimethamine (1mg/kg)
combination is the drug of choice for human toxoplasmosis.
Spiramycin (3g/day) is a safe in pregnant women drug that
concentrates at the placenta and prevents the infection from
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entering the foetus any further. Folinic acid 5mg/kg is also

given to prevent the bone marrow suppression.
• Control measures include basic need for hygiene and
clealiness such as thorough washing of fruits and vegetables
before eating, utensils used for cooking meat, wearing gloves
while gardening and thorough cooking of meat. There is no
vaccine for human toxoplasmosis. The disease is of great
zoonotic importance especially in women as it has the risk of
transfer to babies.

DIAGNOSIS - TOXOPLASMA
• Diagnosis cannot be dependent upon clinical signs.
• Besides symptoms are mild and oocyst production is only for
2 weeks after which there is no oocyst shedding.
• Diagnosis is made by biological, histological and serological
methods.
o Detection of the organism in the tissues collected at
postmortem or biopsy and inoculation of suspected
materials from visceral organs into mice (Bio assay)
o Microscopic examination of impression smears
collected from suspected tissues/organs by Giemsa
staining.
o Immuno histochemical staining ( immunoperoxidase
test)
o Serology
▪ Sabin Feldman dye test (DT) is considered as the
gold standard in the diagnosis of toxoplasmosis.
▪ The principle is that antibodies in the presence of
an accessory factor like properdin modifies the cell
wall of tachyzoites so that they fail to take up the
dye methylene blue at pH 11. But the use of live
antigen has unpopularised its use .
▪ Indirect haemagglutination test (IHAT), latex
agglutination test (LAT), ELISA, modified
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agglutination test (MAT), immunofluroscence are

the various tests employed. Of these, IFAT, ELISA
and MAT have been modified to detect IgM
antibodies too.
▪ MAT is the test of choice for Toxoplasma in all
species of animals and man.
▪ Another developed technique is the carbon
immuno assay (CIA) where carbon in India ink
(dye) stains the cell walls of antigen antibody
complexes and is visualized microscopically.
o Molecular detection
▪ Recent progress made at the molecular level has
simplified the detection of toxoplasmic DNA by
polymerase chain reaction even in autolysed
tissues/aborted foetus.

TREATMENT - TOXOPLASMA

• Not very satisfactory.

• Monensin or lasolacid @ 0.02% in cat feed will
prevent oocyst shedding.
• Clindamycin & roxithromycin have been found
effective as antibiotics in experimental infection.
Last modified: Tuesday, 13 March 2012, 11:53 A
CONTROL - TOXOPLASMA
• Do not feed raw meat to cats.
• Dispose the carcasses of rodents, birds and aborted foetuses
in a proper manner.
• Exterminate flies, cockroaches and rodents from the
surroundings.
• Immunisation
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o “Toxovac” is a live toxoplasma vaccine marketed in the

UK to protect ewes used for breeding and to check
sheep abortion.
o The vaccine contains live tachyzoites of S48 strain.
o Dose is 2 ml intramuscularly in the neck region.
o Given to sheep from the 5th month onwards or 4 months
prior to mating.
o Not used in sheep less than 6 weeks of age and in
pregnant ones.
o Chevon of vaccinated animals not recommended for
human consumption after 42 days.

Immunity

• The extracellular organisms are destroyed by antibodies

(humoral immune response) while the intracellular
protozoans by cell- mediated immune response.
• Toxoplasma gondii evades the humoral immune response by
hiding in the macrophages.
• During cell- mediated immune response, lymphokines
produced by T cells activate the macrophages causing
intracellular killing of the organisms.
• A life long immunity is elicited in the intermediate hosts.

MODULE-22: SARCOCYSTIS
Learning objective

• Sarcocystis sp. follows a prey predator life cycle in which all

carnivores are D/H and herbivores and small mammals act
as I/H. Here also we come across the tissue cysts as
in Toxoplasma and when predator feeds on the prey, it gets
infected.

SARCOCYSTIDAE
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• Suborder: Eimeriina
• Family: Sarcocystidae
• These are cyst forming isosporan coccidia differing from the
family Eimeriidae in that its species are heterogeneous with
a prey predator life cycle consisting asexual stages in the
intermediate hosts and sexual stages in the definitive hosts,
both being vertebrate hosts.

SARCOCYSTIS
Genus: Sarcocystis

• The genus Sarcocystis has an obligatory life cycle with the

formation of asexual stages like tachyzoites and bradyzoites
in the vascular endothelium of visceral organs and muscular
and neural tissues of intermediate hosts like cattle, sheep,
goat, pig, horse, rabbit, chicken and man and the formation
of sexual stages like gamonts and oocysts in the intestinal
epithelial cells of definitive hosts like dogs and cats.
• Each intermediate host may have one or more species for
which the definitive hosts will be from either dogs or cats.
• Since the intermediate hosts are vertebrates, it is preferred to
call them as secondary hosts.

LIFE CYCLE - SARCOCYSTIS

• Sporulated oocysts or free sporocysts discharged in the
feeces of definitive hosts like dogs/cats infect the
intermediate hosts per os by contamination of feed and
water.
• Sporozoites excyst in the intestine penetrate the intestinal
epithelium and reach the endothelial cells of the mesenteric
arteries.
• They undergo schizogony to form I and II generation
schizonts in the endothelial cells of the blood vessels of
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various visceral organs leading to the formation of actively

multiplying type of merozoites called tachyzoites.
• The tachyzoites are also termed as Rainey’s corpuscles.
• Merozoites or tachyzoite liberated from the terminal
generation will enter striated musculature to initiate the
sarcocyst formation.
• Sarcocysts (sarkos-flesh, kystis-bladder in Greek) are the
terminal asexual stages found encysted in the striated
musculature of the intermediate hosts.
o They vary in size and shape depending on the species
like round, ovoid, cylindrical, filamentous, rice grain
appearance etc.
o They may be microscopic (S. cruzi of cattle) or
macroscopic cysts ( S. fusiformis of buffalo and S.
gigantea of sheep).
o Macro sarcocysts are always found in the skeletal and
oesophageal muscles and will be filamentous, spindle,
globular or rice grain like.
o Sarcocysts are always located in a parasitophorous
vacuole in the host cell cytoplasm.
o The cyst wall histologically will be either smooth or
striated or with protrusions which are called as
cytophaneres.
o An immature sarcocyst initially consists of globular
merozoites called as metrocytes (mother cells).
o These metrocytes undergo asexual multiplication by
endodyogeny leading to the formation of crescent
/banana/ sickle shaped zoites called bradyzoites which
are slowly multiplying type.
o The metrocytes are located in the periphery and the
bradyzoites in the medulla of the sarcocyst.
o The sarcocyst internally will carry groups of zoites
divided into compartments by septa.
o Live sarcocysts are fluid filled with the metrocytes and
bradyzoites moving in the fluid.
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o A mature sarcocyst carrying the bradyzoites alone is the

infective stage to definitive hosts like dogs and cats.
o Sarcocysts become infective 75 DAI and can survive in
the intermediate hosts as long as they are alive.
o Ingestion of meat or flesh with mature sarcocysts
results in infection in these definitive hosts.
• Upon ingestion, the sarcocyst will be broken by proteolytic
enzymes releasing the bradyzoites in the stomach and
intestine.
o Bradyzoites penetrate the intestinal mucosa
transforming to schizonts, male and female gamonts,
gametes zygote and finally to oocysts.
o The entire process of gamogony and oocyst formation
takes place within 24 h in the intestinal epithelial cells.
o Oocysts sporulate in the lamina propria.
o As the sporulation is asynchronous both sporulated and
non- sporulated oocysts are found in the intestine.
• The sporulated oocyst , an isosporan type, is colourless, thin
walled and contains 2 elongate sporocysts with 4 elongated
sporozoites within.
o As the oocyst wall is thin, it ruptures immediately
releasing free sporocysts in the intestine which are
expelled in the faeces of definitive hosts like dogs and
cats.
o For most Sarcocystis sp. the oocysts are shed first in the
faeces between 7 and 14 days after ingesting sarcocysts.

HOST SPECIFICITY - SARCOCYSTIS

• Sarcocystis sp. are generally more host specific for their
intermediate hosts than for their definitive hosts.
• Eg. for S. cruzi, ox and bison are the only intermediate hosts
while there is a range of canine species as definitive hosts.
• It should be noted that none of the species transmitted via
dogs can be transmitted by cats and vice versa.
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PATHOGENESIS - SARCOCYSTIS
• Generally Sarcocystis sp are less pathogenic to the hosts.
• The tachyzoites in the visceral organs in the intermediate
hosts give rise to pathogenic symptoms specific to that
organ.
• Intact sarcocyst is not pathogenic but it produces a powerful
endotoxin that is highly toxic to birds and rabbits.
• The gametes and oocysts in the intestine of dogs and cats
may result in anorexia and diarrhoea.

SARCOCYSTIS IN CATTLE
There are 4 species of Sarcocystis in cattle.
• Sarcocystis cruzi (S. bovicanis)
o Found throughout the world with bovines as
intermediate host and dogs, coyotes, red foxes,
raccoons and wolves as definitive hosts.
o Sarcocysts are microscopic found in striated muscles,
Purkinge fibres of heart and CNS.
o It is highly pathogenic to ox, causing fever, anorexia,
anaemia, and emaciation, loss of hair, neurological
signs, prostration and even death in calves.
o Pregnant cows may abort and a drastic drop in milk
production is noted in lactating cows.
o Cattle that do not recover will enter into a chronic stage
with continuous weight loss, excitability and loss of hair
at the rump, neck and tail switch.
o Sporadic cases of bovine abortion and neonatal
mortality have been reported in New
Zealand, Australia, the USA, Canada and Cuba.
• Sarcocystis hirsuta (S. bovifelis)
o World wide prevalence with macro and microscopic
cysts seen in the muscles of oesophagus.
o Calves showed fever, mild diarrhoea and anaemia.
• Sarcocystis fusiformis
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o Involves cats and water buffaloes and is non-

pathogenic to buffaloes.
o Macroscopic cysts are found in the muscles of
oesophagus, eye balls,tongue and diaphragm of the
buffaloes.
• Sarcocystis levinei
o Involves dogs and water buffaloes , is more common
than S. fusiformis and is mildly pathogenic to buffaloes
causing weakness, emaciation and anemia.
o Cysts are microscopic found in the muscles of
oesophagus, heart and diaphragm of the buffaloes.
o All these species are widely prevalent in India, where
unhygienic conditions prevail.
SARCOCYSTOSIS IN SHEEP AND GOATS
There are 4 species in sheep.

• Sarcocystis tenella (S. ovicanis)

o This is highly pathogenic to lambs causing fever,
anorexia, weight loss, loss of wool, abortion, premature
birth nervous signs and death.
o Cysts are microscopic and located in the muscles of
oesophagus, diaphragm, heart, tongue and CNS.
• Sarcocystis arieticanis
o This is less pathogenic than the above, involves dogs as
final hosts and is found in India.
• Sarcocystis gigantea (S.ovifelis)
o This is moderately pathogenic to sheep with
macroscopic cysts fond in the muscles of oesophagus,
larynx and tongue.
• Sarcocystis medusiformis
o This involves cat as the definitive host and is found in
India.

There are two species of Sarcocystis known to occur in goats in

India.
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• Sarcocystis capracanis
o Involves goats and dogs.
o Most pathogenic in goats causing fever, anorexia,
weight loss, abortion, etc.
o The highest intensity of infection is found in the striated
muscles especially the thigh muscles followed by
oesophagus, heart and massetters.
o Kids as young as 7 days have revealed sarcocysts
indicatng a transplacental transmission.
• Sarcocystis hircicanis
o Involves dogs as the definitive hosts.
o It is non pathogenic and is prevalent in India.

MODULE-23: SARCOCYSTOSIS IN PIGS

There are 3 important species in pigs

• Sarcocystis miescheriana (S. suicanis)

o This can depress growth in piglets with purpurea of the
skin of ears, buttocks, dyspnoea, tremors, abortion and
death.
o It is found in India.
• Sarcocystis suihominis
o Man act as the definitive hosts.
o Extremely pathogenic to pigs and and man.
o Cysts are found in the diaphragmatic muscles of the pig.
o It is also found in India.
• Sarcocystis porcifelis
o Cat act as the definitive host.

SARCOCYSTOSIS IN HORSES
• Sarcocystis bertrami
• Sarcocystis equicanis
o Both these are mildly pathogenic to horses with a mild
anaemia, stiff gait and fever.
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o Dogs act as definitive hosts.

o S. equicanis has been identified from the oesophageal
and diaphragmatic muscles from a mare in India.
• Sarcocystis neurona
o The disease condition is called as Equine protozoal
myeloencephalitis (EPM).
o The protozoan is found as intracellular schizonts in the
neurons of equines without transmission to other hosts.
o Horse is the aberrant or dead end host of this organism.
o The life cycle is completed with opossum as the final
host and cat, armadillo, skunk, raccoon, sea otter, etc as
intermediate hosts. Horse acquires the infection from
sporulated oocysts via feed/water.
o The sporozoites enter the vascular endothelial cells
from the intestine, form schizonts, replicates as
tachyzoites and then assumed to enter the CNS via
leucocytes and cytoplasm of endothelial cells.
o The tachyzoites replicate in the neurons and microglial
cells without forming tissue cysts ,gradually destroying
the brain cells, causing incordination and other nervous
signs.
o These schizonts remain non- infective to the other
animals and hence no transmission to other hosts.

SARCOCYSTOSIS IN BIRDS
Sarcocystis gallinarum

• Involves dogs and chicken , causes myositis in chicken.

Sarcocystis rileyi

• Involves dogs/cats and ducks.

• Sarcocysts lead to meningoencephalitis.

SARCOCYSTOSIS IN MAN
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• In India, human beings serve as definitive hosts

for Sarcocystis hominis( cattle) and Sarcocystis suihominis(
pig).
• Infection is acquired by man by ingestion of uncooked or
undercooked beef or pork containing the sarcocysts.
• Gametes and oocysts develop in the intestinal epithelium of
man.
• It is quite common among people living in the slums.
• Sarcocystis suihominis is more pathogenic than the other
resulting in nausea, stomach ache, diarrhoea and dyspnoea.
• Muscular sarcocystis infection has been found in man as an
incidental finding.
• There is one species, Sarcocystis lindemanni where man is
the intermediate host exhibiting fever, myositis, stiffness of
muscles and subcutaneous swellings.

ABORTIONS DUE TO SARCOCYSTOSIS IN

ANIMALS
• Pregnant cattle, sheep and goat may abort or have retained
placenta due to Sarcocystis infections.
• Mechanism of abortions is not fully known since none of the
schizonts or lesions are seen in the ovaries, placenta or
aborted material.
• It is thought that merozoites developing in the endothelial
cells of the visceral organs may induce vascular lesions and
inflammation in the adjacent parenchyma which will lead to
a series of reactions finally resulting in the production of
prostaglandin F2α from the myometrium.
• Being a luteolytic hormone, it causes regression of the corpus
luteum and thus drastic reduction in the progesterone level
and termination of pregnancy.
• It also causes vascular constriction which induces localized
anoxia resulting in foetal death.
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• It may also induce abortions by strong muscular contractions

of the uterus.
• It is yet to be ascertained at what point the organism initiates
these chain of reactions.

DIAGNOSIS - SARCOCYSTOSIS
• Examination of faeces of dogs and cats for sporulated oocysts
or free sporocysts- Oocysts will be isosporan type. Free
sporocysts will be dumb bell shaped.
• Symptoms like fever, anaemia, anorexia and loss of hair
especially at the tail switch
• Serological tests like ELISA, IHAT and IFAT have been
employed to detect circulating antibodies.

TREATMENT AND CONTROL - SARCOCYSTIS

Interruption of the life cycle is the prime method to minimize the
spread of sarcocystosis. This can be done by:

• Keeping away dogs/cats from animal sheds and from feed/

water/ bedding.
• By not feeding uncooked meat or offal to dogs/cats.
• Freezing meat at 20ºC for 3 days or exposing to heat above
55ºC for 20 min to render it non- infective.
• burying or incinerating dead birds or livestock to avoid
access to carnivores.
• Using anticoccidials
o Calves – Amprolium Hcl @ 50 mg/kg for 5 days.
o Pigs and goats –Salinomycin @ 4 mg/kg in divide doses
for 30 days.

IMMUNITY - SARCOCYSTOSIS
• Definitive hosts donot elicit any type of immunity.
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• They suffer from the disease whenever oocysts develop in

them.
• But a certain amount of immunity is elicited in the
intermediate hosts due to the presence of schizonts and
sarcocysts.

NEOSPOROSIS IN CATTLE
• One of the most recently identified causes of abortion is
neosporosis, however recent studies suggest that neosporosis
causes over 10% of all abortions in UK cattle

What is neosporosis?

• Neosporosis is caused by infection with the

protozoan Neospora caninum. Neospora has been found
world-wide and in many species other than cattle. Currently
abortion due to Neospora has been shown in cattle, sheep
and dogs. The dog and other canids (such as foxes) are the
definitive host. That is they are the animals in which the
parasite becomes sexually mature and reproduces.
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Life cycle

• The life cycle of N. caninum in dogs is very similar to that

of T. gondii in cats. An infected dog has parasites multiplying
sexually in the intestine and the infective oocyst is passed in
the dog’s faeces. Meanwhile, parasites are also multiplying
asexually in other tissues.
• Harbouring the sexual form of N. caninum in the intestine
makes domestic dogs the definitive host of the parasite. It’s
not known whether other animals are capable of serving as a
definitive host, but wild dogs, such as foxes, wolves, coyotes,
etc. may do so.
• Animals other than dogs that ingest either oocysts in dog
faeces or animal tissue in which the parasite is present
become intermediate hosts – they have only the asexual
stage, multiplying in the tissue. Thus, dogs pass on the
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parasite in their feces, in their tissue if they are eaten by

other animals, or to an unborn foetus. No animals other than
dogs have been known to spread the parasite in faeces.

Neosporosis in dogs

• Neospora caninum infects domestic dogs worldwide with

varying prevalence. Studies testing dogs for antibodies to the
parasite suggest that more than 30% of dogs are infected in
some areas, with the highest numbers in South American
countries and in rural dogs, especially those living on cattle
farms.
Most infected dogs have no symptoms. When symptoms
occur, neosporosis is most severe in newborn puppies,
infected during gestation when the parasites move from the
bitch’s tissues to the foetus. Puppies suffer paralysis,
particularly of the hind legs and often do not survive. Adult
dogs may suffer from an illness similar to toxoplasmosis in
cats, or they may develop dermatitis.

Neosporosis in cattle

• Like dogs, cattle everywhere harbour N. caninum, and most

show no signs of it. In some herds, close to 90% of cattle are
infected and the parasite is thought to account for more than
40% of abortions – a significant cause of economic loss for
cattle farmers. Many infected foetuses and calves appear
normal, however, and it is still unclear what factors cause or
prevent disease symptoms.
• In cattle, N. caninum is transmitted only from a pregnant
cow to her foetus—the parasite does not pass between cows
in a herd. Some cows, then, must acquire the parasite from
dogs, consuming oocysts while grazing where dogs have
defecated. It’s easy to imagine how farm dogs and livestock
(sheep, goats, and horses can also be infected) may have
increased the prevalence of the parasite, with dogs eating the
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remains of aborted young, becoming infected, and then

passing infective oocysts in faeces deposited where livestock
graze. Calves born without symptoms, meanwhile, pass the
parasite on to their own young.

Clinical Signs

• Abortion, between 3 and 9 months of pregnancy (particularly

5 to7 months)
• Still birth or premature calf
• Occasionally, calves will have brain disease at birth
• No other signs seen in the mother
• Repeat abortions possible in the same cow

Diagnosis

• Clinical signs are of little help

• Characteristic heart and brain damage in aborted calf
• Identification of parasite in the calf tissue
• Antibodies in the mother's blood

However, as a large number of healthy calves can be infected

with Neospora it is important to eliminate other causes of
abortion, particularly BVD or leptospirosis before a diagnosis of
neosporosis is made

Treatment

• No treatment of any proven benefit

Prevention

Dogs are potentially a source of disease. So prevention must

include:

• Keeping cattle food and water away from dogs and foxes
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• High hygiene standards at calving. Dispose of placental

membranes and aborted or dead calves before dogs can get
them

However, transmission from mother to calf (known as vertical

transmission) is far more important. Over 90% of calves born to
mothers with antibodies to Neospora will have been infected in
utero. The importance of transmission between cattle is less clear.
Nevertheless, vertical transmission alone can maintain infection
in a herd. Neospora control programme would consider the
following

• Identify infected cattle and cull them: All cattle with

antibodies to Neospora are sources of infection to their
calves, have a significantly increased risk of abortion, and, on
average, produce less milk than antibody negative cows.
• Select only sero negative cattle for breeding. Heifers
with antibodies should be sold for meat and not bred

These strategies look expensive to achieve, however, the cost of

neosporosis far outweighs the cost of eliminating it from the herd

MODULE-24: PLASMODIIDAE
Learning objective

A very old disease of man but still the human race struggles to win
over. Here we shall confine to malaria of animals which is equally
as devasting as human disease.

PLASMODIIDAE
Has characters of the Suborder: Haemosporina

• Plasmodium in the microgamont produce moderate number

(8) flagellate sporozoites and merozoites lack conoids.
Gamonts are similar and develop independently.
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• Zygotes are motile.They are heteroxenous. Merogony is seen

in vertebrate host and Sporogony in invertebrate host. No
sporocysts and sporozoites are naked in oocysts.
• Sporozoites and merozoites have polar rings rhoptries,
micronemes, subpellicular microtubules, micropores. In
RBC, pigment haemozoin is formed from host
haemoglobin.
• Three genera
o Haemoproteus
o Plasmodium
o Leucocytozoon
• Transmitted by blood sucking arthropods.

GENUS:PLASMODIUM

Plasmodium
• Malarial organism of man and animals.
• Schizogony occurs in endothelial cells of inner organs.
• Sexual phase in blood sucking insects.
o Mammals- Anopheline mosquitoes
o Avian- Culicine mosquitoes
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Schizonts in Plasmodium Signet ring

PLASMODIUM GALLINACEUM
• P.cathemeriyum
• P.juxtra nuclear relictum

Avian malaria

Developmental cycle

• Culicine mosquitoes introduce sporozoites into birds. Pre-

erythrocytic schizogony occur in macrophages and
Fibroblasts of skin near point of entry, referred to as
cryptozoites.
• Merozoites from first generation pre-erythrocytic schizonts
form a II generation pre-erythrocytic schizonts known as
metacryptozoites.
• Merozoites from this enter RBC and other cells of body
(endothelial cells) where exo erythrocytic schizogony occurs
leading to formation of phenarozoites.
• Erythrocytic cycle is initiated 7-10 days after infection by
merozoites from metacryptozoites and/or merozoites from
exo -erythrocytic schizogony.
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• In RBC, merozoites become round and form trophozoites

with large vacuoles displacing cytoplasm of parasite and
nucleus at poles giving a signet ring shape.
• Trophozoites become schizonts to produce merozoites.
During schizogony, parasite takes in host cell cytoplasm by
invagination. Haemoglobin is digested resulting in haematin
deposits in granules with in food vacuoles.
• Schizogony may continue indefinetly. Release of merozoites
from all schizonts occur synchronisingly in host. In human
malaria this is associated with paroxysm of fever. Fever is
not important in avian host. After a number of asexual
generation , the sexual cycle occurs.
• Macrogametes with haploid number of chromosomes are
more than male microgamonts and stain more intensively
blue than male-microgamete. The nucleus of microgamont is
more diffused than in female cells . Further development
takes place when the blood is ingested.
• Development in mosquitoe is rapid within 10-15 minutes.
Nucleus of microgamete divides and through a process of
exflagellation . About 6-8 long thin flagella like microgamete
are extruded from parent cell which remain attached to
parent cells for few minutes lashing actively. They detach
and run away to fertilise macrogamete to form zygote.
• The zygote is motile and is called as ookinete . The ookinete
penetrates midgut and lies on outer surface of stomach
forming early oocyst. They are 50-60µm in diameter. In 10-
20 days, large number of sporozoites are produced by
repeated division of oocyst nucleus which make the oocyst
rupture to release the sporozoites .The liberated sporozoites
migrate all over the body, reach salivary gland of mosquitoes.
• The mosquitoes are infective to new host and infection
occurs when mosquitoes takes a blood meal.The mosquito
remains infected for its life span transmiitting malarial
parasites every time the mosquito takes blood meal.
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PLASMODIUM GALLINAE
• Domestic fowl, pheasants, peacock, wild birds.
• Gamonts round, possess pigment granules of large size and
few in number.
• Schizonts: Round to irregular- 8-30 merozoites. Gamonts
and schizonts displace host cell nucleus.
• Schizony is 36 hr cycle.
• Peak of segmentation or schizogony is seen during noon and
midnight. Exoerythrocytic cycle is seen in endothelial cells
and REC of spleen, brain and liver.
• experimentally Aedes and Armigyrus sp can be infected.

Pathogenesis

• Mortality is upto 80% in certain areas. progressive

emaciation, anaemia, enlargement of spleen and liver,
paralysis due to massive exoerythrocytosis forms in
endothelial cells of brain capillaries.

MODULE-25: GENUS-HAEMOPROTEUS
Species: Haemoproteus columbae

• Gametocytes occur in RBC

• They are halter shaped encircling the nucleus of RBC.
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Merogony

• Merogony occurs in endothelial cells of blood vessels

especially in lung, liver, spleen and not in RBC as
in Plasmodium.
• The parasites are transmiited by hippoboscid flies and in
some cases by Culicoides sp. Sporozoite from salivary gland
are injected into new host through fly bite.
• Sporozoites enter bloodstream ,penetrate endothelial cells of
blood vessels and develop into early schizonts . By growth
and nuclear division , 15 or more small unpigmented masses
or cytomeres each with single nucleus is produced.
• Each cytomere continues to grow and divides into enormous
number of minute merozoites. Endothelial cells break down
and cytomeres are released out.
• They accumulate in capillaries which they block.They
rupture and liberate merozoites into bloodstream, enter RBC
to become gamonts.

Gametogony

• The gamonts are tiny to elongate crescent shaped encircling

the host cells.
• The nucleus of macrogamonts stain dark blue with
Romanowsky stains, nucleus is compact staining dark purple
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to red and the pigment granules are dispersed throughout

the cytoplasm.
• Microgametes stain pale blue to pink. Nucleus is pale pink
and diffused. Pigment granules are collected into a spherical
masses.

Pathogenesis

• Adult birds show no evidence of of disease. An acute form of

the infection is reported in pigeon nestling (squabs) with
heavy mortality.

Clinical signs: Anorexia, anaemia,

Post mortem findings: Liver and spleen enlarged, dark in

colour.

Diagnosis

• Presence of gamonts in blood smear.

• Presence of schizonts in endothelial cells of blood vessels,
liver, lung, spleen and kidney.

Treatment: Quinacrine is effective against young gamonts.

Control: Vector control.

GENUS: LEUCOCYTOZOON
• Macrogamonts and Microgamonts are seen in leucocytes and
RBC.
• PM: Haemozoin not formed.
• Merogony in parenchyma of heart, liver, kidney.
• Meronts form large cytomeres- no merogony in erythrocytes
and WBC.
• Vector: Simulium or midges,Culicoides
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LEUCOCYTOZOON CAULLERYI
Synonym: Akiba caulleryi

Host: Chicken, Guinea fowls.

• Gamonts are seen in RBC.

• Mature gamont is round, 20µm diameter, a dark band
extends about 1/3rd way around parasite.

Life cycle

• Vector: Culicoides sp.

• Zygote: Ookinete in mid-gut of the fly, penetrate the wall and
they become subspherical.They occur in the outer wall of
midgut and undergo sporogony.Numerous sporozoites are
formed and are released to enter salivary gland. They are
transferred to another host when fly bites.
• Host: Exo - erythrocytic meront occur in kidney, liver, lung,
also blood spaces of heart, spleen, pancreas, thymus, muscle,
intestine, trachea, ova, adrenal, brain, single or lobed
meronts divide into cytomere which fuse to form
megalomerozoites, 25-300µm.These merozoites become
gamont in periphery of RBC or erythroblast which disrupt
host cell. When mature, they break out of cell and lie in
plasma.
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Pathogenesis: Some are pathogenic and others not.

• Bangkok heemorhagic disease caused in 1954 in Thailand

might be due to L. caulleryi.
• Affected chicken have anaemia, listless, diarrhoea, pale comb
and wattle, haemorrhage in lung, liver, kidney- signs are due
to exo- erythrocytic megalomeronts which cause
haemorrhages.
• Haemorrhage into pelvic cavity for kidney.

Treatment: Pyrimethamine and sulphadiazine, Clopidol.

Prevention: Elimination of Culicoides.

LEUCOCYTOZOON SABRAZESI
• Chicken, jungle fowls.
• Anaemia, pyrexia, diarrhoea, paralysis of legs, ropy
discharge from mouth.

LEUCOCYTOZOON SIMONDI
Ducks and geese and wild anserines.
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Vector: Simulium.

Pathogenesis

• Heavy loss in young birds.

• Suddeness of onset- flock of normal duckling become ill and
die next morning.
• In acute , affected ducks dont eat, breathing rapid,
obstruction of lung by megaschizonts.
• Adult: characterised by listlessness, slow disease,
splenomegaly, liver hypertrophy, degeneration, anaemia,
WBC increased, blood clots slowly.

Diagnosis

• Gamonts in blood smear.

• No effective treatment.
• Black fly control.

LEUCOCYTOZOON SMITHI
Turkeys- domestic and wild.

Pathogenesis

• Heavy loss. but less affected than fowl. Affected birds tend to
sit and move with difficulty when run, there is in-
coordination, suddenly fall over, gasping, comatose and die.
They recover within 2-3 days and become chronic disease.
Birds will never regain their vigour. Males are stunted, moist
rales, cough, attempt to clear throat, die suddenly under
stress.
• Duodenal infection: Small intestine, anaemia, emaciation
with flabby flesh and muscles.
• Adult: carrier, liver icterus, enlarged, cirrhosis.

MODULE-26: HEPATOZOON
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• Learning objective
• More or less a disease of chronic nature this parasite is
almost found in all crossbred dogs with tick infestation. In
India this is of little importance.

HEPATOZOON CANIS
Brief life cycle

• Merogony takes place in viscera of vertebrates.

• Gamonts are seen in leucocytes . Fertilization and sporogony
is demonstrated in ticks.

Hepatozoon canis (Leucocytozoon canis, Hemogregarine canis)

• This parasite is reported from dogs,cats and reported from

wild animals like jaguars, civet cats and hyena

Structure

• Gamonts are elongated rectangular body with rounded ends

in neutrophils,
• 8-12 X 3-6µ with a central compact nucleus.
• Cytoplasm is pale blue, nucleus is red with Giemsa stain
surrounded by a delicate capsule. Sometimes gamonts are
seen free in blood.
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Life cycle

• The vertebrate host gets infected by ingesting the infected

intermediate host,brown dog tick, Rhipicephalus
sanguineus which contains sporocysts in the body cavity.
• Sporozoites are released in the intestine of vertebrate
host like dogs. They reach liver, lungs, spleen or bone
marrow through bloodstream. In tissues they become
schizonts . From this,merozoites are produced by multilple
fission.
• Two types of meronts are reported . Macromeronts lead to
micromeronts.
• Macromerozoites and micromerozoites later enter blood
cells and become gametocytes or gamonts. There is no
demarcation between two gamonts and no further
development takes place until it reaches tick.
• In the vector, gamonts leave WBC in the alimentary tract of
ticks and become associated in pair, a process known as
syzygy. Microgamont produces two non- flagellate
microgametes, one of which fertilises macrogamete and
produces zygote which is motile (ookinete). The ookinete
penetrates intestinal wall, enters haemocoel of tick wherein
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it grows and forms a oocyst.Sporoblast become sporocyst

and sporozoites develop in sporocyst.
• Oocyst (100-150µ) : It forms 30-50 sporoblasts. Each
sporoblast forms 16 sporozoites. Vertebrate hosts ingest
invertebrate hosts(tick) . Oocyst and sporocyst
reach intestine of dog and release sporozoites.

Pathogenesis

• Schizonts are found in the myocardium of domestic cats in

the capillary lumen.
• Dogs appear healthy and can cause a severe disease and
death.
• Clinical signs such as fever, progressive emaciation,
anaemia, splenomegaly, lumbar paralysis are noticed.
• Death occurs in 4-8 weeks.

Treatment: No Known treatment

Control: Vector control.

MODULE-27: BABESIDAE
Learning objective

Piroplasm means pear shaped bodies which are present inside

RBC. Genus Babesia is economically important in that it produces
an acute disease resulting in mortality among high yielding
animals and crossbred calves. The different species
of Babesia produce various degree of disease.

PIROPLASMIDA
▪ Phylum: Apicomplexa
▪ Class: Sporozoa
▪ Order: Piroplasmida
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• Piroplasms are blood cell parasites of vertebrates. They are

pyriform, round, amoeboid or rod shaped depending on the
genus.
• Occur in RBC, some in WBC or some other cells.
• Have an apicomplex at some stage.
• Not all structures are present.
• Theileria have rhoptries, MN,SPM while Babesia have polar
rings, SPMT, possible micronemes, micropores present in
some stage.
• Pigment haemozoin is not formed.
• No spores or oocyst or cilia or flagella- locomotion by body
flexion or gliding.
• Reproduction
o Sexual life cycle is seen in vertebrates
o schizogony is seen in vector by binary fission or
merogony.
o Budding is also seen more by endodyogeny or
endopolygony which form 2,4 daughter cells.
o Piroplasms are heteroxenous, Vectors are ixodid or
argasid ticks.

MORPHOLOGY
• Family: Babesiidae
• They are large, pyriform seen in RBC. They are round or
amoeboid.
• Schizogony is seen in RBC.
• Vector: Ixodid ticks.

GENUS: BABESIA
• Organisms are present in RBC, multiply by asexual division
producing 2,4 or more non- pigmented amoeboid parasites.
when stained with Romanowsky stain, they show a blue
cytoplasm, red chromatin masses at narrow end (not form
cap like as in Theileria). They are pleomorphic,
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characteristically pear shaped at an angle with narrow end

oppostions.
• There are two forms: large form 3- 5µm and small forms less
than 2.5µm.

Life cycle

• Indirect, heteroxenous, multiplication in RBC takes place by

budding to form 2 or more trophozoites.These are liberated
from erthrocytes and invade other cells. This is repeated
until large percentage of RBC are invaded.
• Blood forms are transportable by mechanical means.
Reproduction of merozooites in RBC takes place by binary
fission under natural condition. Babesia are transmitted by
ticks (Smith and Gilbourn, 1893). Transmission
of Babesia by ticks is through eggs(transovarian) or stage to
stage transmision(transtadial).
• The former happens only in one - host tick since after
attachment of larvae, the rest of the tick development occurs
in the same animal. With 2 or 3 host ticks, transtadial
transmission is common.
• Babesia bigemina in Boophilus ( Rhipicephalus ) microplus,
one -host tick
• Babesia canis in Rhipicephalus sanguineus , three -host tick

BABESIA BIGEMINA
• Disease: Cattle tick fever, Red water fever, Texas fever
(North America), Piroplasmosis.
• Host: Cattle and Buffalo
• Distribution: Tropics and Sub tropics.
• Morphology: Large- 4.5 x 2.5µm, Round forms- 2-3 µm,
Characteristic pear shaped lie in pairs at acute angles in
RBC. Round, Oval, irregular forms occur depending on stage
of development.
• Vectors: Boophilus annulatus & B.microplus in India.
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Life cycle

• Ticks during feeding inject sporozoites into blood stream of

the host . They enter erythrocytes and multiply by series of
binary fission( budding- endodiogeny , ectodiogeny
endopolygony and ectopolygony) producing merozoites
which later probably differentiate into precursors of sexual
stages.
• When ticks suck blood, infected merozoites are lysed ,while
the ovoid forms develop into uninucleate stralenkorper
bodies(Ray bodies).
• Ray bodies attach with each other- cytoplasm of one raybody
denser than that of other. Cells of ray bodies fuse to form
single dense line at place of attachment giving way to fusion
of cytoplasm.
• Two nuclei are seen close to form young zygotes.
• Zygotes transform into a motile vermiform kinete.They are
rounded in anterior end narrow posteriorly (16µm long).
• Kinetes leave intestine enter haemocoel ,invade other cells
such as ovary via haemolymph.

Development in organs of ticks

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• Asexual reproduction is initiated in cells of the (sporogony)

hemocyte, muscle, malphigian tubule, female ovarian cells
including oocyte. Kinete lies directly in the hemocyte
cytoplasm, transformed into polymorrphic structure.
• They subdivide into several uninuclear cytomeres. This
division can be observed in light microscope called Fission
bodies.
• Cytomeres differentiate into new kinete,releasedby rupture
of vacuoles in cells.
• They enter another cell repeating asexual multiplication.
This asexual multiplication results in production of kinetes
known as Sporokinete.

Development in Salivary gland

• Kinetes enter salivary gland undergo sporogony each giving

rise to minute sporozoites. Those kinetes which enter ovary
penetrate become rounded up. they divide few times
becoming very small individuals ( Sporokinete). They
remindormant in the larval tick until the larval tick hatches
from the egg.
• when the larva hatches they enter salivary gland and
multiply further becoming smaller and filling the entire cell.
• Each host cell may contain 1000s of minute parasites.These
form vermiform sporozoites and break up the host cell
Sporzoites transfer to host during feeding of nymphal ticks
(5-10x103).

Pathogenesis

• Babesiosis is highly pathogenic disease. Mortality is more

seen in adult than young calves(inverse age reaction).
• The resistance of the calves disappear between 9 and 12
months . The symptoms are more marked in exotic breeds.
The incubation period is 1-2 weeks. Fever-41-45.50 C marked
dullness, listlessness,inappetance, severe anaemia with
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destruction of RBC, haemoglobinuria,(Coffee coloured

urine) mucous membrane is pale to icteric ,spleen enlarged
soft dark red pulpy, diarhoea, constipation, faeces yellow
except in peracute cases affected animal lose condition,
emaciated, die.
• Death due to multiple organ failure due to destruction of
RBC and odema, icterus but also due to clogging of blood
vessels supplying important organs by parasitic cells or free
parasites.
• Causes degradation of endothelial cells of small blood
vessels, anorexia, development of toxic metabolites, capillary
fragility, perivascular escape of RBC, hemorrhage, shock,
death.
• Haemolysis in B.bigemina is due to increased phagocytosis
of non infected RBC due to increased Reticulo endothelial
activity.

Haematological changes

• PCV, RBC concentration, Haemoglobin- reduced by 5o%,

osmolytic fragility of RBC increased by B.bigemina infection.
• In acute phase, anaemia is normocytic later become
macrocytic and increase MCV. WBC decrease first, increase
to 2-3 folds after recovery. When Haemoglobinuria is seen ,
the temperature becomes subnormal
• In serum, increased SGOT,SGPT, BUN, Alkaline phosphate,
later stages calcium levels decrease- Serum urea kinin for
enzyme, kallikrenin activated several days before parasite
reach detectable levels in peripheral vessels leads to shock,
decreased PCV.
• Due to increased vascular permeability vasodilatation
leading to circulatory stasis- shock. Intravascular coagulation
occurs. These effects are seen before effects of RBC
destruction are seen.
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• Destruction of RBC, decreased PCV, results in destruction to

organ from anaemic anoxia superimposed on that cause by
shock.
• Release Hb overloads kidney- red cell stroma and tissue
product accelerate kinin release leading to intravascular
coagulation.
• Final stage of disease, pathogenesis process that persistently
originated from biological active substance of parasites are
reinforced by effects of Haemolytic anaemia and produce
tissue destruction.
• Apart from RBC destruction, evidence of direct removal of
non-infected erythrocytes by phagocytosis, increased
osmotic fraility of non- infected cells predisposes
spontaneous lysis in small blood vessels.
• Circulatory Antigens form circulatory complexes with
antibody and complement which lodges in kidney and cause
glomerulo nephritis. This reaction depletes body which
disposes anaphylotoxin- augment shock.

Symptoms

• Appear subdued, rumination suspended, lachrymation,

dripping saliva, staggering gait, death in 4 days. If recovered,
chronic symptoms like intermittent fever and emaciation.
• Chronic case: Organism in blood smear is seen for 3-8
weeks- course extended several weeks with intermittent
temperature rise upto 40-420C, animal thin and emaciated,
no marked haemoglobinuria, finally animal recovers, loss of
weight, icterus, hard yellow faeces.
• Cerebral form: Onset is sudden- Temperature- 41.70C in few
hours, death in 12-36 hrs. Parasites appear to accumulate
and multiply in cerebral capillaries since organisms are
rarely seen in blood smears .

Post mortem lesions

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• Sub cutaneous or Intra muscular oedema with icterus, fat

yellow gelatinous, blood thin watery. Urine dark (coffee
coloured dark brown or red), Spleen enlarged with soft dark
pulp, liver enlarged wth yellow colour distension of gall
bladderwith dark bile, Plasma reddened. Kidney congested
with high concentration of parasitised RBC. Thrombosis of
lung liver and Kidney.
• Cerebral form: Perivascular, Perineuro and interstitial
odema through brain and spinal cord.

Immunity

• Inverse age susceptibility, calves in enzootic area have low

parasitemia. No cross immunity
between B.bigemina and B.bovis.
• Acquired immunity: Clinical recovery, absence of Parasites
in peripheral blood, latent infection for many years and on
spleenectomy, organism is demonstrated. Spleenplays an
important role in immunity. Splenectomy result in relapse
and fatal infection Antibodies can be transmitted through
colostrum.

Diagnosis

• Clinical signs: Detection of parasites in blood, thick and thin

smear.
• Cerebral forms: Examination of cerebral capillary smears.
Hemoglobinuria in endemic areas.
• Immuno diagnosis: CFT, IFA, IHA, SELISA, IPT, PCR.

Treatment

• Trypan blue 100ml of 1-2% solution in normal saline given

I/V.
• Acriflavin: 20 ml 5% solution I/V
• Pyrivon, Acaprin, Babesan, Quinuronium Sulphate- 1 ml 5%
solution S/C for 50 kg Body wt.
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• Phenamidine 12 mg kg S/C in 40% aqueous solution.

• Diminazine aceturate : 2-3.5 mg kg Body wt deep I/M, 0.8-
1.6 G/100 kg.
• Diamprom amicarbalide: 10 mg kg I/M or S/C.
• Imidocarb: Therapeutic and Prophylactic. 1mg/kg S/C.
• Supportive therapy: Shock, Calcium, blood transfusion, lot of
water and saline.

Control: Tick control, immunization with with mild strain,

Exoantigen

BABESIA BOVIS (B. ARGENTINA, B. BERBERA)

• Host: Cattle, deer, stag.
• Disease: Bovine Babesiosis, Piroplasmosis, Red water
except USA, Canada.
• Morphology: Merozooites in RBC, pyriform, round,
irregular, vacuolated signet ring forms are common.
Merozoites are 2.4x1.4 µm in centre of erythrocytes.
• Vectors: Boophilus calcaratus, Rhipicephalus bursa in
Europe, B. microplus (S.America), B. australis and B.
microplus (Australia). Transmission through egg
in Boophilus and stage to stage transmission
in Rhipicephalus. Intra -uterine transmission is also
possible.
• Pathogenesis: Similar to disease by B.bigemina, high fever
week- 10 days, haemoglobinuria, cerebral form reported.
Convulsion, incordination, coma, congestion of white mater,
dilatation of capillaries packed with RBC. Perivascular
neuronal interstitial oedema through brain.
• Immunity: Same as B. bigemina. Cell free antigen for
immunisation.

BABESIA DIVERGENS
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• Northern Europe form in cattle, small 1.5x0.5µm, appear as

paired diverted from centre in RBC, pyriform, circular up to
2 µm seen.
• Transmission by Ixodes ricinus, Dermacenter reticulatus.
• Pathogenesis: Less severe than B.bigemina.
Hemoglobinuria, jaundice, Severe infection, death. Gastro -
intestinal upset with thin watery diarrhoea followed by
constipation , progressive appetite loss- death or recovery.

BABESIA MAJOR
• Resemble B. bigemina- smaller- lies in RBC, 2.6x1.5 µm at
an angle- <90%.
• Less pathogenic than B.bovis. Temperature not marked.
• Haemoglobinuria and anaemia mild.
• Indirect fluorescent antibody test is useful for diagnosis

MODULE-28: B.CANIS

• Synonym: Piroplasm canis

• Disease
o Canine babesiosis

o B.canis and B.gibsoni- Canine babesiosis, biliary

fever, malignant jaundice, Nambivu (bloody

ears).
o B. vogeli, B. felis- insignificant.

• Host: Dog, Wolf, Jackal, Racoon.

• Morphology: Large forms 4-5 µ long, pear shaped
amoeboid 2-4 µ in diameter, generally contain a
vacuole. Pleomorphic forms also seen. Multiple
infection of RBC with the organism. Organism in REC
of lung, liver, macrophages due to
erythrophagocytosis.
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• Development in Vector: R.sanguineus (in

India), H.leachi, Dermacenter sp,
H.marginatum (USSR).
• Development: Presence of spike rayed stages in tick
gut- gametes- zygotes enter into epithelium form club
shaped form- enter haemocoel- salivary gland- ova-
transovarian possible. Also S/C muscle- enter salivary
gland. In the salivary gland, numerous binary fissions
follow resulting in pyriform sporozoites within 2-3
days.
Pathogenesis
• Varies with strain- mild to highly pathogenic. Young
and old dogs susceptible. Clinical disease as severe as
seen in adult dogs. Incubation period- 10-21 days.
• Peracute: Haemoglobinuria, death.
• Acute: Fever- anaemia, icterus, inappetance, marked
thirst, weakness, prostration and death.
Haemoglobinuria is occasional.
• Chronic: Mild fever for few days, little icterus, severe
anaemia, weakness, listlessness, emaciation- other
forms of disease
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o Involvement of circulatory system- oedema,

purpura, ascites, stomatitis.
o Respiratory system- catarrah, dyspnoea,
bronchitis.
o Eyes- Keratitis, iritis, petechial haemorrhage.
o Muscle: Myositis, rheumatic muscular pain in
legs.
o CNS: Locomotor disturbance, paresis, epilepsy,
other CNS signs- Acute cerebral babesiosis,
clogging of cerebral capillaries -confused with
rabies.
o Bleeding of ear, muzzle in young dog- Nambiuva
(gurani)- S.Africa.
PM changes
• Spleenomegaly with dark red soft pulp. liver enlarged-
yellow coloured congestion- centrilobular necrosis.
• Heart pale and yellow. Kidneys yellow- nephrosis and
nephritis, muscle pale yellow- fat yellow- fluid in
cavities, hemorrhages on heart, Pleura, bronchi,
intestines. Chronic cases less icteric.
Immunity: Recovered animals are pre immune.
Diagnosis: Endemic areas- signs of fever, anemia, icterus
with or without hemoglobinuria- Canine babesiosis
confirmed by blood smear.
Treatment
• Trypan blue single I/V injection 4.5 ml of 1-2 %
solution.
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• Phenamidine- 10 mg of 5% per kg s/c repeat 24 hrs

later.
• Pyrivon 0.5 % at 0.5 %at 0.05 ml/kg s/c repeated 24
hrs.
• Berenil-3.5 mg/kg,
• Imidocarb: 1 mg/kg.
Prevention and Control
• Tick control.
• Dog kennels and human habitats are treated with
acaricides.
BABESIA GIBSONI
• Synonym: Babesiosis, Nuttalia gibsoni.
• Dog, jackal, wolf, India wild dog, fox, mongoons, badgers.
Jackal - Natural host in India.,
• Small pleomorphic trophozoites are annular, oval, signet
ring forms occur. 1/8 of RBC- bigger forms are also seen.
• Life cycle: H.bispinosa, R.sanguineus- Vector
• Transmission: Transtadial in Haemaphysalis sp. and R.
sanguineus.
• Pathogenesis: Slightly pathogenic to jackals, highly
pathogenic to dogs, anaemia, fever, haemoglobinuria,
constipation, splenomegaly, hepatomegaly- usually chronic
with relapse, no cross immunity between B.gibsoni
and B.canis.
• Treatment: Berenil-11 mg/kg as 1% solution in two divided
doses for five days .

BABESIA FELIS
• Domestic Cat: Small species, round or oval, 1.5-2µm,
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anaemia, icterus, emaciation, splenomegaly,

haemoglobinuria.
• Vector: Haemaphysalis sp.
BABESIA VOGELI
Dog

• Similar to Babesia canis, larger, life cycle similar

to B.canis, R. sanguineus, egg and transtadial transmission.
• Clinical signs similar to B.canis, less pathogenic. Other -
similar to B.canis.

PIROPLASMA OF POULTRY
• B.moshkawsky or Aegyptienella
• Chicken and turkey.
• Asia, USSR, Africa
• Anaplasma like granules, small marginal elongate body with
thin cup 0.5-2.5 µm. Four merozoites are formed.
• Life cycle: Unknown-Ornithodorus cancanensis (soft tick)
may be the vector.

MODULE-29: BABESIA IN SHEEP, GOAT,

HORSE AND PIG
• Learning objective
• We shall see the importance of babesia in small ruminants,
horse and pigs in this module.

BABESIA MOTASI
• Sheep and Goats - Europe, Middle East, USSR, Africa and
other tropics.
• Structure: Large 2.5-4x2µm, single or pair, pyriform
resemble B.bigemina, organism meet atan acute angle.
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• Development: Similar to B.bigemina

• Vectors: R.bursa, Dermacenter sylvarum, Haemaphysalis
punctata, stage and transovarian in R.bursa.
• Pathogenesis
o Acute or chronic.
o Acute: Comparable to B.bigemina- high fever,
haemoglobinuria, with prostration leading to death.
o Chronic : No characteristic signs. Recovered animals
are immune.
• Diagnosis: Clinical signs and blood smear- during acute
fever.
• Treatment: Trypan blue, 10-25 ml of 1% solution in normal
saline given I/V.

BABESIA OVIS
• Sheep and Goats - Tropics and Subtropics.
• Small spherical - 1-2.5 µm - round, occuring at the margin of
RBC. Pyriform rare in pairs, form obtuse angle, organism lie
at the margin of RBC.
• Vector: R.bursa- two - host tick, stage to stage transovarian.
• Pathogenesis:
o Less severe than B. motasi.
o Acute form: Fever, Jaundice, Hemoglobinuria,
anaemia.
o Chronic form: 1% RBC infected- recovered animals
become immune.
• Treatment: Trypan blue ineffective, Pyrevon 2 ml of 0.5%/
10 kg body wt, Berenil- 3 mg/kg.

BABESIA FOLIATA

• Seen in India.
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• Similar to B.ovis but lie central to RBC.

BABESIA TAYLORI

• Goat
• Small, 1.5-2 µm, ovoid to round, 1µ in diameter, 8-16
parasites seen due to fusion in RBC.
• Pathogenesis: Low, haemoglobinuria is not common.
BABESIA CABALLI
• Horses, Donkeys, Mules.
• Europe, Asia, Africa, USA, USSR, etc.
• Morphology: Large, similar to B.bigemina in pairs,
pyriform, 2.5-4 µm- acute angle, round form- 1.5-2 µ also
occur.
• Vector: Dermacenter sp, Hyalomma excavatum,
H.dromederi, R.bursa, R.sanguineus. Transmission- Stage
to stage- Ovarian.
• Pathogenesis
o Acute or chronic, mild or severe, ends in death.
Persistent in fever, anaemia with icterus occur,
haemoglobinuria rare.
o CNS disturbance leading to posterior paralysis.
o Clinical signs consist of restlessness, nervousness,
walking in circles, incordination, inverse age resistance,
recovered animals are pre-immune. In the absence of
infection, again they are susceptible.
• Diagnosis and Treatment
o Trypan blue 50-100 ml of 1% solution, Pyrivon- 1-2
ml/100 kg body weight of 5%, haemosporidin S/C as
2% solution 5-6 ml/horse.
o Imidocarb 0.5-1 mg/kg.
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BABESIA EQUI
• Severe in horses, donkeys and mules.
• Small, 2µm- characteristically appear as "maltese cross"
rounded or amoeboid.
• Developmental cycle: Hyalomma excavatum, H.dromoderi,
R.bursa, R.dronicus, R.sanguineus, exo -erythrocyitc
schizogony is reported. in vivo and in vitro development of
macroschizonts and microschizonts and invasion of RBC by
merozooites. Lymphoblast noticed.
• Pathogenesis: Marked increase in temperature up to 41.70C.
Appearance with organism in blood. Anemia. Peracute cases-
1-2 days after onset of clinical disease, anaemia,
haemoglobinuria, listlessness, inappetance, oedema of
dependant parts, Gastro -intestinal upsets. Hard dung with
yellow tinge. Posterior paralysis is not seen.
• PM leisions: Spleen and liver, kidney flaccid, petechial
hemorrhage, oedema of lung, pneumonia.
• Treatment: Trypan blue and Pentamidine used.

BABESIA TRAUTMANNI
• Pigs, Wart hog
• 2.5-4 µm x 1.5-2 µm.
• Oval, round, amoeboid seen.
• R.sanguineus, B.decolaratus, Dermacenter reticulatus
• Pathogenesis: Seasonal incidence of fever, anaemia,
jaundice, oedema and incordination.
• Treatment: Trypan blue-20-25 ml of 1% solution.
Phenamidine 1.5 ml of 40% / 45 kg.

MODULE-30: THEILERIA
• Learning objective
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• Another important protozoa of crossbred animals, Theileria

annulata is an important species in India causing 10-90%
mortality.A tick- borne parasite of animals. it is very difficult
to control. Treatment should be attempted at the early stage
of the disease to minimise the losses.

GENUS: THEILERIA
Morphology

• Highly pleomorphic with small, round, ovoid, irregular

bacilliform merozoites.
• Apicomplex reduced only rhoptries are present.
• No polar rings, conoids.
• Microneme and Sub-pellicular microtubules at certain
stages; micropore in RBC stage;
• merogony in lymphocytes, histiocytes, erythroblasts followed
by invasion of RBC.
• Forms in RBC may or may not reproduce.

Vector

• Ixodid ticks.

Synonym

• Gonderiae, Cytauxzoon, Haematoxzoon.

Species

• T. parva, T. lawrenci, T.annulata, T.mutans.

THEILERIA ANNULATA
• Synonym: Piroplasma annulata, T. dispar,T.sergenti,
G.annulata.
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• Disease: Tropical bovine theileriosis, Tropical piroplasmosis,

Egyptian fever, Medicoast fever,Mediterrenean fever
• Host: Cattle, Zebu, Water-buffalo - Bos indicus
• Distribution: North Africa, Southern Europe, Soviet USSR,
Asia (India).
• Mortality: 10-90%

Structure

• Forms in bovine RBC are called as merozoites. They are

predominantly round or oval but rod shaped forms are also
present
o Comma - 1.2 x 0.5 µm.
o Round - 0.75 x 2.5 µm.
o Oval - 2.0 x 0.6 µm.
o Anaplasma like - 0.5 µm.

• 2-4 forms seen in the form of cross.

• Schizonts in lymphocytes, lymph nodes to spleen and any
other organ Schizont stage of Theileria is known as Koch's
blue bodies.
• They grow from 8µm diameter up to 27µm.
• Two types of schizonts are noticed - one type of schizont is
macro -schizonts with chromatin granules 0.4 - 1.4 mm
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diameter. After nuclei divide further,they become

micromeront or micro schizont which contains chromatin
granules 0.3-0.8µm diameter which produces merozoites of
0.7- 1µm diameter.
• In ticks, spindle shaped forms that measure 8-12µm long and
0.8µm diameter are noticed

Life cycle

• Vectors
o Hyalomma detritum, Hyalomma anatolicum
anatolicum (Hyalomma excavatum), Hyalomma
marginatum isaaci (H.savignyi), H.
aegyptium, H.dromedarii, H.
truncatum and H. sucupense.
• Developmental cycle
o Cattle are infected from infected ticks by innoculation
of large number uninucleated sporozooites from
salivary glands.
o Sporozoites reach the nearest lymph node through
lymphatic system to develop initially into
macroschizonts known as Koch's blue bodies.
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• Schizogony
o Sporozoites after entry with saliva of ticks rapidly enter
lymphocyte cells.They penetrate in 10 minutes.Parasites
ingest host cell cytoplasm by a typical process.
o Nucleus divide repeatedly by binary fission resulting in
large number of schizonts containing specific number of
nuclei (chromatin granules). They are now known as
Koch's blue bodies which is visible in light microscope.
o Schizonts stimulate host cell (lymphocyte do not
multiply on its own accord) which undergo cell division
during which schizonts also divide and is distributed by
action of host cell spindle apparatus to the daughter
cell.
o Infected cell displaces uninfected lymph node tissue
and in few days produces symptoms identical to those
of leucosis.Only a single type of merozoites are formed.
Merozoites become free and penetrate actively RBC
from 8 days after infection in T.annulata, 13 days in T.
parva. Usually 4-7 days after schizogony , main
pathological effect in host are found leading to death.

Development in RBC

• Two different forms are seen.1) Slender comma shaped

forms measuring 1-1.5µm to 2µm divide by binary fission.
These may destroy host cell and may induce
erythrocytopaenia.2) Spherical forms which measure 0.5-
0.6µm representing probably gamonts from which gamete-
like stages are formed in intestine of ticks fed on infected
animals. They don't produce pigments as that
of Plasmodium sp.

Development in intestine of ticks

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• Ray bodies are discovered by Schein (1965) now proved by

Mehlhorn et al. under electron microscope and observed by
Mehlhorn and Schein (1976).
• Ray bodies seen in 2-4 days after repletion in the gut of ticks
and formed from comma shaped bodies. Spherical bodies
dont divide, considered as macrogametes and then syngamy
observed 12-13 days after feeding.
• Transformation of ovoid or spherical zygotes to club shaped
mobile club shaped structures called Kinetes.
• They enter intestinal cells and are seen in haemolymph when
tick moults.
• They penetrate cells of salivary glands after moult. Kinete is
not observed in any other organ of the tick.

Development in salivary glands

• Kinetes in cytoplasm of host cell i.e. salivary alveoli type 3

acinus which contains 3 glandular cell types, salivary acini
which contains secretory granules, cells close to acinar ducts
containing spotted granules. These two types of cells are
affected by the kinetes. Nucleus of kinetes divides with
repeated nuclear division, nucleus becomes small with 1000s
of sporozoites being formed.
• Numerous invagination formed cytomere - like
compartments on 2nd day of attachment of new adult.
• Infected salivary glands are completely filled with cytomeres
with few nuclei.
• Under light microscope, parasites seem to have a compact
form as the cytomeres are closely packed together and this
development is a continuous process and cytoplasm of host
cell is damaged considerably and remnants of cytoplasm are
seen scattered between cytomeres.
• Nucleus of host cell increases in size and seen at the
periphery of alveolus.
• Cytomere formation ends by 5th day after attachment,
formation of infected sporozoits isthen observed.
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• After 5th day following attachment, parasitised alveolus is

filled with ovoid sporozoites of 1µm- these infected particles
are ready for transmitting number of sporozoites/ salivary
gland can hardly be estimated 50,000 sporozoites are there.
This amounts to enormous inoculum of tick.

View animated life cycle

Pathogenesis and Clinical signs

• Lymphoproliferative disease clinical syndrome with T.

annulata associated with schizogony- acute, subacute or
chronic illness is seen in all breeds of cattle at all stages (both
young and adults) in buffaloses which recover readily.very
young calves showed infection. The infection is seen in
summer and rainy season.
• Incubation period 8-25 days. Course of the disease is 10-19
days;, 3-4 days in acute form, 1-2 days of febrile symptoms,
enlargement of lymph nodes, hypertrophy of all lymph node
with schizonts seen in spleen and liver.
• Fever- 410C- high until death or recover, recession of fever
by about 5th day.
• In early stages animal eats, later anorexia.
• Rapid loss of weight, coat harsh, cessation of rumination,
tachycardia, weakness, decreased milk yield, swelling of
eyelids, lachrymation, nasal discharge, anemia in few days.
• Haemoglobinuria- Bilirubinemia, bilirbinuria also present,
diarrhoea at later stages.
• Stools containing blood and mucous shreads.
• Soft sporadic cough.Conjunctiva is icteric and may show
petechial hemorhages.
• Affected animals become emaciated.
• RBC- 1 million/cu.mm.
• Death - 8-15 days.
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• Acute form- Terminal stages oedema of lung, soft cough

becomes severe respiratory distress, nervous signs include
urticarial skin, grinding of teeth.
• Peracute- Animal die in 3-4 days lasts.
• Subacute- Fever, irregular intermittent- lasts up to 10-15
days after which animal recovers. Pregnant animals abort.
• Chronic- Intermittent fever, inappetance, marked
emaciation, anaemia, icterus- 4 weeks or longer 0r 2 months.
Some cases acute form supervenes and animals die in 1-2
days. In mild form, mild fever, inappetance, listless, digestive
distress, lachrymation, lasting few days, moderate anaemia,
nodules in s/c and internal organs seen, skin erruptions seen
in later stages. Skin erruption smears reveal Koch's blue
bodies. Involvement of CNS also noticed. Staggering gait,
convulsions and other nervous symptoms seen. Progressive
leucocytosis during the course from normal of 10,000-12 to
36000/cu. mm. - increase due to lymphocytes. RBC count
low- more prolonged with T.annulata due to removal of
infected of RBC by spleen and liver not by destruction by
intra - erythrocytic parasites. Greater cell removal results
bilirubinemia and bilirubinuria.

Post mortum lesion

• Spleen, liver, muscles, infarcts includes (due to

compensatory lymphopoiesis) grey hepatisation lung
congested ,haemorhages in endocardium, epicardium
especially left ventricle. Petechial haemorhages in serous and
mucous surface.
• Mucous membrane of abomasum and small intestinte
swollen and reddened show characteristic ulcers (punched
out), 2-12 mm surrounded by zone of inflammation. Body fat
depleted and gelatinous subcutaneous lesions are seen.
• Greater red cell destruction in T.annulata infection results
in watery blood with pale mucous membranend yellow
connective tissue.
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• Immunity: Recovered animal are premune. No cross -

immunity with T. parva.

Diagnosis

• Blood smear examination and lymph node biopsy for

piroplasm of T.annulata and Koch's blue bodies .
• Serology: IFAT, extensively used, CAT, HI used. ELISA, dot -
ELISA are used .

Treatment

• Chlortetracycline or Oxytetracycline- 4mg/kg I/v, early

stage.
• Schizonticidal (after OTC treatment macroschizont
disappear in the place vacuoles appear).
• Menoctone - 11mg/kg body weight I/V given 5 days, 1st day 5
mg/kg followed by 1.5 mg/kg for 4 days.
• Chloroquine- 10 mg/kg B.Wt.
• Berenil- 2-3.5mg/kg.
• Halofugione- Anticoccidial, given early stage- 1.2 mg/kg
B.Wt.
• Buparvaquone- 2.5 mg/kg B.Wt I/m (Butalex), single
injection.
• Supportive treatment- Liver extract, vitamins, emolliative
therapy- Parvaquone 10mg/kg- 2 doses, 48 hrs interval.
• Diethyl carbamazine- 50mg/kg, I/m.
• Anti histamine- severe anemia- blood transfusion.

Control

• Tick control by repeated dipping.

• Quarantine measures.
• Immunization
o Virulent field strain passaged in vitro
o Schizont culture- Calf innoculated from cell culture
withstood homologous strain.
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o Now in India RAKSHAVAC -T

o Young calves vaccinated with attenuated schizonts, 2
months later, tick stabilates given.
• Infection and treatment method
o By infecting calves with infected ticks or tick stabilates
(GUTTs) and administering Chlortetracyclines at 16
mg/kg B.Wt for 8 days prevents severe reaction, but
allows resistance to homologous strain.
o Acaricide and tick control.

MODULE-31: THEILERIA PARVA

• Synonym: T. lawrenci
• East Coast Fever , Bovine theileriosis, Corridor's disease.
• Animals affected: Cattle, Water buffalo , Synceres cafer
• Highly fatal encephalitis of cattle in E.Africa known as
"Turning Sickness".

Morphology

• Piroplasm form 80%- rod shaped. 1.5x0.5-1µm, round, oval

comma occur.
• T. lawrenci- 65%- round or oval.

Life cycle

• Schizogony life cycle occur in reticulo endothelial system--(

different from T.annulata) found in spleen, lymph node.
Schizonts smaller, circular and irregular.
• Rhipicephalus. appendiculatus, R.evertsi, Hyalomma
excavatum, H. dromadarii, H. truncatum- Transtadial
transmission.
• PP- 4-12 days, others as previously described .

Pathogenesis
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• Highly pathogenic- 90% die, mortality low in endemic area,

calves- 5-50% die.
• Incubation period- 8-24 days.
• Disease runs 4-12 days.
• Acute
o Fever (1070C). Continue up to or after 7-11 days, other
symptoms appear- cessation of rumination, ,
lachrymation, swelling of lymph node, iris, jowl,ears,
tachycardia, general weakness, decrease in milk yield.
diarrhoea with blood, marked emaciation, cough,
icterus, breathing rapid with dyspnoea at death,
oligocythemic anaemia, no haematuria.
• Sub -acute
o Similar to acute, less severe pronounced-recover but
after several days.
• Mild
o Mild fever, lasting several days, lymph node swelling.
• Leisions: Similar to T.annulata
• Immunity: Recovered animals are solidly immune. Parasites
clear up completely. No premunity.
• Diagnosis: Similar to T.annulata
• Treatment: No drug is effective . Same drugs indicated
for T.annulata can be used.
• Control: Repeated dipping every 3 days. No cross-immunity.

THEILERIA MUTANS
• Synonym: T.orientalis, T.buffeli, G. mutans, cattle-Beningn
Theileriosis- non fatal form in erythrocytes, round, oval, 1-
2µm, 55%- round or oval. Schizonts not readily detected, 2-4
parasites in a single RBC can be seen as a result of multiple
infection.
• Ticks: R.appendiculatus, R.evertsi, H. bispinosa, H.
punctata, stage to stage transmission.
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• Pathogenesis: Not so pathogenic,acute form impossible.

when exposed to massive parasites,mortality is less than 1%.
Signs, course and lesions are similar to mild T.annulata,
anaemia, icterus, lymph node swollen, liver, lungs, swollen
infarcts in kidneys, haemoglobinuria absent. T.mutans is
reported in Sub -Saharan,transmiited by Amblyomma sp.
Benign tumor in , T.orientalis (T.mutans in
part, T.sergenti in part). Bacillus thuringiensis in other
places it is to be determined, transmission by H.longi- Asia,
Australia, H.punctata in Europe.

THEILERIA HIRCI

• Similar to T.annulata in cattle, but in sheep and goat.

• 50-100% most highly fatal.
• Morphology: Similar to T.annulata, schizogony in
lymphocytes of spleen
• Vector : Rhipicephalus bursa
• Infection is mild in young animals
• Acute sub -acute and chronic disease seen
• Emaciation, fever listlessness, atony of rumen,
weakness anaemia icterus, haemoglobinuria,swollen
lymph nodes,
• Liver and spleen enlarged
• Lung oedematous, infarction in kidney
• Petechiae in abomasum
• Diagnosis by blood smear examination
• Treatment Similar to T.annulata
Last modified: Tuesday, 6 Decem
THEILERIA OVIS
• Sheep and Goat: smaller than T.hirci.
• Morphology: Resemble T.hirci, relatively scarce.
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• Ticks: Rhipicephalus sp., Dermacenter, Haemaphysalis sp,

Ornithodorous.
• Non Pathogenic, fever, swelling of lymphnode, anemia, no
cross immunity between T. hirci and T.ovis.

THEILERIA FELIS
• Cytoxayzoon felis
• RBC and lymph node of cat in USA.
• 1-1.5µ merozoites in histiocytes. Spleen, lymph node, liver,
lung-Koch's blue bodies.
• Pathogenesis: Abortion or fatal pyrexia, depression, icterus
and fever may be present. Lymph node enlarged and
reported in rabbit, sheep , goat, etc. Cause abortion and still
births.

MODULE-32: CILIATES
• Learning objective
• Balantidium coli is a commensal parasite which is
opportunistic pathogen of pigs cattle and human being.
Being transmitted through contaminated water and food
sometimes more fatal in young piglets.

BALANTIDIUM COLI
• It is an enteric protozoan disease and a commensal in early
days . Now in warm climates, marked disease is reported in
pigs.

Structure
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• Organism posses cilia for locomotion.

• Posses two nuclei-large macronucleus and vesicular

micronucleus concerned with reproduction. Reproduction is
asexual transverse binary fission. Sexual reproduction is bt
conjugation 50-60 µ m rarely 100µ m oval or ellipsoidal.
• Body surface is covered with oblique longitudinal rows of
cilia. Peritstome is sub terminal at narrow end .
Macronucleus is kidney shaped. Micronuclus lies at the
notch of it.A pair of contractile vacuole and food vacuoles are
seen.
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• Cysts are produced ovoid or spherical. yellowish green in

colour Macronucleus is seen inside the cysts. Transmission
by cysts

• Pathogenesis seen in pigs. Lumen of intestine without any

change in mucosa.Mild to severe enteritis with dysentry may
occur due to invasion of organism into mucosa causing
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superficial or deep ulceration. Organism is seen deep upto

muscularis layer os caecumand colon. Lymphocytic
infilteration . In Man deep ulcers may be produced. So it is
a zoonosis. In buffaloes it causes severe diarrhoea
Ingestion of cysts contaminated with food stuf is the cause of
disease in man.
• Diagnosis symptoms lesions and ulcers in large and small
intestine of pigs due to more number of B.coli
• Treatment tetracycline-250mg/kg

MODULE-33: INTERNATIONAL CONTROL

REGULATIONS FOR DIFFERENT PROTOZOAN
PARASITES (AS PER OIE,2010)
LEISHMANIOSIS

• Leishmaniosis is not a single entity but comprises a variety

of syndromes due primarily to at least 16 species and
subspecies of Leishmania . Dogs are commonly affected
by L. infantum and L. chagasi ( now regarded as synonyms )
, but canine infections with L. tropica, L. major and L.
braziliensis have also been reported. In humans, the clinical
spectrum ranges from asymptomatic infections to those with
high mortality, with three distinct forms being classically
described: visceral ( VL ), cutaneous ( CL ) and
mucocutaneous ( MCL ). When clinical signs and
characteristic lesions are present in affected humans and
animals, the demonstration of the parasites in stained
smears of splenic, bone marrow and lymph node aspirates, of
skin scrapings, and in tissue biopsies, gives a positive
diagnosis. If the infection is low grade, detection of parasites
is possible only by attempting in-vitro or in-vivo isolation or
by polymerase chain reaction ( PCR ) . Serology is the
preferred method for diagnosis of canine leishmaniosis and
VL, even during the early stages of the disease. In subclinical
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forms, seropositive cases are confirmed by parasitological

diagnosis or PCR. Of the several serological techniques
available, the indirect fluorescent antibody test and the
enzyme-linked immunosorbant assay are the most suitable.
The leishmanin skin test is useful for determining the
distribution of human infections, distinguishing immune
from nonimmune cases. The test is positive in CL, MCL and
cured VL, but negative in active VL.
• Requirements for vaccines and diagnostic
biologicals: There is no effective vaccine available at
present for use in dogs or humans. Leishmanin is no longer
available commercially and needs to be standardised.

TRYPANOSOMA EVANSI INFECTION (SURRA)

• Trypanosoma evansi causes a trypanosomosis known as ‘

surra’ . It affects a large number of wild and domesticated
animal species in Africa, Asia, and Central and South
America. It is an arthropod-borne disease; several species of
haematophagus flies, including Tabanids and Stomoxys, are
implicated in transferring infection from host to host, acting
as mechanical vectors. The general clinical signs of T.
evansi infection are not sufficiently pathognomonic for
diagnosis. Laboratory methods for detecting the parasite are
required. a variety of antibody detection tests have been
introduced for laboratory and field use. Some have been
partially validated, but await large-scale evaluation and
standardisation. The most relevant are immunofluorescence
test ( IFAT ) , enzyme - linked immunosorbant assays (
ELISA ) and card agglutination test ( CATT/ T. evansi). For
field use, only CATT /T. evansi can be applied. Estimates of
predictive values indicate that ELISA for detecting IgG is
more likely to classify correctly uninfected animals, while the
CATT is more likely to classify correctly truly infected
animals. ELISA would thus be suitable for verifying the
disease-free status of animals prior to movement or during
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quarantine. CATT can be used to target individual animals

for treatment with trypanocidal drugs. For declaring a
disease-free status, serial testing – CATT and ELISA
followed by re-testing of suspect samples – is recommended,
preferably completed by PCR. No vaccines are available for
the disease.

TRICHOMONOSIS

• Bovine venereal trichomonosis is caused by Tritrichomonas

foetus, a flagellate protozoan parasite. It is world-wide in
distribution and at one time was of major economic
importance as a cause of abortion and infertility, especially
in dairy cattle. Tritrichomonas foetus is a flagellate, pyriform
protozoan parasite seen in of preputial samples of infected
bulls and vaginal washings or cervico-vaginal mucus of
infected cows, or sometimes in aborted fetuses. The standard
diagnostic method for bulls involves the appropriate
collection, examination and culture of smegma from the
prepuce and penis. Smegma can be collected by a variety of
means including preputial lavage or scraping the preputial
cavity and glans penis at the level of the fornix with a dry
insemination pipette. A number of in-vitro culture media
exist, but more recently a commercially available field
culture test2 has been introduced that allows for
trichomonad growth and direct microscopic examination.
Bovine trichomonosis may also be detected by polymerase
chain reaction amplification. In the past, an agglutination
test using mucus collected from the cervix and an antigen
made from cultured organisms has been used as a herd test.
Similarly, an intra - dermal test using a trichloracetic acid
precipitate of the organism has been used in herds.
• Requirements for vaccines and diagnostic
biologicals : A partially efficacious, killed whole-cell
vaccine is commercially available as either a monovalent, or
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part of a polyvalent vaccine containing Campylobacter and

Leptospira .

CRYPTOSPORIDIOSIS

• Cryptosporidiosis is caused by protozoan parasites of the

genus Cryptosporidium , in which there are 18 ‘valid’ species.
In livestock, C. parvum, C. andersoni, C. baileyi, C.
meleagridis and C. galli have been reported to cause
morbidity and outbreaks of disease. Laboratory
identification is required to confirm diagnosis. There is no
prescribed test for Cryptosporidium infection. The
demonstration of Cryptosporidium species oocysts
or Cryptosporidium antigen in a properly collected and
submitted sample is sufficient for a positive diagnosis.
Diagnosis is established microscopically, with the acid-fast
Ziehl–Neelsen or auramine phenol methods using
unconcentrated or concentrated faecal smears. Microscopy-
based methods for detecting oocysts and enzyme-linked
immunosorbant assays for
detecting Cryptosporidium antigens are relatively
insensitive, but are sufficiently sensitive for detecting clinical
cases. The polymerase chain reaction ( PCR ) and restriction
fragment length polymorphism ( RFLP ) and/or sequencing
can be used to determine some or
all C ryptosporidium species/genotypes or subtypes. Those
typing and sub typing systems used for veterinary ( and
human ) samples should also be used for environmental
samples, to avoid any confusion arising from using different
systems during the investigation of disease outbreaks with
both veterinary and public health implications. Specimens
for primary diagnosis should be collected during acute
infection, and should be processed as soon as possible,
ideally, within 24 hours. Transportation to the laboratory
should be in accordance with the International Air Transport
Association regulations. There are no international
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standards for the preparation of purified oocysts, antisera,

antigens, monoclonal antibodies or hybridomas, although a
variety of purified oocysts and coproantigen detection kits
using monoclonal antibodies are available commercially.
• Serological tests Cryptosporidiosis is often a disease of the
newborn and unless there has been exclusion of exposure to
infectious oocysts, serological tests do not offer any benefit.
• Requirements for vaccines and diagnostic
biologicals There is no control programme for
cryptosporidiosis, neither is there a rigorously tested and
accepted vaccine available.

TOXOPLASMOSIS

• Toxoplasmosis is a zoonotic infection of animals caused by

the protozoan parasite Toxoplasma gondii . It has the
capacity to infect all warm-blooded animals and, while
infection does not cause clinical illness in the majority of
animal species, in some it causes acute life-threatening
disease and in others, particularly sheep and goats, it may
manifest itself as a disease of pregnancy by multiplying in
the placenta and fetus.
• Toxoplasma gondii is an obligate intracellular parasite that
has a sexual cycle in felidae and a two-stage asexual cycle in
all warm-blooded animals. In aborting sheep, goats and
pigs, T. gondii is often difficult to find in tissue sections, but
is more likely to be seen in sections of brain and placenta. Its
identity can be confirmed by immune histochemistry, while
the polymerase chain reaction may be used to identify
parasite DNA in tissues. Isolation of T. gondii from samples
is expensive and slow but, if required, is best achieved by
inoculation of mice with tissue homogenate derived from
fetal brain or placenta. The dye test is the longest established
serological method, and in many ways represents the ‘gold
standard’, at least in humans. The test has proven unreliable
in some species. In addition, as live Toxoplasma is used, the
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test carries a potential risk of human infection as well as

being expensive to conduct. The indirect fluorescent
antibody ( IFA ) test is safer, gives titres comparable with the
dye test and can be used to differentiate IgM and IgG
antibodies. The direct agglutination test and the latex
agglutination test are both relatively rapid and neither
requires complex laboratory facilities. The enzyme-linked
immunosorbant assay requires more sophisticated
laboratory equipment but can handle large numbers of
samples and does not rely on human interpretation for the
result.
• Requirements for vaccines and diagnostic
biologicals A vaccine composed of live T. gondii tachyzoites
is available commercially for use in sheep in certain
European countries and New Zealand. The vaccine is
supplied as a concentrated suspension of tachyzoites with an
approved diluents and delivery system. The vaccine must be
maintained and handled strictly according to the
manufacturers’ instructions as it has a very short shelf life.

BOVINE BABESIOSIS

• Babesiosis is a tick-borne disease of cattle caused by the

protozoan parasites Babesia bovis, B. bigemina, B.
divergens and others. Rhipicephalus (Boophilus) spp., the
principal vectors of B. bovis and B. bigemina , are
widespread in tropical and subtropical countries. The major
vector of B. divergens is Ixodes ricinus . Other important
vectors include Haemaphysalis and
other Rhipicephalus spp. In the case of live animals, thick
and thin films of capillary blood should be taken from, for
example, the tip of the tail. Demonstration of parasites in
dead animals is possible by microscopic examination of
smears of peripheral blood, brain, kidney, heart muscle,
spleen and liver, provided decomposition is not advanced.
Enzyme-linked immunosorbant assays ( ELISAs ) have
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replaced the indirect fluorescent antibody ( IFA ) test as the

most widely used test for the detection of antibodies
to Babesia spp. , because of processing efficiency and
objectivity in interpretation of results. The IFA test has been
used for detection of antibodies to B. bigemina , but
serological cross-reactions make species diagnosis difficult.
The complement fixation ( CF ) test has also been used to
detect antibodies against B. bovis and B. bigemina .
• Requirements for vaccines Vaccines consisting of live,
attenuated strains of B. bovis,B. bigemina or B.
divergens are produced in several countries from the blood
of infected donor animals or from in-vitro culture. The
vaccines are provided in frozen or chilled forms. Frozen
vaccine has the advantage of allowing thorough post-
production control of each batch, but has a much reduced
post-thaw shelf life compared with chilled vaccine. The risk
of contamination of this blood-derived vaccine makes
thorough quality control essential, but this may be
prohibitively expensive. Whilst in-vitro production methods
offer obvious advantages in terms of animal welfare, vaccine
can also be successfully produced using in-vivo production
systems under strict animal welfare guidelines. With
either in-vivo or in-vitro systems, strict adherence to
production protocols is essential to ensure consistency of
vaccine and to avoid potential changes in virulence,
immunogenicity and consequent protectiveness associated
with continued passage of Babesia spp . organisms in both
culture and splenectomised calves. Live Babesia vaccines are
not entirely safe. A practical recommendation is to limit their
use to calves, preferably less than 1 year old, when
nonspecific immunity will minimise the risk of vaccine
reactions. When older animals are to be vaccinated, the risk
of reaction warrants close surveillance and treatment with a
babesiacide if severe reactions do occur. Protective immunity
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develops in 3–4 weeks. A single vaccination usually provides

life -long immunity.

THEILERIOSIS

• Tick-transmitted Theileria parasites of cattle are a major

constraint to the improvement of the livestock industry in
large parts of the Old World. Theileria annulata and T.
parva , the most economically important species, are
responsible for mortality and losses in production. Bovine
theileriosis is generally controlled by the use of acaricides to
kill ticks, but this method is not sustainable. Acaricides are
expensive, they cause environmental damage, and over time
ticks develop resistance to them requiring newer acaricides
to be developed. More sustainable and reliable methods for
the control of theileriosis that deploy a combination of
strategic tick control and vaccination are desirable. However,
these are yet to be successfully applied on a large scale in
endemic areas. Diagnosis of a variety of disease syndromes
caused by the parasites is principally based on clinical signs,
knowledge of disease and vector distribution, and
• Identification of parasites in Giemsa-stained blood and
lymph node smears. The most widely used diagnostic test
for Theileria species is the indirect fluorescent antibody (
IFA ) test. For the IFA test, both schizonts and piroplasm
antigens may be prepared on slides or in suspension and
preserved by freezing at ≤ –20°C, except in the case of the
piroplasm suspension, which is stored at 4°C. The IFA test is
sensitive, fairly specific, and usually easy to perform.
However, because of the problems of cross-reactivity among
some Theileria species, the test has limitations for large-
scale surveys in areas where species distribution overlaps.
The new indirect enzyme-linked immunosorbant assays
for T. parva , and T. mutans , based on recombinant
parasite-specific antigens, have demonstrated higher
sensitivity and specificity and have largely replaced the IFA
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tests previously used in Africa. In addition, newer molecular

diagnostic tests, particularly those based on the polymerase
chain reaction and reverse line blot hybridisation are proving
to be powerful tools for characterizing parasite
polymorphisms, defining population genetics and generating
epidemiological data.
• Requirements for vaccines and diagnostic
biologicals Reliable vaccines of known efficacy have been
developed for T. parva and T. annulata . For T. annulata ,
the vaccine is prepared from schizont-infected cell lines that
have been isolated from cattle and attenuated during in-
vitro culture.The vaccine must remain frozen until shortly
before administration. Vaccination against T. parva is based
on a method of infection and treatment in which cattle are
given a subcutaneous dose of tick derived sporozoites and a
simultaneous treatment with a long-acting tetracycline
formulation. This treatment results in a mild or inapparent
East Coast fever reaction followed by recovery. Recovered
animals demonstrate a robust immunity to homologous
challenge, which usually lasts for the lifetime of an animal.
Immunisation of animals with a stock ( s ) engendering a
broad-spectrum immunity is desirable to cover a range of
immunological T. parva strains that exist in the field.
Immunised animals usually become carriers of the
immunising parasite stock. Safety precautions must be taken
in the preparation and handling of T. parva vaccines to
protect the workers and to avoid contamination of the
stabilates. Consideration should also be given to the risk of
introducing new isolates into an area where they may then
become established through a carrier state.

EQUINE PIROPLASMOSIS

• Equine piroplasmosis is a tick-borne protozoal disease of

horses, mules, donkeys and zebra. The aetiological agents are
blood parasites named Theileria equi and Babesia caballi .
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Theileria equi was previously designated as Babesia equi.

Infected animals may remain carriers of these parasites for
long periods and act as sources of infection for ticks, which
act as vectors The introduction of carrier animals into areas
where tick vectors are prevalent can lead to an epizootic
spread of the disease. Infected horses can be identified by
demonstrating the parasites in stained blood or organ
smears during the acute phase of the disease. In carrier
animals, low parasitaemias make it extremely difficult to
detect parasites, especially in the case of B. caballi infections,
although they
• may sometimes be demonstrated by using a thick blood
smear technique. Molecular techniques for the detection of
T. equi and B. caballi based on species-specific polymerase
chain reaction ( PCR ) assays, targeting the 18S rRNA gene,
have been developed and continue to expand. These tests
have been shown to be highly specific and sensitive and
promise to play an increasing role in the diagnosis of
infections.
• Serological tests Infections in carrier animals are best
demonstrated by testing their sera for the presence of
specific antibodies. Currently, the indirect fluorescent
antibody ( IFA ) test and the competitive enzyme-linked
immunosorbant assay (C- ELISA ) are the primary tests used
for qualifying horses for importation. Indirect ELISAs may
also be used to detect antibodies to both species in infected
horses, although cross-reactions between T. equi and B.
caballi occur. Application of recombinant T. equi and B.
caballi merozoite proteins in diagnostic assays appear to be
very promising in the accurate determination of equine
piroplasmosis infection.
• Requirements for vaccines and diagnostic
biologicals There are no biological products available.
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