PHYLUM APICOMPLEXA

• Classification
• A. Coccidia are placed in the phylum
Apicomplexa
• B. The phylum name is derived from
organelles at the apical end of the invasive
sporozoites and merozoites.
C. Coccidia are placed in the class Sporozoea. Each produces a
resistant spore-like cyst stage. The structure of each of these
"spores" (oocysts) is characteristic for the species
Members of the phylum Apicomplexa
A. Coccidia and related organisms
1. Eimeria spp.*
2. Isospora spp *
3. Toxoplasma gondii
4. Sarcocystis spp.
5. Cryptosporidium spp.
6. Hemmondia
7. Besnoitia
• Though recently researchers have broadened the term to include other genera, we will restrict
our use of the term coccidia to its classical referral to the Eimeria and Isospora.

B. Malaria and malaria-like organisms

1. Plasmodium spp.
2. Leucocygozoan spp.
3. Haemoproteus spp.

C. Piroplasms
1. Babesia spp
2. Theileria spp
3. Cytauzoon spp
 Subphylum Sporozoa
• Occur intracellular
• Have apical complex(some stage )
• No cilia ,flagella in the trophzoites
• Reproduction involve
– Schizogony hase(asexual)
– Gametogony phas esexual
– Sporogony
 Important veterinary groups
PHYLUM
APICOMPLEXA

Subphylum
SPOROZOA

Coccidiosis: Eimeria in ruminants,

poultry; Isospora in dog, cat, pig Class:
Coccidia

Family:
Family:Sarcocystidae
Eimeriidae

Toxoplasma

Genera:Eimeria Genera:Isopora Genera:Cryptosporidium Sarcocystis

Beseoitita
Neospora caninum
Hammondia
 This figure is a stylized illustration of sporulated oocysts representative of coccidian
genera. Below each oocyst is the name of a genus in which that morphologic form is
found. Above each oocyst is the number of sporocysts and sporozoites found in each
oocyst of that genus.
 Family: Eimeriidae

• The family contain 16 genera (most important is

Eimeria and Isopora
• Homoxenous family with a single host .
• Intracellular parasite of intestinal epithelium
• Schizogony and gametogony occure in the host,
while the Sporulation take place out the host.
 Eimeria
• Eimeria: these species are tetrasporocystic
with dizoic
• Host: poultry , cattle ,sheep , goat ,pigs ,horse
,and rabbits.
• Site :epithelial cells of the intestine and
kidney ,Liver .
 species host/habitat

Eimeria bovis
cattle/ posterior small intestine
Eimeria auburnensis
Eimeria zuernii
Disterbution cattle/small intestine
cattle/small intestine

Eimeria faurei
sheep/small intestine
Eimeria intricata sheep/small intestine, cecum
Eimeria ovina sheep/small intestine
Eimeria ovinoidalis sheep/colon

Eimeria arloingi
goats/intestinal crypts
Eimeria ninakohlyakimovae goats/intestinal crypts
Eimeria christenseni goats/small intestine

Eimeria intestinalis
rabbit/cecum, colon
Eimeria perforans rabbit/small intestine

Eimeria tenella
chicken/cecum
Eimeria maxima chicken/small intestine
Eimeria necatrix chicken/small intestine
Eimeria praecox chicken/small intestine

Eimeria danilovi
ducks/small intestine

Eimeria adenoides
turkey/colon, cecum
Eimeria meleagrimitis turkey/small intestine
 Identification
• Microscopic examination for faeces for
detection the Oocysts.
• Microscopic examination after scraping the
lesion and mixed with NaCl or by ME of
histological section of affecting tissues.
• Oocyst identifed according shape and size.
• Tissue stage :idienfied the mature schizonts
by location ,size ,and the number merozoites
contain .
 Morphology of the typical oocyst
(Eimeria spp.):

Some facts:
there are 4 sporocysts containing 2 sporozoites each
micropyle and its cap do not appear in every Eimeria-
species
bilayer oocyst wall is resisting strong chemical reagents
'stieda body' is removed by enzymatic means - trypsine and
bile salts
(b.e.: taurodeoxycholate for Emeria tenella)
Eimeria oocyst

Eimeria has four sporocysts with

two sporozoites
Isospora has two sporocysts with
four sporozoites
 Oocysts

Eimeria oocyst Isospora cyst

EIMERIA AND ISOSPORA
A. Host specificity - these parasities have a narrow host range -
(stenoxenous).
B. Organ specificity - these parasities are usually found in a specific organ.
C. Site specificity within organ or cell - these parasities inhabit specific
sites within an organ or cell.
D. Monoxenous - coccidia usually parasitize one host, the definitive host.
E. Reproduction
1. Schizogony (Merogony) -multiple fission.
2. Gamogony (syngamy) - union of similar gametes (Isogamy)
F. Structure of sporulated oocyst
1. Eimeria - 4 sporocysts, each with 2 sporozoites
2. Isospora - 2 sporocysts, each with 4 sporozoites
 Life cycle
• Lc divided to three phases :
• Sporogony , Schizogony and Gametogony .
 Detailed Life Cycle of The Coccida
Eimeria and Isospora
Infection of the definitive host begins with the ingestion of infective oocysts containing
fully developed sporozoites (within sporocysts) which are freed in the lumen of the
intestine by enzymic action of digestion upon the oocyst wall. The freed motile
sporozoites penetrate epithelial cells of the intestine and round-up to form
trophozoites which undergo a form of internal budding or cell division which is termed
a schizont at this point (or schizogony the process). The later process (first generation
schizonts) is terminated when the round internal cells elongate or become sickle
shaped (which are termed merozoites, first generation) and are released (rupture host
cells) into the intestinal lumen to enter other cells in their vicinity and repeating a
second and/maybe a third generation of schiogony (merogony). Most merozoites of
the second generation form macrogamethocytes with macrogametes which undergo
no cell division. Those merozoites which develop into microgametocytes undergo
further division forming biflagellated microgametes. The later leave host cells to
penetrate other cells containing macrogametes resulting in fertilization, forming the
zygote. The latter lays down a wall around itself from the eosinophilic plastic granules
in its cytoplasm, thus forming the oocysts which breaks out of the host cells to be
passed in the feces to sporulate or become infective in about 2-3 days under ideal
conditions of temperature (Sporogony
1. Sporozoite entering intestinal cell
2. Trophozoite in ntestinal cell.
3-5. Formation of merozoites by schizogony
6-9. Generation of merozoites detined to produce
gametocytes
10-12 Formation of macrogametocyte and
macrogamete
13-15 Formation of microgametocyte and
microgametes
16 Fertilization
17 Oocyst (zygote with membrane). Passes from hst in
the feces
 Pathology

• Symptoms of Eimeria infection include

bloody diarrhea due to intestinal epithelium
dying off since a large number of oocysts and
merozoites burst out of the cells. Necrotic
tissue clogs the cecum causing the organ to
die.
 Coccidiosis in poutry
Caecal and intestinal based in location and
associated pathology .
E.tenella and E.necatrix are the most pathogenic
and important spp.
E.acervulina ,E.mivati are common and slightly
to moderately pathogenic ,E. brunetti is un
common
E. praecox non-pathogenic
 Caecal coccidiosis
• E. tenella is responsiple for CaCo.
• One of the most serious diseases of poultry and E .tenella is
the main spp. responsible for Caecal coccidiosis .
• Mortality higher in younger birds.3-7 weaks
• Development stage in Caecum .
• Oocysts ovoidal with smooth wall.
• Clinical diseasre occure when lare number of 20,000
Oocysts ingested over short period .
• Soft faeces containing blood ,the great hemorrhage 5-6 day
• Infected chicknes are dull, listless ,drooping feathers.
• Flock coc becomes noticeable at about 72 hours after
infection .
COCCIDIOSIS OF THE SMALL INTESTINE
• E.necatrix most important and pathogenic .
• E .brunetti highly pathogenic
• E .acervulina ,
• E.maxima,E. mitis more commen moderate
pathogenic ,E.praecox minore pathogen.
• The prepatent period 4 to 7 day.
 Different characters of Eimeria in
domestic fowl.
E.tenella E.necatrix E.brunetti E,acervulina E.maxima E.mitis

Region Caeca SI Lower SI Upper Si Mid SI Lower SI

Intestinal lesion Hemorrhage Hemorrhage slight Watery exudate salmone pink No visible lesion
white spot Thickened wall hemorrhage white transverse exudate
white spot Coagulative band thickened walls
necrosis Hemorrhage with
heavy infection

Blood in faeces ++ + + _ _ _
-
Degree of ++++ ++++ +++ ++ ++ ++
pathogenicity

Oocyct size µm 23*19 20*17 25*19 18*14 30*20 16*15

50 % sporlation time in 21 20 38 12 38 19
hours at 29° C
 Diagnosis
• Depend on PM examination
• Microscopic examination the faeces for the
presence of Oocysts or by examination of
scraping or histological section of affected
tissues
• Presence large number is not related with
sever pathological change in the gut .
• At necropsy ,the location of lesion and type of
lesion .
 Treatment
• Sulphonamide 2 period of 3 day
• Sulphaquinoxaline ,some time potentiated
with diaveridine, sulphadimidinn ,
• Mixture of amporolium and ethopate have
given good result .
• In outbreak Toltrazurile or sulphonamide
 Control
• Combination Good management with
anticoccidial compound in the feed or water.
• Food and water not contaminated
• The anti-coccidial agent depend of
management concerned.
• Good ventilation
• Vaccine (live and attenuated)
• Oral vaccine available now
 COOCIDIOSIS IN CATLE
• Bovine coccidiosis occurs under one year old .
• E.zuernii & E.bovis are principle pathogen spp.
• E.zuernii is pathogenic ,attacking caecum and
colon and in sever case causing bloodstained
dysentry .
• E.bovis most commen40% ,also found in
caecum and colon and cousing a sever
enteritisand diarrhoea.
 Diagnosis and treatment
• History and Clincal sign especially
hemorrhage diarrhea in acute casses and
Identification the large number of Oo in faeces.
• PM : scraping of the small and large intestine
mucosa should be examined
 TREATMENT
• Amprolium 20-25 mg/kg daily in the feed for
5 day.
• Sulphadimidine orally or parenterally and
repeated at half dose in the next 2 -3 days.
 Preventation and control
• Good mangment
• Treatment in good sanitation
• The feed should be kept dry and clean
• When outbreaks occur ,bedding and soil may
be sterlized by 1,25 %sodium hydrocloride ,0,5
cresol or phenole by fumigation witg
formaldehyde .
 Coccidiosis in sheep and goat
• Occur in young lamp and kids
• tow of the 11 spp are known to be highly
pathogenic
• E.grandallis and E.ovinoidalis .
• Lambs affected between 4-7 weeks of age
with a peak infection around 6 weaks.
• Outbreak occur when ewe and lambs were
housed in unhygienic condition or grazed
intensively .
 Life cycle
• Oocyst are shed in feces. These are harmless to other
goats.
• Under favourable conditions these undergo sporulation in
1-3 days.
• When the sporulated oocysts are ingested these release
sporozoites which rapidly penetrate the intestinal cells.
• Now coccida pass through several stages of multiplication
durin which large schizonts are formed.
• Intestinal cells are destroyes and thousands of merozoites
break out and invade new cells.
• Eventually these merozoites form oocyst
• The entire cycle from oocyst to oocyst is 2-3 weeks.
www.dvmdocs.webs.com
 Sign and symptoms
• If a young kid is suddenly exposed to coccidia it
become severely ill 1-2weeks later.
• It’ll be off feed, listless and weak, abdominal pain by
crying.
• At first kid might have fever but later it become
normal.
• Diarrhea pasty then becomes watery. The kid may
dehydrate rapidly
• Brownish to yello green diarrhoea.
• The diarrhea is only rarely bloody. Neither is straining
common.
• The lactic acid produced by digestion of milk helps to
inhibit coccidia in nursing kid
• Sever attack may kill young kids. In strong kids
chronic disease develops.
• Kid with chronic disease cannot digest feed
properly
 Diagnosis
Case History
In peracute ,clinical sign may arise befor oocyste are
shed.
Diagnosis is based on clinical signs or microscopical
examination of feces.
The diarrhea that begins with consumption of too
much milk, grain, or lush grass may drag on for days
because of coccidiosis.
Oocyst can be identified if feces are mixed with a conc
sugar soln.
 Treatment
• Variety of sulfa drugs such as sulfaguanidine and
sulfamethazine, tetracyclines and amprolium. If
overdosed these are dangerous.
• Amprolium 50-60 mg/kg with drinking or feeding for
4 day
• Very high levels of amprolium may lead to a nervous
disease polienceaphalomalacia.
• Nitrofurazone
• All these drugs are coccidiostats.
 Preventination
• Feed lots should be kept dry and clean .not
contaminated by faeces.
• The feeding pasture area should be changed
regularly .
• Changed bedding regularly when ewes and
lamb kept in yard to avoid contamination .
• Fecal contamination of feed and water should be
prevented, this means that feeders and waterers should
be outside the pens.
• Daily cleaning the pens can reduce infection because
oocysts need to be sporulated before infection.
• Ordinary disinfectants don’t kill oocyst.
• Oocyst are killed by very hot or cold temperature.
 Isospora (syn.Cystoisospora)
• The important spp. Include I.suis in the pig
I.canis and I.ohioensis in the dog ,
I. felis ,I.rivolta in cat
Isospora belli
Transmission direct, fecal oral, via oocysts
Pathogenic potential low, non-bloody diarrhea common in
immunodeficient hosts, uncommon in others
Clinical signs absent, except in rare cases
Reservoir limited to humans, other anthropoids,strongly
host-specific
Damage low, destroys superficial mucosal cells
Prevalence world-wide, sanitation dependent
Diagnosis by microscopic ID of oocysts in fecal flotation
Treatment usually unnecessary, pyrimethamine + a
sulfa, trimethoprim, when needed
 Life cycle
The life cycle of isoporaspp differe from
Eimmeria in three respects
1. The sporulated oocyct contain tow
sporocysts each with four sporozoites
• Extraintestinal stage occur in the spleen , liver,
and lymph node.
• The rodents may be ingestion of oocysts from
the dog and cat, become infected with
asexual stage and act as reservoirs
Isospora belli oocysts
 Genera:Cryptosporidium
• Historically, numerous species of
Cryptosporidium were each thought to infect a
single host species, but recent studies show that
an isolate of Cryptosporidium from one
mammlian host can infect several mammalian
host species. Transmission is direct. Unusally
small sporulated or unsporulated oocysts are
shed in the feces. On ingestion or inhalation of
sporulated oocysts, sporozoites are released and
infect the epithelium in the digestive or
respiratory tract.
• Although asexual and sexual stages of
Cryptosporidium are morphologically
similar to those of other coccidia, they
possess some unique distinguishing
characteristics. All stages are small and
are located at the microvillar surface of
epithelial cells. When viewed with light
microscopy, these stages appear as dots.
Meronts contain only four to eight
merozoites. Some oocysts sporulate in
situ and contain four sporozoites
 Genera:Cryptosporidium

• C.parvum is the spp responsible for clinical

disease in domestic animal and man.
• C.baileyi and C.meleagridis occur in poultry.
• Unlike Eimeriidae the Cryptosporidium dosn,t
enter the cells of host and lack host specificity
.
Sporozoa, continued

Cryptosporidium parvum
Transmission direct, fecal-oral, via oocysts
Pathogenic potential variable: low in “healthy”,
moderate/high in “deficient” hosts,
depending on immunocompetence level
Clinical signs: non-bloody diarrhea/dysentery,
mild/short-term (~2 weeks) to severe/long-
term (steady or recurrent)
Reservoir: complete spectrum unknown, but
many domestic animals are known
Damage potential and mechanisms vary with
hosts & species, poorly understood
Sporozoa, continued

C. parvum, continued
Prevalence world-wide, sanitation dependent,
Diagnosis: microscopic ID of oocysts in feces by
flotation, acid-fast or immunofluorescent staining;
histologic or immunohistologic exam of biopsy
of intestinal mucosa
Treatment: paramomycin may be suppressive in
specific cases, not curative (no curative
medication known)
Cryptosporidium sp. life cycle
 Sarcocytis
• Important stage of genus found in the
intermediate host
• Both schizonts in the endothelium of the
blood vessels and the bradyzoit cysts in the
skeletal and cardiac muscles .
• Final hosts :dogs ,cat, and man
• Intermdiate host :ruminants ,pigs,and horses
• Site in final host :small intestine
• Site in intermediate host :schizonts in
endothelial cells of the blood vessels ,large
cysts contain bradyzoit in muscle
• Species :important spp with dog as final host
• S.bovicanis
• S.ovicanis
• S.capricans
• Those with the cat as the final host include
• S.bovifelis
• S.ovifelis

Man is final host

S.Bovihominis
S.porcihominis
 Sarcocystis and related parasites

• In Sarcocystis, the
intermediate host is
usually a ruminant, and
the definitive host is a
Sarcocystis cruzi oocysts
dog or other canine. in the feces of an infected
• May be common and dog
benign, although heavy
infestations may cause
death to ruminants.

A section of cattle tongue

showing three sarcocysts
Sarcocystis species Life Cycle
Life Cycle of
Sarcocystis
cruzi
 Clinical signs
• Infection in the final host is normally non-
pathogenic
• In the heavy infection of the intermediat host:
• Anorexia
• fever,
• anemia,
• loss of weight,
• recumbancy ,
• in lambs dog sitting
• In the catle :
• Loss of hair at the end of tail

These signs accompanied by :

Submandibular oedema
Enlargement of lymph node
Abortion
 Diagnosis
• Meat inspection
• Heavy infection of intermediate host based in
clinical signs and histological demonstration of
the schizont in the blood vessels of
organ(kidny,heart) and presence of cycte in
the muscle at biobsy .
• In direct haemagglutination
• In ruminant degenerative muscle
• Examination of faeces from cat and dog for
the presence of sporocyste
 Treatnent and control
• add Amprolium in diet
• Farm dog and cat should not be housed in,not
allowed to defaecate in pens and not fed un
cooked meat.
 The major features of the LF of
important class coccidia
Eimeria Isospora Cryptosporidi Toxoplasma Sarcocystis
um
LF Direct Direct Direct Direct or In direct
indirec
Infective stage Oocyst (4 Oocyst Very small Bradyzoite Bradyzoite
Of final host
sporocysts each (2sporocysts oocyst with 4 Cysts cycts
with 2 each with 4 sporozoites Tachyzoits
sporozoites sporozoites small oocyst
Infective stage _ _ _ Bradyzoite sporocysts
for cycts (4 sporozoites )
intermediate Tachyzoits
host oocyst

Asexual Single host Usually Single host Many host Many host
phase single host
Sexual cat Dog and cat
phase
Toxoplasmosis
 What is toxoplasmosis?

• Toxoplasmosis is an infection caused by a

single-celled parasite called Toxoplasma
gondii. The infection is most commonly
acquired from contact with cats and their
feces or with raw or undercooked meat
Classification
1. Toxoplasma gondii is placed in the phylum Apicomplexa
2. Invasive stages have typical apical complex
3. Part of life cycle in cats and other felids is similar to
Eimeria and Isosopora
4. Toxon = arc; Plastos = form. One stage in the life cycle is
arc- shaped.
5. The species name is derived from the host in which the
parasites was first described:Ctenodactylus gundi =
small African rodent
Geographagic Distribution: worldwide
Epidemiology and Hosts
1. 500 million people worldwide have antibody to T. gondii
2. Prevalenc is the same in men and women
3. Prevalence of T. gondii in other animals.
a. Sheep -20%
b. Cattle - 25%
c. Pigs - 30%
d. Dogs - 30%
e. Cats - 45%
f. Birds - 12%
g. Toxoplasma gondii infects many species of warm-blooded
vertebrates (euryxenous)
4. Modes of transmission:
a. Feline feces containing infective oocyst
b. Eating raw of undercooked meat
c. Congenital and acquired toxoplasmosis
• Toxoplasma is transmitted to cats that ingest
either sporulated oocysts or tissues infected with
tachyzoites, but the most common source of
infection is ingestion of tissues containing cysts.
On ingestion of cysts, bracyzoites released in the
gastrointestinal tract initiate an enteroepithelial
cycle of asexual and sexual multiplication,
followed by oocyst development and shedding of
unsporulated oocysts with feces. An
extraintestinal cycle, like that seen in nonfelids,
also occurs in cats
 Historical Facts--Toxoplasmosis
• 1. First described in 1908, in material from a small
rodent, the gondi.
• 2. Rediscovered in 1935 in the brain tissue of guinea
pigs used for encephalitis experiments.
• 3. In 1939 it was found as the cause of encephalitis
and chorioretinitis in a 31 day old infant. This
stimulated interest in the disease.
• 4. In 1969 infective cysts were detected in the stools
of cats experimentally infected with toxoplasmosis
from mouse tissue.
 Toxoplasmosis
• Domestic cat and other Felidae are the
definitive host

• Vertebrates are the intermediate host

– 1. amphibians
– 2. fish
– 3. reptiles
– 4. all warm-blooded animals including man
 Lifecycle

Toxoplasma gondii exists in 3 forms:

tachyzoite -invasive form, rapidly replicating

bradyzoite -tissue cyst, slowly replicating

sporozoite - oocyst
 Toxoplasma
Host cell/parasite interaction
Toxoplasmosis oocyst
 What factors increase the risk of acquiring
toxo?

• touching your hands to your mouth after gardening, cleaning a cat's

litter box, or anything that came into contact with cat feces
•
eating raw or partly cooked meat, especially pork, lamb, or venison

• touching your hands to your mouth after contact with raw or

undercooked meat
•
organ transplantation or transfusion (this is rare)
 Infection can occur by

• Ingestion of oocysts
• Ingestion of tissue cysts
• Transplacental transmission
• Blood transfusion or organ transplantation
Toxoplasma gondii life cycle.
• The coccidium Toxoplasma gondii infects all
warm-blooded animals, including humans. Felids
(both domestic and wild) are the only definitive
hosts. felids and nonfelids are intermediate
hosts. Toxoplasma can betransmitted to
intermediate hosts via oocysts in feline feces, via
cysts in host tissues (meat), and via techyzoites
transplacentally. Unsporulated oocysts in feline
feces sporulate outside the body and become
infectious. On ingestion, sporozoites excyst and
multiply in the intestine and associated lymph
nodes as tachyzoites..
• Tachyzoites multiply by endodyogeny (for numerous
generations, spreading through tissues and circulation,
and then encyst. Cysts persist most frequently in the
brain, liver, muscles, and retina. They are usually
spherical or elongate, thin-walled structures containing
a few to several hundred slender PAS-positive
bradyzoites or slowly multiplying zoites. Cysts ingested
by a nonfeline host release bradyzoites, which become
tachyzoitesm, and the cycle is repeated. Infection by
either oocysts or cysts during pregnancy can result in
transplacental infection of the fetus with tachyzoites
 Symptoms and Signs
Infections may manifest in several ways:
• Acute toxoplasmosis
• CNS toxoplasmosis
• Congenital toxoplasmosis
• Ocular toxoplasmosis
• Disseminated or non-CNS disease in
immunocompromised patients
 Diagnosing Toxoplasmosis
• Detecting oocysts in the stool
• Serological Testing—ELISA tests
• IGg and IGm
• Titers of IgG can last for years
• Titers of IgM usually persist for only 12 weeks
unless cat has FELV
 Toxoplasmosis - Diagnosis

Antibody testing may be

Followed by prenatal PCR
or by CT or MRI scans

Antibody testing
 ACUTE THERAPY

• Preferred
– Pyrimethamine 200mg po loading dose followed
by 75-100 mg po qd plus folinic acid 15-20 mg po
qd plus sulfadiazine 1-1.5g po q6h - 6 weeks.
• Alternatives
– Pyrimethamine with folinic acid (as standard)
with one of the following:
• Clindamycin 600 mg po q6h
• Clarithromycin 1g po bid
• Azithromycin 1.2-1.5g po qd
• Dapsone 100mg po qd - 6 weeks
 Latent

• In people with latent toxoplasmosis, the cysts are immune to these treatments, as
the antibiotics do not reach the bradyzoites in sufficient concentration.
• Medications that are prescribed for latent toxoplasmosis are:
• atovaquone — an antibiotic that has been used to kill Toxoplasma cysts .
• clindamycin — an antibiotic which, in combination with atovaquone, seemed to
optimally kill cysts in mice


Treatment of pregnant women with primary infection can decrease the incidence
of fetal infection. Spiramycin
 PREVENTION
• To eat well cooked meat - internal temperature of
1160C, or no longer pink inside.
• Proper hand washing.
• Fruits and vegetables should be washed prior to
consumption.
• To avoid contact with materials contaminated with
cat feces, handling cat litter boxes.
• To wear gloves during gardening.
 Prevention and Control

The following preventative measures apply to all persons, but because

toxoplasmosis is most severe in the perintatal period, they should be
emphasized for pregnant women and for young children.
1. Avoid contamination with oocysts from cat feces by:
a. Feeding cats dry, canned or thorougly cooked food
b. Preventing cats from hunting birds and rodents
c. Emptying litter boxes daily, before oocysts sporulate
d. Wearing gloves or thoroughly washing hands after working in the garden or
with soil, and before eating or touching the face
e. Covering children’s sandboxes when not in use
f. Preventing aerosols in the laboratory during centrifugation of potentially
infected biological samples
g. Boiling drinking water from streams, ponds, or lakes frequented by cats

2. Avoid ingestion of tissue cysts by cooking meat to over 660 C and washing
hands after handling raw meat
• The following preventative measures apply to farms and
other animal-rearing facilities. Avoid contamination of feed
or water with oocysts in cat feces by:
• 1. Using rodenticides and traps to prevent cats from
hunting rodents
• 2. covering, closing or locking feed-storage facilities to
prevent cats from entering and defecating
• 3. Promptly removing cat feces from building stalls or
cages; and flushing, burning, or burying them to destroy
oocysts
• 4. Providing adequate dry, canned, or thoroughly cooked
food and separate water to prevent cats from sharing
facilities used by other animals.
Sarcocystis
 Sarcocystis

Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Sarcocystis
 Sarcocystis and Sarcocystosis
• Sarcocystis – parasites of cattle, swine, and sheep
• Domestic animals are intermediate hosts; they pick
up infective cysts while grazing on grass
contaminated with human feces.
• Humans are infected when the meat is consumed.
• Symptoms include diarrhea, nausea, and abdominal
pain.
• No specific treatment

91
 Introduction
In sarcocystosis, the endothelium and muscles and other soft
tissues are invaded by protozoans of the genus Sarcocystis . As the
name implies, Sarcocystis spp form cysts in various intermediate
hosts—humans, horses, cattle, sheep, goats, pigs, birds, rodents,
camelids, wildlife, and reptiles. The cysts vary in size from a few
micrometers to several centimeters, depending on the host and
species.
• Sarcocystis is a genus of cyst-forming coccidia
with an obligatory two-host life cycle. cysts are
found primarily in muscles of wild and domestic
herbivores. Carnivores that prey on herbivore
hosts become infected and serve as definitive
hosts when zoites released by digestion of
mature cysts invade the intestinal epithelium and
develop directly into gamonts. Fertilization is
followed by formation of oocysts, which
sporulate within the intestine and are shed as
infective oocysts or sporocysts in the feces of the
carnivore
 Etiology
• Sarcocystis spp normally develop in 2-host cycles consisting of an
intermediate host (prey) and the final host (predator). Species-specific prey-
predator life cycles have been demonstrated for cattle-dog ( S cruzi )
• , cattle-cat ( S hirsuta )
• , cattle-human ( S hominis )
• , sheep-dog ( S capracanis , S hircicanis ),
• sheep-cat ( S gigantea , S medusiformis ),
• goat-dog ( S capracanis , S hircicanis ),
• goat-cat ( S moulei ),
• pig-dog ( S meischeriana ),
• pig-human ( S suihominis ),
• pig-cat ( S porcifelis ),
• and others. Some wildlife may serve as intermediate hosts (such as raccoons)
or final hosts (coyotes) for some species of Sarcocystis .
 Clinical finding
• Sarcocystis spp infections are quite prevalent in farm animals; In cattle severely
affected by S cruzi , the signs include fever, anorexia, cachexia, decreased milk
yield, diarrhea, muscle spasms, anemia, hyperexcitability, weakness, prostration,
and death. Cows infected in the last trimester of pregnancy may abort.
• . Sarcocystis spp infections are probably most important in growing ruminants and
swine, in which they can result in subclinical anemia and reduced weight gain.
Sarcocystis spp may also induce abortion in sheep
• Sarcocystis spp were considered of doubtful pathogenicity until induced infection with S cruzi sporocysts
from canine feces caused acute disease in calves; eosinophilic myositis in cattle; and abortions, stillbirths,
and deaths in pregnant cows. Two cases of necrotic encephalitis in heifers have been reported. Similar
pathogenicity has been demonstrated for S tenella in lambs and ewes. An outbreak of myositis affecting
20 ewes with flaccid paralysis was a result of heavy Sarcocystis infection. Immune status of the host and
the dose of cysts may be the most important factors for the development of clinical disease.
Immunosuppression may be responsible for tissue invasion of final hosts (eg, dog and cat). Pathologic
changes in myocardium and skeletal muscles were more pronounced in cows with lymphatic leukemia.
“Immunization” using small doses of sporocysts appears to prevent development or reduce severity of
clinical disease in sheep when challenged with large doses later (premunitive immunity). In dogs, a longer
prepatent period and shortened patent period resulted after repeated infection. Pigs can also have
persistent acquired immunity after immunization infections. Humans may also serve as intermediate hosts
and suffer myositis and vasculitis, but this tissue phase is rare, and the source of such human infection has
never been determined. Human intestinal illness, with clinical signs of nausea, abdominal pain, and
diarrhea that lasted up to 48 hr, has followed ingestion of sarcocysts of S suihominis in uncooked pork and
S hominis in uncooked beef. The extent of human illness from ingestion of infected meat has not been

documented .
 Pathology

• Some species of Sarcocystis are pathogenic to the herbivore intermediate

host. Acute lesions characterized by hemorrhage, edema, and necrosis are
associated with the maturation of second generation meronts.
Macroscopic lesions observed postmortem may include generalized
serous atrophy of fat, excessive yellowish fluid in all body cavities, watery
blood, petechical hemorrhage in the heart and pericardium, serosa of the
gastrointestinal tract and urinary bladder, edema and hemorrhage of
lymph nodes, and alternate pale and dark striping or mottling of skeletal
muscles. Microscopically, hemorrhage may be seen in all organs, and
mononuclear cell infiltration into the perivascular tissues of the hear,
skeletal muscles, lung, liver, and kidney may be mild to severe.
Regenerative changes are most often associated with the myocardium.
Chronic lesions charactgerized by muscle atrophy and myositis are
associated with mature saccocysts. Specific macroscopic lesions may not
always be seen postmortem. Microscopic lesions may include myositis and
myocarditis. Most definitive hosts are clinically unaffected by Sarcocystis
infection.
 Transmission
• About 1 wk after ingesting muscle tissue that contains Sarcocystis cysts (sarcocysts), the
final host begins to shed infective sporocysts in the feces; shedding continues for
several months.
• After ingestion of sporocysts by a suitable intermediate host, sporozoites are liberated
and initiate development of schizonts in vascular endothelia.
• Merozoites are liberated from the mature schizonts and produce a second generation
of endothelial schizonts.
• Merozoites from this second generation subsequently invade the muscle fibers and
develop into the typical sarcocysts.
• . Sarcocysts of some species grow so large that they are easily visible with the unaided
eye. The presence of such sarcocysts can cause condemnation of the carcass during
meat inspection.
• S cruzi is probably most important in condemnation of beef cattle for human
consumption. However, S hirsuta has been primarily responsible for dairy cattle
condemnation for visible sarcocysts.
• S meischeriana is usually the species responsible for sarcocyst condemnation of pork
and may affect meat quality.
• Sarcocysts are easily recovered from esophagus, diaphragm, and heart muscle.
Sarcocysts of some species remain microscopic even though tremendous numbers of
cysts may be present in the muscles .
• The heteroxenous (more than one obligatory host in its life cycle) life.
• In outline gametogony and sporogony occur in the intestine of the definitive host while both schizogony
which occurs in various tissues and the formation of sarcocysts (containing bradyzoites and metrocytes)
occurs prinicpally in the muscles of the intermediate host. In some cases a single species may act as both
the definitive and intermediate host.
• Oocysts are passed in the feces of an infected definitive host. The oocyst undergoes sporogony creating
two sporocysts. Once this is complete the oocyst itself undergoes lysis releasing the sporocysts into the
environment. Sporocysts typically contain 4 sporozoites and measure 15-19 by 8-10 micrometres.
• An intermediate host such as a cow or pig then ingests a sporocyst. Sporozoites are then released in the
body and migrate to vessels where they undergo the first two generation of asexual reproduction. These
rounds result in the development of meronts. This stage lasts about 15 to 16 days after ingestion of
sporocysts. Merozoites emerge from the second generation meronts and enter the mononucleate cells
where they develop by endodyogeny. Subsequent generations of merozoites develop downstream in the
direction of blood flow to arterioles, capillaries, venules, and veins throughout the body subsequently
developing into the final asexual generation in muscles.
• Merozoites entering muscle cells round up to form metrocytes and initiate sarcocyst formation. Sarcocysts
begin as unicellular bodies containing a single metrocyte and through asexual multiplication numerous
metrocytes accumulate and the sarcocyst increases in size. As the sarcocyst matures, the small, rounded,
noninfectious metrocytes give rise to crescent-shaped bodies called bradyzoites that are infections for the
definitive host. Time required for maturation varies with the species and may take 2 months or more.
 TRT
• Ponazuril 15%w/w
• Nitazoxanide 11mg/kg 5 day
• Navigator with 30%nitrzoxanide
 Control:
• Livestock become infected by sporocysts from the feces of carnivores.
Because most adult cattle, sheep, and many pigs harbor cysts in their
muscles, dogs and other carnivores should not be allowed to eat raw
meat, offal, or dead animals.
• Supplies of grain and feed should be kept covered; dogs and cats
should not be allowed in buildings used to store feed or house
animals. Amprolium (100 mg/kg, sid for 30 days), fed prophylactically,
reduced illness in cattle inoculated with S cruzi .
• . Therapeutic treatment of cattle and sheep has been ineffective.
Vaccines are not available.
• Experimental work demonstrated that infected pork could be made
safe for consumption by cooking at 70°C for 15 min or by freezing at -
4°C for 2 days or -20°C for 1 day.