Zoonotic parasite; Toxoplasma is an opportunistic pathogen. Infects animals, cattle, birds, rodents, pigs, and sheep. and humans. Causes the disease Toxoplasmosis

2. ClassificationClassification
Phylum: Apicomplexa
Class: Sporozoea
Subclass: Coccidia
Order: Eucoccidia
Suborder: Eimeriina
Genus: Toxoplasma
Species: gondii

3. Toxoplasma gondiiToxoplasma gondii
 Worldwide
 Zoonotic parasite; Toxoplasma is an opportunistic
pathogen.
 Infects animals, cattle, birds, rodents, pigs, and sheep.
 and humans.
 Causes the disease Toxoplasmosis.
 Toxoplasmosis is leading cause of abortion in sheep and
goats.
 Intracellular parasite.
 Final host (Felidae family, cat)
 Intermediate host (mammals )
Toxoplasmosis
1. All parasite stages are infectious.
2. Risking group: Pregnant women, meat handlers (food
preparation) or anyone who eats the raw meat

4.  Definitive (final) host. Domestic cats, who pick up
the organism from eating infected rodents.
 Asexual and sexual division is intracellular.
 Oocysts in feces.
• Intermediate host..
• Asexual tissue cycle.
• Motile, disease producing phase = tachyzoites.
• Non-motile “slow” phase in tissue cyst =
bradyzoites.
Humans (Mammals)
Cats (Mainly domestic and wild cats)

5. Toxoplasma gondiiToxoplasma gondii exists in three formsexists in three forms
All parasite stages are infectiousAll parasite stages are infectious..
1. Tachyzoites 2. Tissue cysts (bradyzoit)
3- Oocysts

6. Tachyzoite stageTachyzoite stage
 Rapidly growing stage observed in the early stage of
infection.
(Acute phase) habits in the body fluid.
 Crescent-shaped. One end is more pointed than the other
subterminal placed nucleus.
 Asexual form.
 Multiplies by endodyogeny.
 It can infect phagocytic and non-phagocytic, cells.

7. BradyzoitesBradyzoites
 Are slow-growing stage inside the tissue cysts.
 Bradyzoites mark the chronic phase of infection.
 Bradyzoites are resistant to low pH and digestive
enzymes during stomach passage.
 Protective cyst wall is finally dissolved and
bradyzoites infect tissue and transform into
tachyzoites.
 Bradyzoites are released in the intestine and are
highly infective if ingested.

8. Oocysts in the feces of catOocysts in the feces of cat
 Cat ingests tissue cysts containing bradyzoites.
 Gametocytes develop in the small intestine.
 Sexual cycle produces the oocyst which is excreted in
the feces.
 Oocysts appear in the cat’s feces 3-5 days after
infection by cysts.
 Oocysts require oxygen and they sporulate in 1- 5
days.

9. The Oocyst
• The oocyst is noninfectious before sporulation.
• Unsporulated oocysts are subspherical to spherical.
• Sporulated oocysts are subspherical to ellipsoidal.
• Each oocyst has two ellipsoidal sporocysts.
• Each Sporocyst contains four sporozoites .
• Shedding occurs 3-5 days after ingestion of tissue cysts
• Sporulated oocyst remain infective for months .

10. Life cycle of T. gondii

11. Sources of infection :
Contaminated water or food by oocysts
Ingestion of tachyzoites and bradyzoites
(cysts) in flesh of infected host.
Undercooked meat.
Mother to fetus.
 Organ transplant (rare).
Blood transfusion (rare).
Toxoplasma Transmission

12. Disease: ToxoplasmosisDisease: Toxoplasmosis
A- Acquired toxoplasmosis(Mild
lymphatic inflammation).
B- Congenital toxoplasmosis:
1-Intracerebral calcification.

13. Congenital ToxoplasmosisCongenital Toxoplasmosis
2- Chorioretinitis .
3-Hydrocephaly.
4- Microcephaly .
5- Convulsions.
6- Mental retardation .
7- Cardiomegaly .

15. Prophylaxis
1- Individuals at risk, particularly pregnant women,
children, and immunocompromised persons should avoid
contact with cat and its feces.
2- Proper cooking of meal.
3- Proper washing of hands and washing of vegetables
and fruits before eating.
4-Blood or blood products from seropositive persons
5- should not be given and screening for T. gondii
antibody
6- should be done in all blood banks.

16. control
It is difficult to control toxoplasmosis because of
wide range of animal reservoirs. Currently, there is
no effective vaccnine available for humans. A
genetically engineered vaccine is under
development for use in cats.
Treatment
Congenital infection is treated with pyrimethamine
and sulfadiazine. For primary prophylaxis
Trimethoprimsulfamethoxazole is the drug of choice

18. ClassificationClassification
Phylum: Apicomplexa
Class: Sporozoea
Subclass: Coccidia
Order: Eucoccidia
Suborder: Eimeriina
Genus:Isospora
Species: belli

19. Morphology
Oocysts of I. belli are elongatedovoid and
measure 25 μm × 15 μm.
Each oocyst is surrounded by a thin smooth 2
layered cyst wall
Immature oocyst seen in the feces of patients
contain two sporoblasts.
The oocysts mature outside the body.

20. On maturation, the sporoblast convert into
sporocysts.
Each sporocyst contain 4 crescentshaped
sporozoites
The sporulated oocyst containing 8 sporozoites
is the infective stage of the parasite.
A B
Oocysts of Isospora belli. A. Immature cyst; B. Mature cyst

21. Life Cycle
I. belli completes its life cycle in one host.
Man gets infection by ingestion of food and water
contaminated with sporulated oocyst.
When a sporulated oocyst is swallowed, 8 sporozoites
are released from the 2 sporocysts in the small intestine
and invade the intestinal epithelial cells.
In the epithelium, the sporozoites transform into
trophozoites, which multiply asexually (schizogony)
to produce a number of (merozoites). The merozoites
invade adjacent epilhelial cells to repeat asexual cycle.

22. Some of the trophozoites undergo sexual cycle (gameto
gony) in the cytoplasm of enterocytes and transform
into macrogametocytes and microgametocytes.
After fertilization, a zygote is formed, which secretes a
cyst wall and develops into an immature oocyst.
These immature oocysts are excreted with feces and
mature in the soil.
Incubation period: 1–4 days.

23. Life Cycle of Isospora belli

24. Clinical Features
Infection is usually asymptomatic.
Clinical illness includes abdominal discomfort,
mild fever, diarrohea, and malabsorption.
The diarrohea is usually watery and does not
contain blood or pus and is selflimiting.
However, protracted diarrohea, lasting for
several years can be seen in immunocompromised
persons, particularly in the human immunodefi
ciency virus (HIV) infected.

25. Indirect evidence
High fecal fat content.
Presence of fatty acid crystals in stool.
Presence of CharcotLeyden crystals in stool.
Direct evidence
It may be diffi cult to demonstrate the transparent oocyst in
saline preparation of stool.
Stool concentration techniques may be required when
direct wet mount of stools are negative.
The staining technique used are Modified ZiehlNeelsen
stain or Kinyoun acid fast staining of stool smear. In these
methods, pink colored acid fast large oocyst (>25 μm) can
be demonstrated. The stool smear can also be stained by
auramine rhodamine and Giemsa stains.
Laboratory Diagnosis
1-Stool Examination

26. 2- Duodenal Aspirates
After repeatedly negative stood examinations,
duodenal
aspirate examination or enterotest can be
performed to
demonstrate oocyst.
3- Intestinal Biopsy
Upper gastrointestinal endoscopy may provide
biopsy specimens for demonstration of oocysts.
4-Others
Eosinophilia, which is generally not seen with
other enteric
protozoan infections, is detectable in case of
isosporoloasis

27. Treatment
No treatment is indicated in self limiting infection in
immunocompetent persons.
Immunodefecient patients with diarrhea and excreting
oocysts in the feces should be treated with cotrimoxazole
(trimethoprimsulfamethoxazole)
in a dose of 2 tablet, 4 times a day for 10 days followed by
2 tablets 2 times a day for 3 weeks.
For patients intolerant to sulfonamides, pyrimethamine
50–75 mg/day is given.Relapses can occur in persons with
AIDS and necessitate maitainance therapy with
cotrimoxazole 1 tablet thrice a week.

29. Classification
•Phylum: Apicomplexa
•Class: Sporozoea
•Subclass: Coccidia
•Order: Eucoccidia
•Suborder: Eimeriina
•Genus:Isospora
•Species: belli

30. Morphology
The infective form of the parasite is oocyst.
The oocyst is spherical or oval and measures about 5 μm
in diameter.
 Oocysts does not stain with iodine and is acid fast.
The wall of the oocysts is thick, but in 20% cases, wall
may be thin. These thin walled oocysts are responsible
for autoinfection.
 Both thin walled and thick walled oocyst contain 4
crescent shaped.
 Oocyst can remain viable in the environment for
long periods, as it is very hard and resistant to most
disinfectants and temperature upto 60°C.
 It can survive chlrorinated water, but sequential
application of ozone and chlorine has been found
effective in eliminating the cysts.

31. The parasite complete its life cycle, sexual and asexual
phases in a single host (monoxenous)
Suitable host: Man.
Reservoirs: Man, cattle, cat, and dog.
Mode of transmission:
Man acquires infection by:
€ Ingestion of food and water contaminated with
feces containing oocysts
€Autoinfection.
Infective form: Sporulated oocysts.
The oocyst contains 4 sporozoites, which are released in
the intestine.

32. Life Cycle

33. Pathogenicity and Clinical Features
Clinical manifestations of c. parvum infection vary
depending upon the immune status of the host.
€ Infection in healthy immunocompetent persons
may be asymptomatic or cause a selflimiting febrile
illness, with watery diarrhea in conjunction with
abodminal pain, nausea, and weight loss. It can also
cause childhood and traveller’s diarrhea, as well as
waterborne outbreaks.

34. In immunocompromised hosts, especially those with
AIDS and CD4+ T cell counts below 100/uL, diarrhea
can be chronic, persistent, and remarkably profuse,
causing significant fl uid and electrolyte depletion,
weight loss, emaciation, and abdominal pain. Stool
volume may range from 1 to 25 L/day. Billary tract
involvement can manifest as right upper quadrant
pain, sclerosing cholangitis, or cholecystitis.

35. Laboratory Diagnosis
Stool Examination
Diagnosis is made by demonstration of the oocysts in
feces.
A direct wet mount reveals colorless, spherical oocyst of
4–5 μm, containing large and small granule. The oocysts
are diffi cult to visualize in unstained wet preparations.
 Modifi ed acid fast staining is the method of
choice and by this method oocysts appear as red acidfast
spheres, gainst a blue background . Yeast closely resembles
oocysts of c. parvum in shape and size
but can be differentiated by using acidfast stain, as they
are not acidfast and appear blue in color. The staining
can also be used for demonstration of oocysts in other
specimens like sputum, bronchial washing, etc.

36. If oocysts load is less and cannot be demonstrated even
after examination of 3 wet mounts of stool
specimen, concentration techniques like Sheather's
sugar floatation technique and zinc sulfate floatation
technique can be applied.
Fluroscent staining with auraminephenol or acridine
orange has also been reported to be a useful technique.
Definitive identification can be made by indirect
immunofl uroscence microscopy using specific antibody.

37. Histopathological Examination:
Cryptosporidia can also be identified by light and electron
microscopy at the apical surface of intestinal epithelium
from biopsy specimen of the small bowel (jejunum being
the preferred site).
Serodiagnosis:
Antibody persists for at least an year and can be
demonstrated by ELISA or immunofl uroscence.
An ELISA for detection of cryptosporidium antigens
in stools using monoclonal antibody has also been
developed and is highly sensitive and specifi c.
Molecular Diagnosis
For seroepidemiological study, western blot technique
is employed by using a 17KDA and 27KDA sporozoite
antigen.
PCR technique has also been applied to detect viable
cysts

38. Supportive therapy with electrolytes and fluids and
early antiretroviral therapy in AIDS patients.