Toxoplasmosis — photos

Symptoms and syndromes in photos

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Toxoplasma gondii in epithelial gut cell of a cat, the natural host.

Photo 1. Toxoplasma gondii in epithelial gut cell of a cat, the natural host. The definitive host of the coccidial protozoan, Toxoplasma gondii is the cat which passes infective oocysts in its faeces. These will develop to a cystic asexual stage in a very wide variety of mammalian hosts, including man. Infection is acquired either from ingesting these from raw meat, or through contamination by oocysts from cat faeces. (X600)

Sporulated oocysts of T. gondii.

Photo 2. Sporulated oocysts of T. gondii. The tiny oocysts (10µ diameter) are passed unsporulated. (x325)

Endozoites of t. gondii in a leucocyte.

Photo 3. Endozoites of t. gondii in a leucocyte. Asexual and sexual reproduction occur in the epithelium of the cat's intestine. In man acute infection may result from ingestion of any stage, a proliferative phase of endodyogeny occurring in many tissues. (Giemsa x 900)

Brain X-ray showing calcification in the ventricles and sub-ependymal tissues.

Photo 4. Brain X-ray showing calcification in the ventricles and sub-ependymal tissues. Transplacental infection, usually from an acutely infected mother, in the fourth month of pregnancy produces congenital toxoplasmosis with typical calcification of the sub-ependymal tissues, and sometimes dilation of the ventricles due to rapid proliferation of the parasites.

Post-mortem appearance of brain.

Photo 5. Post-mortem appearance of brain. Irregular areas of calcification in the lateral ventricles are seen in this brain of a seven-week-old child dying of toxoplasmosis. Mental disorders and blindness are common in children who survive.

Ventricular exudates in congenital toxoplasmosis.

Photo 6. Ventricular exudates in congenital toxoplasmosis. Cross section through brain of six-week-old infant showing fibrinous ventricular exudate and septa, with periventricular necrosis (Case 4 of Frenkel and Friedlander, 1951 U.S. PHS Publication No 141)

Fatal toxoplasmosis relapce secondary to immuno-supression.

Photo 7. Fatal toxoplasmosis relapce secondary to immuno-supression. Brain from a 64-year-old woman who received immuno-suppressive therapy for multiple myelomatosis (Case 3 of Frenkel et el, Human Path 1975, 6, 97).

Fundal changes in congenital toxoplasmosis.

Photo 8. Fundal changes in congenital toxoplasmosis. Congenital toxoplasmosis may produce choroidoretinitis in later years. This painting is of a macular lesion showing ectopic choroidal pigmentation. Defective vision and squint may result.

Histology of lymph glands.

Photo 9. Histology of lymph glands. Acute infection of older individuals may be cryptic, or it may produce a prolonged low fever with lymphadenopathy. Lymph node biopsy shows follicular hyperplasia with active germinal centres containing large, pale histiocytes. These contain ingested plasma cells, not parasites, but T. gondii may be isolated from such biopsies by inoculation into mice. (x20)

Cystozoites in Toxoplasma cysts in brain section.

Photo 10. Cystozoites in Toxoplasma cysts in brain section. As the individual develops a measure of immunity, T. gondii produces typical cysts which contain numerous trophozoites formed by endodyogeny. These resting stages produce no cellular reaction in the surrounding brain tissue.(x 20)

Immunofluorescent test for toxoplasmosis(Negative control).

Photo 11. Immunofluorescent test for toxoplasmosis. (Negative control 11; positive 12.) The Sabin Feldman dye test is also commonly employed. Methylene blue stains T. gondii trophozoites obtained from mouse peritoneal exudate, but in the presence of antibody-containing serum the uptake of dye is inhibited by 50% or more. High titres occur in acute infections but a low positive titre remains indefinitely. Other useful serological tests are the CFT, direct agglutination, and toxoplasmin skin test.

Immunofluorescent test for toxoplasmosis (positive).

Photo 12. Immunofluorescent test for toxoplasmosis (positive).

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