Toxoplasma gondii and toxoplasmosis

1. Toxoplasma gondii and toxoplasmosis Cheng Yanbin April 2005

2. Toxoplasma gondii • Infects most species of warm blooded animals,including humans. • Cause the disease toxoplasmosis. • Found in almost every country. • Estimated to infect 50% of the population of some countries. • Most of infections are asymptomatic.

3. Morphology I • Trophozoite (tachyzoite & bradyzoite) banana form or crescent-shape, 4~7 µm by 2~4 µm. (Pseuocyst) • Cyst: spherical, has a think wall around the masses of bradyzoites.

4. Morphology II • Mature oocyst: contains two sporocysts that contains 4 sporozoites.

5. Life cycle • Cats are the final host; • Mammals, birds and humans are the intermediate host; • The common infectious stages: A) The tachyzoites (in groups or clones); B) The bradyzoites (in tissue cysts); C) The sporozoites (in oocysts) .

6. Life cycle • Human infection may be acquired in several ways: A) ingestion of undercooked infected meats containing Toxoplasma cysts; B) ingestion of the oocyst from fecally contaminated hands or food; C) organ transplantation or blood transfusion; D) transplacental transmission; E) accidental inoculation of tachyzoites

7. Life cycle • In the human body, the actively proliferating trophozoites or tachyzoites are usually seen in the early, more acute phages of the infection. The cysts are formed in chronic infections and are found primarily in muscle, brain and other organs. It is a result of the host immune response.

9. Clinical diseases • The majority of infections are no-symptoms. The most severe symptoms are seen with congenital, transpacental infections or infections in the compromised patients. • Mechanism: When the trophozoites are actively proliferating, they invade adjacent cells from the original infected cells as it ruptures. This process create s focal lesions. The organisms can be disseminated via the lymphatic liquid and the blood stream to other tissues.

10. Congenial infections • It may be particularly severe if the mother acquires the infection during the first or second trimester of pregnancy. • Symptoms in these infants may include retinochoroiditis, cerebral calcification, hydrocephalus or microcephaly. Symptoms of CNS involvement may not appear until several years later. • Asymptomatic congenital infections were common in prospective studies.

11. Acquired infections • In 90% of cases, no clinical symptoms are seen during the acute infection. • However, rare symptoms seen in acquired acute infections would include chorioretinitis, myositis, and symptomatic heart, lung, liver, or CNS involvement. • Infections acquired can be categorized into four groups:

12. Lymphadenitis, fever, headache, and myalgia, with a possibility of spenomegaly. • Typhus-like exanthemous form with myocarditis, meningoencephalitis, atypical pneumonia, and possibly death; • CNS involvement, which is usually fatal; • Retinochoroiditis, which may be severe, requiring enucleation. The most common manifestation in adults is local or generalized lymphadenopathy, and the nodes most commonly involved are those of the neck.

13. Infections in the immunocompromised patients • Infections in the compromised patients can lead to severe complications (Hodgkin’s disease, non- Hodgkin’s lymphomas, leukemias, solid tumors, AIDS and transplant recipients). • The CNS is primarily involved, with diffuse encephalopathy, meningoencephalitis or cerebral mass lesions

14. Laboratory diagnosis • Observation of T.g in patient specimens, such as bronchoalveolar lavage material, or lymph node biopsy. • Isolation of T.g from blood or other body fluids, by intraperitoneal into mice or tissue culture. • Serological tests using killed antigens. • Detection of T.g DNA by PCR.

15. Treatment • Treatment is not needed for a healthy person who is not pregnant. • Treatment may be recommended for pregnant women or persons who have weakened immune systems. • Oral administration of pyrimethamine, usually accompanied by sulfadiazine, is the treatment of choice at this time.