Toxoplasmosis is of world wide distribution and is caused by a small protozoon, Toxoplasma gondii which exists in three forms i.e. trophozoites, cysts and oocysts.

The trophozoites are mainly responsible for acute infection while cysts are pathologic hallmark of chronic infection and remain latent in immunologically normal hosts. The later are formed in the intestinal mucosal cells of cats which have ingested them either in poorly cooked meat or those shed by other animals.

For completion of its life cycle it requires a definitive host e.g. a cat, sheep or pig and an intermediate host i.e. a human. There are three modes of transmission is either by ingestion of material containing either of the two, inadvertent direct or by congenital route.

Most commonly it occurs by taking improperly cooked meat (lamb, pork or beef) contaminated by T. Gondi cysts or by handling cats which are passing oocysts in their faeces.


Clinical features of Toxoplasmosis

Toxoplasmosis may present in different forms i.e. congenital or acquired.


It is transmitted from the mother infected during pregnancy to the fetus and these results in congenital type. If it is acquired in early pregnancy abortion may result but infection acquired in late pregnancy the infant at birth is free from any signs of the disease but develops symptoms of disease in 2 or 3 months.

The infant presents with neurological features such as encephalomyelitis, internal hydrocephalus chorioretinitis, convulsions and cerebral calcification. Them is wide spread involvement of C.N. system.


It may remain asymptomatic in large number of healthy adults and children where it is largely self limiting. But it is immuno competent persons who develop indications in a week to three weeks after acquiring the infection. It is mainly in the type of cervical lymphadenopathy (one or several discrete nodes, which are non-tender).

Other group of glands in the body (anterior and posterior cervical, post auricular, mediastinum and retroperitoneum) may also be enlarged. There maybe splenemegaly. A large majority of patients with lymphadenopathy may have no associated indications while some (20-40%) have features of low grade fever, malaise, arthralgia, headache and a maculopapular rash. In some people, a more complicated type of the disease may show with prolonged fever, pneumonia, pleural effusion, myocarditis, pericarditis, hepatitis, uveitis and retino choroiditis.

These generally resolve within one to three weeks. Rarely a chronic syndrome of lymphadenopathy may be seen. Immuno deficient patients such as patients of Hodgkins disease.

Lymphomas, AIDS or those receiving corticosteroids or immuno suppressive agents are more likely to suffer from a widely disseminated infection in the form of encephalopathy meningo encephalitis, high fever, myocarditis, hepatosplenomegaly etc. In such patients, lymphadenopathy may or may not be present.

Depending upon the cysts breakdown and resultant inflammatory reaction, a reactivated form of the disease mainly confined to the central nervous system may be seen. Mass lesions in the brain show with focal neurological signs such as altered mental status convulsions and features which may progress to coma.


Serologic tests are the main stay of diagnosing Toxoplasmosis. Specific anti- toxoplasma 1gM antibody can be detected in the serum using an 1gM fluorescent antibody assay (1gM- WA). Since 1gM titers appear within the first week after infection, and disappear more rapidly than IgG antibodies, testing for 1gM antibodies is useful for detecting acute infection.

Complement fixing antibodies appear and decline more quickly. T. gondi can be isolated by injecting mice intra-peritoneally with human tissue extracts (bone marrow, fetal blood, body fluids or CSF) suspected of being infected.

Peritoneal fluid of the animal is examined after 4-6 weeks for the presence of trophozites. CT scan/MRI may be done in those suspected of mass lesions in the brain. CSF generally shows a moderate rise in proteins and pleocytosis.


Asymptomatic patients of toxoplasmosis require no treatment. Immuno compromised or those with active or congenital disease shall require treatment. In adults oral pyrimethamine (25-50 mg three times a day) and sulfadiazine (4-8 g/day in divided doses) are given for 4 weeks.

Other drugs which can be used are clindamycin, spiramycin. Those with ocular form of toxoplasmosis shall require steroids (60 mg per day) in addition to a combination of pyrimethamine and sulfadiazine.

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