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USMLE – Toxoplasmosis

Toxoplasma gondii is a coccidian protozoan parasite that commonly causes subclinical infection or mild lymphadenopathy in normal persons yet produces severe opportunistic infections in infants in utero and patients with AIDS, both of whom lack intact cell-mediated immune systems.

Toxoplasma infects a wide range of animals, but human infections are predominantly caused by one strain. Sexual reproduction occurs only in the intestinal epithelium of the cat, but humans can be infected either by ingesting oocysts from cat feces or incompletely cooked lamb or pork; the latter contains Toxoplasma cysts filled with intracystic organisms called bradyzoites. Entering through the gut, T. gondii spreads systemically and penetrates into any type of host cell, a unique property of this parasite. Bow-shaped T. gondii tachyzoites spread from cell to cell until T cell-mediated immunity develops and macrophages are activated to kill the intracellular parasites. One strong inducer of T cell-mediated immunity may be a superantigen of Toxoplasma, which, like that of staphylococci that causes toxic shock, binds directly to receptors on many T cells and causes release of large quantities of interferon-gamma. Some T. gondii cysts containing bradyzoites, however, remain dormant for years in muscle and visceral cells.

After primary T. gondii infection of the mother during the first trimester of pregnancy, disseminated and often fatal parasitemias occur in 25% of fetuses. T. gondii tachyzoites travel through the placenta into the fetus and destroy the developing heart, brain, and lung tissues. Congenital infection with T. gondii is also the most common cause of chorioretinitis in the United States, which may result in blindness in one or both eyes. In patients with AIDS, Toxoplasma reactivated from dormant cysts causes encephalitis, which frequently produces mass lesions. Iatrogenic immunosuppression in organ transplant patients results in toxoplasmosis from (1) reactivation of the cysts within the grafted kidney, heart, liver, or lungs or (2) the recipient’s own tissues after bone marrow graft.

T. gondii is able to infect all types of cells because the parasites bind the extracellular matrix protein laminin to their surface, in turn attaching to laminin receptors on the surface of host cells. While bacterial invasion of epithelial cells is dependent on host actin, invasion of host cells by Toxoplasma is dependent on parasite actin. During host cell penetration, Toxoplasma releases numerous proteins from its secretory organelles. This route of entry of the T. gondii parasites appears to be important in preventing acidification, because organisms covered with anti parasite antibodies and entering host cells by Fc receptors enter acidified vacuoles.

In otherwise normal adults, Toxoplasma causes lymphadenitis characterized by follicular hyperplasia; focal proliferation of transformed, histiocytoid B cells; and scattered accumulations of enlarged, epithelioid type macrophages, which do not form well-defined granulomas. Lesions are more frequent in young women than in men, posterior cervical lymph nodes are most often affected, and the diagnosis can be confirmed by serologic titers to Toxoplasma antigens or by staining for parasite antigens by immunohistochemical techniques.

In neonatal toxoplasmosis, destructive lesions of the central nervous system are composed of microglial nodules containing many tachyzoites located about the ventricles and aqueduct, which may be obstructed and so cause hydrocephalus. These lesions are often accompanied by extensive central nervous system necrosis, vascular thrombosis, and intense inflammation. In addition, the liver, heart, lungs, and adrenals may become necrotic.

In Toxoplasma chorioretinitis, destruction of the retina by tachyzoites is accompanied by a granulomatous reaction in the choroid and sclera.

Lillian Thompson By Lillian Thompson

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