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Toxoplasmosis is caused by infection with the obligate intracellular parasite Toxoplasma gondii. Acute infection acquired after birth may be asymptomatic but is thought to result in the lifelong chronic persistence of cysts in the host’s tissues. In both acute and chronic toxoplasmosis, the parasite is responsible for clinically evident disease, including lymphadenopathy, encephalitis, myocarditis, and pneumonitis. Congenital toxoplasmosis is an infection of newborns that results from the transplacental passage of parasites from an infected mother to the fetus. These infants may be asymptomatic at birth, but many later manifest a wide range of signs and symptoms, including chorioretinitis, strabismus, epilepsy, and psychomotor retardation. In immunocompetent individuals, toxoplasmosis can also present as acute disease (typically chorioretinitis) associated with food- or waterborne sources.
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T. gondii is an intracellular coccidian that infects both birds and mammals. There are two distinct stages in the life cycle that are transmissible to humans (Fig. 223-1). Tissue cysts that contain bradyzoites are transmitted in undercooked meat. After an intermediate host (e.g., a human, mouse, sheep, pig, or bird) ingests the cyst, it is rapidly digested by the acidic-pH gastric secretions. Sporulated oocysts that contain sporozoites are products of the sexual cycle in feline intestines and are acquired by ingestion of food or water contaminated with infected cat feces. Bradyzoites or sporozoites are released, enter the intestinal epithelium, and transform into rapidly dividing tachyzoites. The tachyzoites can infect and replicate in all mammalian cells except red blood cells. The parasite actively penetrates the cell and forms a parasitophorous vacuole. Parasite replication continues within the vacuole. After the parasites reach a critical mass, intracellular signaling within the host and the parasite, including calcium fluxes, results in parasite egress from the vacuole. The host cell is destroyed, and the released tachyzoites infect adjoining cells. Parasites can disseminate throughout the body as free tachyzoites or within phagocytic cells in the bloodstream or via lymphatics. Tachyzoites actively invade host cells and can cross epithelial barriers.
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The tachyzoite replication cycle within an infected organ causes cytopathology and clinical symptoms. Most tachyzoites are eliminated by the host’s humoral and cell-mediated immune responses. Tissue cysts containing bradyzoites develop 7–10 days after systemic ...