oral contact with feces of cats shedding oocysts; and (4) transplacental fetal infection with tachy-zoites from acutely infected mothers.
Primary infection with T. gondii produces clinical symptoms in ~10% of immunocompetent individuals. The acute illness is usually self-limiting and rarely requires treatment. It can cause serious disease in pregnant women, often leading to abortion. Immunocompromised individuals may develop toxoplasmic encephalitis from reactivation of tissue cysts deposited in the brain. Toxoplasmic encephalitis typically is seen in patients with AIDS and can be fatal. Clinical manifestations of congenital toxoplasmosis vary widely, but chorioretinitis is the most common finding. The primary treatment for toxoplasmic encephalitis is the antifolates pyrimethamine and sulfadiazine. Therapy must be discontinued in ~40% of cases because of toxicity, primarily of the sulfa drug; clindamycin can be substituted for sulfadiazine without loss of efficacy. Alternative regimens combining azithromycin, clarithromycin, atovaquone, or dapsone with either trimethoprim-sulfamethoxazole or pyrimethamine and folinic acid are less toxic but also less effective than the combination of pyrimethamine and sulfadiazine.
Spiramycin, which concentrates in placental tissue, is used to treat acute acquired toxoplasmosis in pregnancy to prevent transmission to the fetus. If fetal infection is detected, the combination of pyrimethamine and sulfadiazine is administered to the mother (only after the first 12—14 weeks of pregnancy) and to the newborn in the postnatal period.
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