(Toxoplasmosis)

Infants with congenital infection are asymptomatic at birth in 70% to 90% of cases, although visual impairment, learning disabilities, or mental retardation will become apparent in a large proportion of children several months to years later. Signs of congenital toxoplasmosis at birth can include a maculopapular rash, generalized lymphadenopathy, hepatomegaly, splenomegaly, jaundice, and thrombocytopenia. As a consequence of intrauterine infection, meningoencephalitis, cerebrospinal fluid (CSF) abnormalities, hydrocephalus, microcephaly, chorioretinitis, seizures, and deafness can develop. Some severely affected infants die in utero or within a few days of birth. Cerebral calcifications may be demonstrated by radiography, ultrasonography, or computed tomography of the head.

Toxoplasma gondii infection acquired after birth may be asymptomatic, except in immunocompromised people. When symptoms develop, they are nonspecific and include malaise, fever, sore throat, and myalgia. Lymphadenopathy, frequently cervical, is the most common sign. Occasionally, patients may have a mononucleosis-like illness associated with a macular rash and hepatosplenomegaly. The clinical course usually is benign and self-limited. Myocarditis, pericarditis, and pneumonitis are rare complications.

Isolated ocular toxoplasmosis commonly results from reactivation of untreated congenital infection but also occurs in a small percentage of people with acquired infection. However, because many people become infected with T gondii after birth, even this small percentage results in a large proportion of all toxoplasmic ocular disease being attributable to infection after birth. Characteristic retinal lesions (chorioretinitis) develop in up to 85% of young adults after untreated congenital infection. Acute ocular involvement manifests as blurred vision. Ocular disease can become reactivated years after the initial infection in healthy and immunocompromised people.

In chronically infected immunodeficient patients, including people with human immunodeficiency virus (HIV) infection, reactivated infection can result in encephalitis, pneumonitis, or less commonly, systemic toxoplasmosis. Rarely, infants who are born to HIV-infected mothers or mothers who are immunocompromised for other reasons and who have chronic infection with T gondii may have acquired congenital toxoplasmosis in utero as a result of reactivated maternal parasitemia.