T. gondii is a coccidian parasite ubiquitous in nature. Members of the feline family are definitive hosts. The organism exists in 3 forms: oocyst, tachyzoite, and tissue cyst (bradyzoites). Cats generally acquire the infection by feeding on infected animals such as mice or uncooked household meats. The parasite replicates sexually in the feline intestine. Cats may begin to excrete oocysts in their stool for 7–14 days after infection. During this phase, the cat can shed millions of oocysts daily for 2 weeks. After excretion, oocysts require a maturation phase (sporulation) of 24–48 hours before they become infective by oral route. Intermediate hosts (sheep, cattle, and pigs) can have tissue cysts within organs and skeletal muscle. These cysts can remain viable for the lifetime of the host. The pregnant woman usually becomes infected by consumption of raw or undercooked meat that contains cysts or by the accidental ingestion of sporulated oocysts from soil or contaminated food. Ingestion of oocysts (and cysts) releases sporozoites that penetrate the gastrointestinal mucosa and later differentiate into tachyzoites. Tachyzoites are ovoid unicellular organisms characteristic of the acute infection. Tachyzoites spread throughout the body via the bloodstream and lymphatics. It is during this stage that vertical transmission from mother to the fetus occurs. In the immunocompetent host, the tachyzoites are sequestered in tissue cysts and form bradyzoites. Bradyzoites are indicative of the chronic stage of infection and can persist in the brain, liver, and skeletal tissue for the life of the individual. There are reports of transmission of toxoplasmosis through contaminated municipal water, blood transfusion, organ donation, and occasionally as a result of a laboratory accident.
Acute infection in the adult is often subclinical (90% of the cases). If symptoms are present, they are generally nonspecific: mononucleosis-like illness with fever, painless lymphadenopathy, fatigue, malaise, myalgia, fever, skin rash, and splenomegaly. The vast majority of congenital toxoplasmosis cases are a result of acquired maternal primary infection during pregnancy; however, toxoplasmic reactivations can occur in immunosuppressed pregnant women and result in fetal infection. Approximately 84% of women of childbearing age in the United States are seronegative and thereby are at risk to acquire T. gondii infection during gestation. Placental infection occurs and persists throughout pregnancy. The infection may or may not be transmitted to the fetus. The later in pregnancy that infection is acquired, the more likely is transmission to the fetus (first trimester, 17%; second trimester, 25%; and third trimester, 65% transmission). Infections transmitted earlier in gestation are likely to cause more severe fetal effects (abortion, stillbirth, or severe disease with teratogenesis). Those transmitted later are more likely to be subclinical. Infection in the fetus or neonate usually involves the central nervous system (CNS) or the eyes with or without disseminated systemic infection. Approximately 70–90% of infants with congenital infection are asymptomatic at birth; however, visual impairment, learning disabilities, or mental impairment becomes apparent in a large percentage of children months to several years later.