Clinical Information

Toxoplasma gondii is an obligate intracellular protozoan parasite that can infect a variety of intermediate hosts, including humans. Infected definitive hosts (cats) shed oocysts in feces that rapidly mature in the soil and become infectious.(1,2) Toxoplasmosis is acquired by humans through ingestion of food or water contaminated with cat feces or through eating undercooked meat containing viable oocysts. Vertical transmission of the parasite through the placenta can also occur, leading to congenital toxoplasmosis. Following primary infection, T gondii can remain latent for the life of the host; the risk for reactivation is highest among immunosuppressed individuals.

Seroprevalence studies performed in the United States indicate that approximately 9% to 11% of individuals between the ages of 6 years and 49 years have antibodies to T gondii.(3)

Infection of immunocompetent adults is typically asymptomatic. In symptomatic cases, patients most commonly present with lymphadenopathy and other nonspecific constitutional symptoms, making definitive diagnosis difficult to determine.

Severe-to-fatal infections can occur among patients with AIDS or individuals who are otherwise immunosuppressed. These infections are thought to be caused by reactivation of latent infections and commonly involved the central nervous system.(4)

Transplacental transmission of the parasites resulting in congenital toxoplasmosis can occur during the acute phase of acquired maternal infection. The risk of fetal infection is a function of the time at which acute maternal infection occurs during gestation.(3) The incidence of congenital toxoplasmosis increases as pregnancy progresses; conversely, the severity of congenital toxoplasmosis is greatest when maternal infection is acquired early during pregnancy. Most infants infected in utero are asymptomatic at birth, particularly if maternal infection occurs during the third trimester, with sequelae appearing later in life. Congenital toxoplasmosis results in severe generalized or neurologic disease in about 20% to 30% of the infants infected in utero; approximately 10% exhibit ocular involvement only and the remainder are asymptomatic at birth. Subclinical infection may result in premature delivery and subsequent neurologic, intellectual, and audiologic defects.

Detection of T gondii DNA by polymerase chain reaction (PCR) has proven to be a rapid and reliable alternative or supportive method for the diagnosis of toxoplasmosis. When performed on blood, it may detect circulating parasite DNA and thus confirm or support the results of serologic testing. PCR testing on peripheral blood has been used successfully to detect cases of ocular toxoplasmosis (3) as well as invasive disease in allogeneic stem cell recipients.(4,5) However, blood may not be a sensitive specimen for detecting organ specific disease (eg, ocular or cerebral toxoplasmosis). In this case, other specimens (eg, ocular fluid, CSF, fresh tissue) should be considered (order PTOX / Toxoplasma gondii, Molecular Detection, PCR, Varies).