Toxoplasma gondii is an obligate intracellular protozoan parasite with a worldwide distribution. Although cats are the definitive host, the organism can infect almost all mammals and birds. (...)
Toxoplasma gondii is an obligate intracellular protozoan parasite with a worldwide distribution. Although cats are the definitive host, the organism can infect almost all mammals and birds. Serological data indicates that approximately 30% of the population of most industrialized nations is chronically infected with the organism, although the prevalence varies among different populations.
Toxoplasma exists in three forms: trophozoite, cysts, and oocysts. The trophozoite is the invasive form present during the acute phase of infection. Tissue cysts are formed after multiplication of the organism within the host cell cytoplasm and may contain up to several thousand organisms. Oocysts develop in the intestinal epithelial cells of cats and are not found in other hosts. Oocysts are excreted in the feces of cats and mature after a few days. Infection of man and other animals occurs after ingestion of either cysts in raw or undercooked meat, or mature oocysts in material contaminated with cat feces. Once ingested, the parasites are liberated from cysts or oocysts by digestive enzymes and invade the intestinal mucosa. The parasites multiply locally and are then transported to other organs forming tissue cysts which persist for the life of the host. Cysts are found predominantly in brain, heart, and skeletal muscle.
Infection with T. gondii is asymptomatic in the majority (80 - 90%) of cases. The most common clinical manifestation of acute toxoplasmosis in the adult is asymptomatic lymphadenopathy involving single or multiple nodes. Lymphadenopathy may be accompanied by fever, malaise, and atypical lymphocytosis symptoms which mimic infectious mononucleosis. Very rarely will more serious complications, such as encephalitis, myocarditis or pneumonitis, be seen in the normal host.
When a seronegative woman becomes infected with T. gondii during pregnancy, the organism is often transmitted across the placenta to the fetus. The severity of infection in the fetus varies with the trimester during which the infection was acquired. Infection during the first trimester may lead to spontaneous abortion, stillbirth, or overt disease in the neonate. Infection acquired later during pregnancy is usually asymptomatic in the neonate, and may not be recognized. Approximately 75% of congenitally infected newborns are symptomatic. However, nearly all children born with subclinical toxoplasmosis will develop adverse ocular or neurologic sequelae later in life. Approximately 80 - 85% develop chorioretinitis and some may also experience blindness or mental retardation. A variety of serologic tests for antibodies to T. gondii have been used as an aid in diagnosis of acute infection and to assess previous exposure to the organism. The more widely used tests include the Sabin-Feldman dye test, direct agglutination, indirect hemagglutination, latex agglutination, indirect immunofluorescence, and ELISA. Serologic procedures that measure IgM class antibodies to T. gondii include indirect immunofluorescence, immunosorbent agglutination, and ELISA. High affinity IgG antibodies to T. gondii, if present in a sample, may interfere with the detection of IgM specific antibody. High affinity IgG antibody may preferentially bind to T. gondii antigen leading to false negative IgM results; also, rheumatoid factor, if present along with antigen-specific IgG, may bind to the IgG causing false positive IgM results.