Toxoplasmosis is caused by infection with the protozoan Toxoplasma gondii, an obligate intracellular parasite. The infection produces a wide range of clinical syndromes in humans, land and sea mammals, and various bird species. T gondii has been recovered from locations throughout the world, except Antarctica (see the image below). (See Etiology and Pathophysiology.)
Toxoplasma gondii tachyzoites (Giemsa stain).
Nicolle and Manceaux first described the organism in 1908, after they observed the parasites in the blood, spleen, and liver of a North African rodent, Ctenodactylus gondii. The parasite was named Toxoplasma (arclike form) gondii (after the rodent) in 1909. In 1923, Janku reported parasitic cysts in the retina of an infant who had hydrocephalus, seizures, and unilateral microphthalmia. Wolf, Cowan, and Paige (1937-1939) determined that these findings represented the syndrome of severe congenital T gondii infection.
There are 3 major genotypes (type I, type II, and type III) of T gondii. These genotypes differ in their pathogenicity and prevalence in people. In Europe and the United States, type II genotype is responsible for most cases of congenital toxoplasmosis.
T gondii infects a large proportion of the world’s population (perhaps one third) but uncommonly causes clinically significant disease.
However, certain individuals are at high risk for severe or life-threatening toxoplasmosis. Individuals at risk for toxoplasmosis include fetuses, newborns, and immunologically impaired patients. (See Etiology and Pathophysiology and Epidemiology.)
Congenital toxoplasmosis is usually a subclinical infection. Among immunodeficient individuals, toxoplasmosis most often occurs in those with defects of T-cell–mediated immunity, such as those with hematologic malignancies, bone marrow and solid organ transplants, or acquired immunodeficiency syndrome (AIDS).In most immunocompetent individuals, primary or chronic (latent) T gondii infection is asymptomatic. A small percentage of these patients eventually develop retinochoroiditis, lymphadenitis, or, rarely, myocarditis and polymyositis. (SeePresentation and Workup.)
Primary prevention based on prenatal education could be an effective strategy to reduce congenital toxoplasmosis. Educate the public in toxoplasmosis-prevention methods, such as protecting children’s play areas from cat litter. Mothers with toxoplasmosis must be completely informed of the disease’s potential consequences to the fetus.