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Congenital toxoplasmosis: Clinical features and diagnosis

Nicholas G Guerina, MD, PhD
Jennifer Lee, MD, MS
Ruth Lynfield, MD
Section Editors
Sheldon L Kaplan, MD
Leonard E Weisman, MD
Deputy Editor
Carrie Armsby, MD, MPH


Toxoplasma gondii is a ubiquitous protozoan parasite that infects animals and humans. Toxoplasma infection typically is asymptomatic in immunocompetent hosts. However, serious disease can occur, most frequently in the setting of immunosuppression or congenital infection. The fetus, newborn, and young infant with congenital Toxoplasma infection are at risk of infection-associated complications, particularly retinal disease that can occur into adulthood.

The clinical features and diagnosis of congenital toxoplasmosis in infants and children will be reviewed here. The treatment, outcome, and prevention of congenital toxoplasmosis and acquired toxoplasmosis in pregnancy, immunocompetent hosts, and HIV-infected patients are discussed separately. (See "Congenital toxoplasmosis: Treatment, outcome, and prevention" and "Toxoplasmosis and pregnancy" and "Toxoplasmosis in immunocompetent hosts" and "Toxoplasmosis in HIV-infected patients".)


Congenital toxoplasmosis is caused by T. gondii, an intracellular protozoan parasite. Toxoplasma has a unique biphasic life cycle that consists of a sexual cycle that occurs exclusively in felines and an asexual cycle that can occur in other animals and humans (figure 1). Cats acquire the infection by ingesting oocysts in soil or tissue cysts from small prey. Replication occurs in the intestine of the cat, and oocysts are formed, excreted, and become infectious after 24 hours. During the primary infection, the cat can shed millions of oocysts daily for up to three weeks. Humans who come in contact with cat feces containing Toxoplasma oocysts may inadvertently ingest contaminated material, and the asexual phase of Toxoplasma replication begins. Oocysts rupture to release sporozoites that divide and become tachyzoites, which are characteristic of the acute stage of infection. Tachyzoites spread throughout the body via the bloodstream and lymphatics. With an adequate immune response, the tachyzoites are sequestered in tissue cysts and form bradyzoites. Bradyzoites are indicative of the chronic stage of infection and can persist for the life of the individual.


Congenital toxoplasmosis occurs throughout the world. The prevalence varies geographically according to the risk of primary Toxoplasma infection in women of child-bearing age [1-3]. (See "Toxoplasmosis and pregnancy", section on 'Incidence'.)

The highest rates of infection with T. gondii have been reported in Europe, Central America, Brazil, and Central Africa [1]. The environment plays a key role in perpetuating the life cycle of T. gondii, and warm, humid climates are ideal. In parts of Central America, seropositivity starts around one year of age, when children begin playing in contaminated soil, and it reaches 50 to 75 percent by adolescence. In other areas, transmission occurs primarily through the ingestion of undercooked meat. In these areas, depending on eating customs, seropositivity may begin in adolescence (or sooner) and can continue throughout adulthood. In many parts of the world, the pattern is mixed. (See "Toxoplasmosis in immunocompetent hosts", section on 'Prevalence of infection'.)


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Literature review current through: Sep 2016. | This topic last updated: Mar 2, 2016.
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