Congenital toxoplasmosis

Crystal L Walker MSN CPNP (

Crystal Walker of Atrium Health - Levine Children’s Hospital has no relevant financial relationships to disclose.

Daniel J Bonthius MD PhD (

Dr. Bonthius of Atrium Health/Levine Children’s Hospital has no relevant financial relationships to disclose.

Nina Schor MD PhD, editor. (

Dr. Schor of the National Institutes of Health and Deputy Director of the National Institute of Neurological Disorders and Stroke has no relevant financial relationships to disclose.

Originally released February 1, 1995; last updated November 27, 2019; expires November 27, 2022


Toxoplasma gondii is an important cause of congenital infections. When the infection occurs during pregnancy, the parasite can cross the placenta and severely damage the fetus, where the fetal brain and retina are particularly vulnerable. Microencephaly, intellectual disability, vision impairment, hydrocephalus, and epilepsy are common outcomes. In this updated article, the authors discuss the pathogenesis of congenital toxoplasmosis and explain the ways in which infection with this parasite can be differentiated from other congenital infections. In addition, the authors discuss the controversy surrounding prenatal screening for congenital toxoplasmosis, management strategies for treatment before and after birth of an affected infant, and the cost-effectiveness of prenatal screening programs.

Key points


Toxoplasma gondii is an intracellular parasite that can gravely damage the human brain and retina when infection occurs during pregnancy.


• The severity of fetal pathology is greatest when maternal infection occurs early in pregnancy, but likelihood of transmission to the fetus is greatest when maternal infection occurs in later pregnancy.


• Classic signs of congenital toxoplasmosis infection include intrauterine growth retardation, liver dysfunction, rash, chorioretinitis, and intracranial calcifications.


• Congenital toxoplasmosis is most commonly diagnosed serologically, but can also be diagnosed by real-time PCR or by the detection of parasites in fetal tissues.


• Newborns with suspected or confirmed congenital toxoplasmosis should be treated with a combination of pyrimethamine, sulfadiazine, and folinic acid for 1 year.

Historical note and terminology

Toxoplasma gondii, an obligate intracellular parasite, was first observed in 1908 in cells from the spleen and liver of the gondii, a North African rodent, from which the parasite derives its name. Twenty years later, chorioretinitis was recognized as a complication of human infection with T gondii. In 1939, observations linked congenital toxoplasmosis to intrauterine transmission of the parasite. The first serologic tests for toxoplasmosis were developed in 1948. It was not until the 1960s that cats were identified as the principal host of T gondii and the vector through which the pathogen most commonly reaches humans. In the mid-1970s, it became recognized that past infection with toxoplasmosis could reactivate in immunocompromised patients. Today, toxoplasmosis is recognized as 1 of the most common and important of the prenatal infections and accounts for the TO in the TORCH acronym guiding physicians in the workup of suspected congenital infections.

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