Cerebral toxoplasmosis

John E Greenlee MD (

Dr. Greenlee of the University of Utah School of Medicine received consulting fees from Wheeler Trigg O'Donnell LLP.

Originally released May 23, 2000; last updated December 8, 2019; expires December 8, 2022

This article includes discussion of cerebral toxoplasmosis and Toxoplasma gondii encephalitis. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Toxoplasma gondii is a parasite that is present worldwide, infects multiple mammalian and avian species, and is a significant cause of asymptomatic and symptomatic human infection. The disorder is capable of causing devastating prenatal neurologic injury. In adults, cerebral toxoplasmosis remains a highly prevalent disorder in HIV infection and AIDS, despite the advent of highly active antiretroviral therapy (HAART). Infection with Toxoplasma gondii is also an important issue in severely immunocompromised individuals who are not given prophylactic treatment. Less frequently, T gondii can cause central nervous system infection in apparently immunocompetent individuals. In AIDS patients, cerebral toxoplasmosis can coexist–and be difficult to distinguish from–cerebral cryptococcal infection and primary central nervous system lymphoma. Considering that persons with toxoplasma encephalitis have a high probability of early death, prophylaxis should be maintained in immunosuppressed patients who experience failure of antiretroviral therapy, and HAART should be initiated as soon as possible after toxoplasma encephalitis diagnosis. "Encephalitic" forms of toxoplasmosis in non-AIDS patients have also been described.

Key points


Toxoplasma gondii is a widely distributed protozoan that is found in multiple animal species. The definitive hosts, with regard to human infection, are felines. Human infection is common, and may result in lifelong persistence of the organism.


• Prior to the advent of the acquired immunodeficiency syndrome (AIDS), symptomatic invasion of the central nervous system in adults was unusual, most frequently occurring in the setting of immunosuppression.


• The advent of acquired immunodeficiency syndrome brought a marked increase in cerebral toxoplasmosis. Numbers of cases of cerebral toxoplasmosis in HIV infected individuals has fallen with the advent of highly active antiretroviral therapy (HAART).


T gondii modulates gene expression of brain endothelial cells to promote its own migration through the blood-brain barrier.


• Prevention of congenital toxoplasmosis requires an active antenatal screening program, and prevention of toxoplasmosis in immunosuppressed individuals requires prophylactic antibiotic therapy. Seropositivity for toxoplasmosis of >200 IU/mL in serum is of great help in the antemortem diagnosis.


• Mortality is higher in antiretroviral naive immigrants with neuro-AIDS treated on a neurologic intensive care unit.


• The incidence of cerebral toxoplasmosis during pregnancy is low.

Historical note and terminology

Although Toxoplasma gondii was probably first identified in 1900 in Java sparrows by Laveran (Laveran 1900), the organism was given its current name following its recovery from the tissues of a hamster-like African mammal, Ctenodactylus gundi (Dubey 2008). Association of the agent with humans was first described in 1908 in Panama, where the organism was present in muscle biopsies (Darling 1908). However, for several decades thereafter, toxoplasma was confused with either Sarcosporidia or Encephalitozoon. The first case of congenital toxoplasmosis infection was described in 1923 (Janku 1923). This patient had typical clinical features of congenital toxoplasmosis with unilateral micro-ophthalmia, hydrocephalus, and seizures. At postmortem, aqueductal stenosis and retinal lesions were present, and “sporocysts” were described in the retina. Sixteen years elapsed before toxoplasma was established as a causative agent for neurologic disorders in children, now termed “congenital toxoplasmosis,” in an extensive review by Wolf and colleagues (Wolf et al 1939).

Acquired toxoplasmosis was first described in 1940 in a Peruvian man who was immunosuppressed due to a preceding Bartonella infection (Pinkerton and Weinman 1940). Although this patient had lymphadenopathy at autopsy, lymphadenopathy was not recognized as a characteristic sign of toxoplasmosis until 1951, when it was described during pregnancy (Gard and Magnusson 1951).

Prior to the advent of AIDS, symptomatic central nervous system by T gondii was uncommon and was most often seen in the setting of immunosuppression (Townsend et al 1975). The first cases of CNS toxoplasmosis complicating HIV infection were described in 1983 (Luft et al 1983), and the agent was rapidly recognized as a significant cause of CNS infections in HIV-infected patients (Levy et al 1985). Toxoplasma chorioretinitis and cerebral toxoplasmosis have been associated with treatment with anti-TNF-alpha agents (Lassoued et al 2007), as well as with aggressive immunosuppression following hematopoietic stem cell or solid organ transplant (Dard et al 2018).

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