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  • Updated 05.24.2023
  • Released 05.23.2000
  • Expires For CME 05.24.2026

Cerebral toxoplasmosis



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 also capable of causing devastating prenatal neurologic injury. In adults, cerebral toxoplasmosis remains an important 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—including encephalitis—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. Patients developing toxoplasma encephalitis have a high probability of early death. For this reason, antitoxoplasma prophylaxis should be maintained in HIV-infected patients who experience failure of antiretroviral therapy, and HAART should be initiated as soon as possible after toxoplasma encephalitis diagnosis. Prophylactic treatment should also be initiated in severely immunocompromises patients with other disorders.

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 in systemic tissues and/or within the central nervous system or eyes.

• Infection with Toxoplasma gondii in children or adults is most commonly acquired from ingestion of material contaminated with cat droppings or by eating undercooked meat containing toxoplasma cysts. Less frequently, the organism can be transmitted by blood transfusion or organ transplantation.

• 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.

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

• 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).

• 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.

• 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 (63), the organism was given its current name following its recovery from the tissues of a hamster-like African mammal, Ctenodactylus gundi (29). Association of the agent with humans was first described in 1908 in Panama, where the organism was detected in muscle biopsies (26). However, for several decades thereafter, T gondii was confused with either Sarcosporidia or Encephalitozoon. The first case of congenital toxoplasmosis infection was described in 1923 (50). 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 (107).

Acquired toxoplasmosis was first described in 1940 in a Peruvian man who was immunosuppressed due to a preceding Bartonella infection (89). 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 (39).

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 (102). The first cases of CNS toxoplasmosis complicating HIV infection were described in 1983 (68), and the agent was rapidly recognized as a significant cause of CNS infections in HIV-infected patients (66). Toxoplasma chorioretinitis and cerebral toxoplasmosis have since been associated with treatment with anti-TNF-alpha agents (62), as well as with aggressive immunosuppression following hematopoietic stem cell or solid organ transplant (25; 71).

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