Cerebral toxoplasmosis

Tarakad S Ramachandran MD (Dr. Ramachandran of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
John E Greenlee MD, editor. (Dr. Greenlee of the University of Utah School of Medicine received an honorarium from Merck for authorship.)
Originally released May 23, 2000; last updated September 14, 2015; expires September 14, 2018

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

Overview

Cerebral toxoplasmosis remains a highly prevalent disorder of the CNS, even in the advanced highly active antiretroviral therapy (HAART) era, particularly among severely immunosuppressed patients and in absence of prophylaxis. In children, incidence of cerebral toxoplasmosis is rare even in the presence of immunocompromise. In patients who are seronegative for toxoplasmosis or are on prophylactic therapy for toxoplasmosis, with positive imaging studies, other diagnoses should be considered, including tuberculosis, cryptococcosis, and fungal abscess. Primary cerebral lymphoma can coexist with cerebral toxoplasmosis. 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. An autopsy-confirmed "encephalitic" form of toxoplasmosis in a non-AIDS patient has been reported.

Key points

 

• In concert with acquired immunodeficiency syndrome, there has been a marked increase in cerebral toxoplasmosis.

 

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

Toxoplasma was first observed in animals (Java sparrows) in 1900 (Laveran 1900). The first human patient was 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, immune-suppressed due to a preceding Bartonella infection (Pinkerton and Weinman 1940). Although this patient had lymphadenopathy at autopsy, lymphadenopathy was recognized as a characteristic sign of toxoplasmosis in 1951, when it was described during pregnancy (Gard and Magnusson 1951). The incidence of cerebral toxoplasmosis markedly increased during the 1980s in concert with the AIDS pandemic. The first cases of CNS toxoplasmosis complicating HIV infection were described in 1983 (Luft et al 1983). Toxoplasmic chorioretinitis and cerebral toxoplasmosis during treatment with anti-TNF-alpha agents have been reported (Lassoued et al 2007).

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