Other meanings of Toxoplasmic encephalitis
Infectious disease
Toxoplasmic encephalitis is a severe opportunistic infection of the brain caused by the protozoan parasite Toxoplasma gondii. It occurs almost exclusively in immunocompromised individuals, particularly those with advanced HIV/AIDS, and is the most common cause of cerebral mass lesions in this population. The condition is covered under the broader topic of Toxoplasmosis, which encompasses all clinical manifestations of the infection.
Toxoplasmic encephalitis results from reactivation of latent Toxoplasma gondii cysts in the brain when cell-mediated immunity wanes, typically when CD4+ T-cell counts fall below 100 cells/µL in HIV-infected patients.1 The parasite transforms into rapidly dividing tachyzoites, causing focal necrotizing encephalitis with microglial nodules and abscess formation.2 Clinically, patients present with headache, fever, confusion, and focal neurological deficits such as hemiparesis or seizures. Neuroimaging typically reveals multiple ring-enhancing lesions, most commonly in the basal ganglia and corticomedullary junction. Without treatment, the disease is uniformly fatal, but with prompt therapy, mortality is reduced to less than 10%.
Diagnosis is usually presumptive, based on clinical presentation, characteristic imaging findings, and positive serology for anti-Toxoplasma IgG, as the sensitivity of brain biopsy is limited and invasive. Definitive diagnosis requires histologic demonstration of tachyzoites or PCR detection of T. gondii DNA in cerebrospinal fluid or brain tissue. Standard treatment consists of pyrimethamine plus sulfadiazine and folinic acid, with clindamycin as an alternative for sulfa-allergic patients.3 Acute therapy is given for at least 6 weeks, followed by maintenance therapy until immune reconstitution occurs with antiretroviral therapy. In resource-limited settings, trimethoprim-sulfamethoxazole is often used due to cost and availability.
The incidence of toxoplasmic encephalitis has declined dramatically in developed countries since the introduction of highly active antiretroviral therapy (HAART), but it remains a major cause of morbidity and mortality in low- and middle-income countries where access to ART is limited.4 Primary prophylaxis with trimethoprim-sulfamethoxazole is recommended for HIV-infected patients with CD4 counts below 100 cells/µL and positive Toxoplasma serology. Secondary prophylaxis is continued until CD4 counts rise above 200 cells/µL for at least 3 months. Screening for latent toxoplasmosis is a standard part of HIV care, and seronegative patients are counseled to avoid undercooked meat and cat feces.
Beyond HIV/AIDS, toxoplasmic encephalitis can occur in other immunocompromised states, including organ transplant recipients, patients receiving immunosuppressive biologics, and those with hematologic malignancies.5 In transplant settings, the infection often arises from a seropositive donor organ transplanted into a seronegative recipient, leading to primary infection rather than reactivation. Congenital toxoplasmosis can also cause encephalitis in neonates, with a classic triad of hydrocephalus, chorioretinitis, and intracranial calcifications. A rare but notable phenomenon is the 'immune reconstitution inflammatory syndrome' (IRIS), where paradoxical worsening of cerebral lesions occurs after starting ART due to an overly robust inflammatory response.6 Additionally, T. gondii has been shown to manipulate host behavior in rodents, though the relevance to human neuropsychiatric symptoms remains controversial.
This article is part of the Toxoplasmosis topic.
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