Cerebral toxoplasmosis is the most common cause of focal brain lesion in people living with HIV (PLWH) and usually causes multifocal encephalitis with little or no meningeal involvement. Classically, only subtle cerebrospinal fluid (CSF) abnormalities are described. There are no prior case reports in the literature on eosinophilic meningitis associated with cerebral toxoplasmosis in PLWH. We report on an HIV-positive man from Brazil who presented to the emergency department with headache, nausea, vomiting, and hemiparesis. He had a T-CD4+ lymphocyte count of 145 cells/mm3, and antiretroviral failure was identified. Brain computed tomography showed a contrast-enhancing lesion with mild mass effect and trimethoprim–sulfamethoxazole and dexamethasone were started. Examination of CSF showed 194 cells/mm3 (74% eosinophils, 18% lymphocytes, 4% monocytes, and 2% neutrophils), protein = 83 mg/dL, and glucose = 49 mg/dL. Detection of Toxoplasma gondii on CSF by polymerase chain reaction confirmed the diagnosis of cerebral toxoplasmosis. An exhaustive laboratorial investigation excluded other possible etiologies. After 14 days, the patient showed complete resolution of neurological and CSF alterations and substantial improvement in the brain lesion and was discharged home. We suggest that eosinophilic meningitis should be included in the spectrum of manifestations of HIV-related cerebral toxoplasmosis, especially in countries with high prevalence of toxoplasmosis in the general population.
The reactivation of Chagas disease in HIV infected patients presents high mortality
and morbidity. We present the case of a female patient with confirmed Chagasic
meningoencephalitis as AIDS-defining illness. Interestingly, her TCD4+ lymphocyte
cell count was 318 cells/mm3. After two months of induction therapy, one
year of maintenance with benznidazol, and early introduction of highly active
antiretroviral therapy (HAART), the patient had good clinical, parasitological and
radiological evolution. We used a qualitative polymerase chain reaction for the
monitoring of T. cruzi parasitemia during and after the treatment. We emphasize the
potential value of molecular techniques along with clinical and radiological
parameters in the follow-up of patients with Chagas disease and HIV infection. Early
introduction of HAART, prolonged induction and maintenance of antiparasitic therapy,
and its discontinuation are feasible, in the current management of reactivation of
Chagas disease.
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