Multifocal enhancing brain lesions in immunocompetent patients have broad causes including infectious, inflammatory and neoplastic processes that may overlap clinically and radiographically. Key infectious etiologies include neurocysticercosis, tuberculous meningoencephalitis, and toxoplasmosis. These are especially important to consider in individuals from regions where such infections are common. Although rare in healthy hosts, Toxoplasma gondii can cause necrotizing encephalitis with hemorrhage and severe intracranial pressure elevation. We report a case of rapidly progressive, fatal encephalitis due to this organism.

A 21-year-old man from rural Guatemala with no prior medical history presented with two months of progressive headaches, confusion, behavioral changes, and 20–30 lb weight loss. Two weeks prior, he developed staring spells and poor appetite. On presentation, he was disoriented and agitated. Examination revealed encephalopathy without focal deficits. CT showed multifocal cortical hypodensities and MRI demonstrated multiple bilateral enhancing cortical and subcortical lesions with vasogenic edema, concerning for infectious or metastatic etiologies. CSF analysis revealed WBC 179/µL (mixed cells), protein <6 mg/dL, and glucose 53 mg/dL. Extensive infectious workup including HIV, fungal, tuberculosis and meningoencephalitis PCR was negative. Empiric therapy for neurocysticercosis with empiric levetiracetam was initiated.

Within four days, he developed worsening encephalopathy and fever requiring intubation and subsequently developed fixed dilated pupils with an ICP >90 mm Hg. Repeat MRI showed numerous bilateral hemorrhagic enhancing lesions with mass effect. Despite maximal ICP management, neurological function deteriorated and he was declared brain dead. Brain biopsy revealed acute and chronic cerebritis with T. gondii bradyzoites, confirming fulminant cerebral toxoplasmosis.

This case shows the difficulty of diagnosing multifocal brain lesions in healthy patients from endemic areas. Although treatment initially targeted neurocysticercosis, the patient’s rapid decline and severe ICP crisis suggested a more aggressive cause. Cerebral toxoplasmosis, though rare in immunocompetent individuals, should be considered when standard therapies fail.