Chagas disease, caused by Trypanosoma cruzi, remains an important public health problem in the Americas. Although the most prevalent chronic form is cardiac, central nervous system reactivation is rare but severe, particularly in immunosuppressed patients. We report three cases diagnosed in 2024, highlighting diagnostic and therapeutic challenges. Case 1: A 58-year-old woman, heart transplant recipient 6 months earlier for Chagas cardiomyopathy, developed acute confusional state, tremors, and focal motor deficit. Brain MRI showed a periventricular space-occupying lesion with heterogeneous contrast enhancement, suggesting infectious etiology. Brain biopsy revealed fibrinonecrotic material with inflammatory reaction, and T. cruzi genetic material was detected by molecular methods in tissue and CSF. She was treated with benznidazole for 60 days and immunosuppression was adjusted to reduce the risk of further reactivation. Case 2: A 64-year-old woman, heart transplant recipient 10 years earlier for Chagas cardiomyopathy, on maintenance immunosuppression, presented with motor deficit, dysarthria, and progressive cognitive changes initially attributed to chronic ischemic vascular disease. Due to persistent symptoms, CSF analysis was performed and T. cruzi genetic material was detected. She was treated with benznidazole, but neurological outcome was unfavorable, highlighting the severity of disease. Case 3: A 61-year-old man with advanced Chagas cardiomyopathy and dual-chamber pacemaker developed subacute neurological changes, including ataxia, dysphagia, dysarthria, and cognitive decline. Cranial CT showed nonspecific white matter changes, initially attributed to microangiopathy. CSF revealed mild inflammatory reaction and detection of T. cruzi genetic material. Brain biopsy showed chronic encephalitis without other etiologies, reinforcing the diagnosis of neuro-Chagas. Benznidazole treatment led to partial improvement. CNS reactivation of T. cruzi is a rare and severe complication that should be considered in patients with intense or dysfunctional immunosuppression. Diagnosis requires integration of imaging, CSF analysis, and, when necessary, brain biopsy. Molecular diagnosis proved important for management. Antiparasitic treatment, along with immunosuppression control, is essential.
Aguiar et al. (Sun,) studied this question.