Despite effective anti-mycobacterial therapy, tuberculosis (TB) remains a major global cause of mortality, and tuberculous meningitis (TBM) is its most lethal manifestation. We present a 61-year-old woman with no history of immunosuppression who presented with acute inattention, mild aphasia, and right-sided weakness after several days of progressive cognitive decline. She had recently traveled to Nigeria, where she was treated for malaria and typhoid fever. Initial brain imaging was unrevealing. Extensive infectious testing was inconclusive. Her condition within the first few days after hospital admission was fluctuating, with periods of transient improvement followed by clinical deterioration eventually requiring intubation on Day 5. Computed tomography (CT) scan of the brain demonstrated hydrocephalus. An empiric treatment for bacterial and viral meningitis as well as a trial of intravenous immunoglobulin (IVIG) for suspected autoimmune encephalitis yielded no improvement. On day 11, a lymph node biopsy done after a CT scan of the abdomen and pelvis revealed extensive lymphadenopathy and confirmed acid-fast bacilli (AFB), establishing disseminated tuberculosis. However, soon after this revelation, she became unresponsive, with imaging demonstrating subarachnoid hemorrhage and diffuse cerebral edema. She progressed to tonsillar herniation and eventually succumbed to the disease. This case underscores the diagnostic challenge of TBM, often underrecognized in the modern era despite its high global prevalence and its ability to be transmitted rapidly when exposure occurs. Given the high mortality associated with delayed treatment, clinicians must maintain a high index of suspicion and consider early empiric therapy in patients with subacute meningitis and epidemiologic risk factors, even when initial testing is inconclusive.
Ashwinee et al. (2026) studied this question.