To the Editors: Central nervous system tuberculosis (CNS-TB) remains one of the most severe manifestations of Mycobacterium tuberculosis infection, contributing disproportionately to mortality and long-term neurologic sequelae in pediatric populations. In Brazil, hospitalizations due to CNS-TB have increased by 59% between 2014 and 2023, with mortality approaching 11%, underscoring its persistent public health impact.1 We report a fatal case highlighting key diagnostic challenges in early CNS-TB. A previously healthy 15-year-old female presented with fever, headache and vomiting, followed by rapid neurologic deterioration, including progressive lower limb weakness, dysphagia, aphasia and reduced oral intake, evolving within 1 week to acute respiratory failure. On admission, she was critically ill, with depressed consciousness, tetraparesis and areflexia. Cerebrospinal fluid (CSF) analysis showed mild pleocytosis (55 cells/µL), elevated protein (71 mg/dL), glucose of 52 mg/dL and predominance of polymorphonuclear cells (59.5%), an atypical but recognized early pattern in CNS-TB that may mimic bacterial meningitis.2,3 Initial cranial computed tomography was unremarkable, while chest radiography demonstrated diffuse bilateral infiltrates. Within 7 days, imaging showed progression with cavitary pulmonary lesions (Fig. 1), and molecular testing confirmed rifampicin-sensitive M. tuberculosis in both sputum and CSF. Chest computed tomography revealed a “tree-in-bud” pattern with cavitation, consistent with disseminated tuberculosis. Standard antituberculous therapy was initiated alongside broad-spectrum antibiotics and supportive care. Despite these measures, the patient developed severe systemic inflammation and remained dependent on mechanical ventilation. On day 21, a bilateral pneumothorax occurred during preparation for extubation, followed by cardiorespiratory arrest and death.FIGURE 1.: Chest radiographs demonstrating disease progression. (A) Diffuse, bilateral, heterogeneous alveolar–interstitial opacities, predominantly in the middle and lower lung fields, without lobar consolidation or significant pleural effusion. (B) Progression to more extensive bilateral infiltrates, more pronounced on the left, with the development of cavitary lesions.This case illustrates that early CNS-TB may present with neutrophil-predominant CSF and initially normal neuroimaging, potentially delaying diagnosis. In endemic settings, these atypical findings require a high index of suspicion and early integration of clinical, radiologic and molecular data. Prompt recognition remains critical to improving outcomes in this frequently fatal condition.2–4
Muinhos et al. (Wed,) studied this question.