Abstract
Tuberculous meningitis (TBM) is the most severe form of extrapulmonary tuberculosis (TB). In a high TB-burden setting, TBM comprises over 10% of TB cases. After a patient inhales droplet micronuclei, which harbor mycobacteria, the alveolar macrophages will be infected. Spread throughout the body can occur afterward. In TBM, three different types of granuloma represent three different stages in the development of the same pathological process: (1) nonnecrotizing cellular granuloma, (2) necrotizing gummatous granuloma, and (3) necrotizing “abscess”-type granuloma, all present mainly in the leptomeninges. The two main cytokines that form an integral part of the pathophysiology of TB granuloma are tumor necrosis factor alpha (TNF-α) and interferon-γ. Specific candidate genes and variants first associated with pulmonary TB such as LTH4H have been identified with increased susceptibility to TBM. TBM in childhood is diagnosed based on a combination of clinical, laboratory, and neuroimaging findings. The treatment of susceptible TBM consists of an initial 2-month intensified period with four first-line drugs; isoniazid (INH), rifampicin (RIF), pyrazinamide, and ethambutol, followed by an additional 7–10 months with only INH and RIF. Many of the sequelae seen in TBM can be attributed to a dysregulated host immune response. Effective host-directed therapies, such as inhibition of TNF-α, are therefore likely to be critical in improving outcomes and survival. The Bacillus Calmette–Guerrin (BCG) remains the only licensed and widely used vaccine against TB. BCG vaccine has consistent high efficacy against acute forms of childhood TBM. Lasting neurological abnormalities in children due to TBM can occur with prevalence ranging from 12.5% to 100%.
Published Version
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