[PS6-1B-K] Tubercular Meningitis --Recent advances
Tubercular meningitis is especially common in young children and causes death or disability in nearly half of those affected. HIV co-infection is associated with higher complications and case fatality rate.
The mycobacteria spread from the lungs by hematogenous seeding into the CNS forming caseous lesions in the cerebral cortex or meninges. These rupture into the subarachnoid space, leading to basal exudates, obstruction of vessels, infarction and hydrocephalous. Symptoms are often non-specific with fever, malaise, lethargy and behavior changes and therefore diagnosis is delayed. Convulsions, stupor or coma with neurodeficits occur later. The CSF typically shows 10-500 WBCs, with predominance of lymphocytes, glucose <40 mg/dl and moderately elevated (150-200mg/dl) protein. CSF can be normal in children with unruptured tuberculomas. Isolation of mycobacteria is possible in only a small fraction of the cases; PCR, ADA, ELISA and several newer tests have varying degrees of accuracy; Gene Xpert is helpful. Neuroimaging characteristically shows basal exudates, infarcts and hydrocephalous. Antitubercular therapy is required for at least one year; simultaneous corticosteroid use reduces the risk of death or disabling residual neurological deficit in HIV-negative children. Even after adequate treatment, prognosis is guarded. In an analysis of 350 children with CNS TB, the mortality was 24.6% and 56.1% had neurological sequelae. Multi drug resistant TB is increasing and is not easy to diagnose and manage in children.
Prevention of CNS tuberculosis is a huge challenge. Several tuberculcosis vaccines are being explored. WHO has emphasized involvement of the community towards achieving national strategic TB control plans.
The mycobacteria spread from the lungs by hematogenous seeding into the CNS forming caseous lesions in the cerebral cortex or meninges. These rupture into the subarachnoid space, leading to basal exudates, obstruction of vessels, infarction and hydrocephalous. Symptoms are often non-specific with fever, malaise, lethargy and behavior changes and therefore diagnosis is delayed. Convulsions, stupor or coma with neurodeficits occur later. The CSF typically shows 10-500 WBCs, with predominance of lymphocytes, glucose <40 mg/dl and moderately elevated (150-200mg/dl) protein. CSF can be normal in children with unruptured tuberculomas. Isolation of mycobacteria is possible in only a small fraction of the cases; PCR, ADA, ELISA and several newer tests have varying degrees of accuracy; Gene Xpert is helpful. Neuroimaging characteristically shows basal exudates, infarcts and hydrocephalous. Antitubercular therapy is required for at least one year; simultaneous corticosteroid use reduces the risk of death or disabling residual neurological deficit in HIV-negative children. Even after adequate treatment, prognosis is guarded. In an analysis of 350 children with CNS TB, the mortality was 24.6% and 56.1% had neurological sequelae. Multi drug resistant TB is increasing and is not easy to diagnose and manage in children.
Prevention of CNS tuberculosis is a huge challenge. Several tuberculcosis vaccines are being explored. WHO has emphasized involvement of the community towards achieving national strategic TB control plans.