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Central Nervous System (CNS) tuberculosis (TB) meningitis, a severe extrapulmonary manifestation of TB, poses significant diagnostic and therapeutic challenges due to its high morbidity and mortality rates, especially in immunocompromised individuals such as those with HIV. The pathogenesis involves hematogenous dissemination of Mycobacterium tuberculosis from a primary infection site, often the lungs, leading to invasion of the central nervous system. This process triggers a robust immune response characterized by neuroinflammation, cerebral edema, and vasculitis, ultimately causing neurological damage. Genetic factors, such as LTA4H polymorphisms, also influence the severity of inflammation and patient outcomes. CNS TB is disproportionately prevalent in regions where TB and HIV are endemic, notably in sub-Saharan Africa and Southeast Asia. Recent data from 2024 show that HIV-positive individuals are particularly vulnerable, with CNS TB accounting for up to 10% of all TB cases in this population. In India, where TB-HIV co-infections are common, diagnostic delays and limited access to advanced molecular diagnostics exacerbate the disease burden. In a clinical setting, patients may exhibit general symptoms like headache, fever, stiff neck, and altered mental status. Diagnostic evaluation includes cerebrospinal fluid (CSF) analysis and imaging studies, with nucleic acid amplification tests (e.g., GeneXpert MTB/RIF) providing rapid confirmation of the disease. Treatment follows World Health Organization (WHO) guidelines, including an intensive two-month phase of anti-TB therapy followed by a continuation phase. Adjunctive corticosteroid therapy, particularly with dexamethasone, helps reduce mortality by controlling neuroinflammation. On the other hand, careful observation for medication toxicity and side effects like immune reconstitution inflammatory syndrome (IRIS) is critical, particularly in HIV-TB co-infected patients. Early diagnosis, prompt treatment, and targeted public health interventions are crucial in reducing the impact of CNS TB, particularly in high-burden regions.
Central Nervous System (CNS) tuberculosis (TB) meningitis, a severe extrapulmonary manifestation of TB, poses significant diagnostic and therapeutic challenges due to its high morbidity and mortality rates, especially in immunocompromised individuals such as those with HIV. The pathogenesis involves hematogenous dissemination of Mycobacterium tuberculosis from a primary infection site, often the lungs, leading to invasion of the central nervous system. This process triggers a robust immune response characterized by neuroinflammation, cerebral edema, and vasculitis, ultimately causing neurological damage. Genetic factors, such as LTA4H polymorphisms, also influence the severity of inflammation and patient outcomes. CNS TB is disproportionately prevalent in regions where TB and HIV are endemic, notably in sub-Saharan Africa and Southeast Asia. Recent data from 2024 show that HIV-positive individuals are particularly vulnerable, with CNS TB accounting for up to 10% of all TB cases in this population. In India, where TB-HIV co-infections are common, diagnostic delays and limited access to advanced molecular diagnostics exacerbate the disease burden. In a clinical setting, patients may exhibit general symptoms like headache, fever, stiff neck, and altered mental status. Diagnostic evaluation includes cerebrospinal fluid (CSF) analysis and imaging studies, with nucleic acid amplification tests (e.g., GeneXpert MTB/RIF) providing rapid confirmation of the disease. Treatment follows World Health Organization (WHO) guidelines, including an intensive two-month phase of anti-TB therapy followed by a continuation phase. Adjunctive corticosteroid therapy, particularly with dexamethasone, helps reduce mortality by controlling neuroinflammation. On the other hand, careful observation for medication toxicity and side effects like immune reconstitution inflammatory syndrome (IRIS) is critical, particularly in HIV-TB co-infected patients. Early diagnosis, prompt treatment, and targeted public health interventions are crucial in reducing the impact of CNS TB, particularly in high-burden regions.
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