IM27.{1-4,12} | Tuberculosis Foundations — Summary & Reflection

KEY TAKEAWAYS

Tuberculosis is India's most consequential infectious disease, with 2.8 million new cases annually. Key foundations:

Epidemiology: India = 26% of global TB burden; men aged 15–49 most affected; poverty, crowding, and migration are proximate determinants; the NTEP aims for elimination by 2025 with universal free treatment and Ni-kshay digital notification.

Microbiology: M. tuberculosis complex, slow-growing (18–24 hr doubling time), acid-fast due to mycolic-acid-rich cell wall. Transmitted exclusively by airborne droplet nuclei (1–5 μm) from smear-positive cases. Culture on Lowenstein-Jensen medium takes 4–8 weeks.

Pathogenesis: Inhalation → alveolar macrophage ingestion → Ghon focus → haematogenous spread → hilar nodes (primary complex). At 3–8 weeks, Th1 CD4+ response forms caseating granuloma. In 90–95% of adults: LTBI (dormant, TST-positive). Reactivation: upper-lobe cavitation. Extrapulmonary (via haematogenous spread): lymph nodes (most common), Pott's disease, meningitis, miliary, pleural, renal, pericardial.

Comorbidities: HIV = 50–100-fold risk at CD4 <200 — atypical presentation, smear-negative, disseminated; start ART within 2–8 weeks of ATT. Diabetes = 2–3-fold risk; screen all TB patients for DM. Malnutrition = immune suppression + poor drug absorption.

Drug resistance: Chromosomal mutations only (no plasmids); MDR-TB = H + R resistant; pre-XDR = MDR + fluoroquinolone resistance; XDR = MDR + fluoroquinolone + bedaquiline/linezolid. Caused by inadequate treatment (mono/dual therapy, interruption, poor adherence) + primary transmission. Never add one drug to a failing regimen.

BCG: Intradermal at left deltoid at birth; highly protective against meningeal/miliary TB in children (70–80%); variable adult pulmonary efficacy (0–80%); complications — local lymphadenitis, disseminated BCG-itis in severe immunodeficiency. Does not convert TST to active TB.

REFLECT

Ramesh, from the opening scenario, was diagnosed with smear-positive pulmonary TB. His six-year-old daughter was also coughing. Think through the chain of events that led to his diagnosis and the obligations it creates: what epidemiological data in his history most raised the pre-test probability? What are the NTEP contact-tracing obligations for his dormitory co-workers and his daughter? If you were the NTEP counsellor explaining Ramesh's diagnosis, what would you say about the duration of treatment, the importance of daily dosing, and the meaning of the Ni-kshay nutritional support? And if three months into treatment Ramesh stops responding — sputum remains positive — what is the single question you must ask before changing the regimen, and what must you never do? These connections between microbiology, epidemiology, programme, and patient communication define what it means to practise TB medicine in India.