**MYCOBACTERIUM TUBERCULOSIS **
definition – Mycobacterium tuberculosis is the obligate aerobic, non‑sporing, non‑motile bacillus that causes tuberculosis (TB) in humans
cause – inhalation of aerosol droplets containing viable bacilli from a coughing TB patient
types (clinical)
- primary (first infection, usually in children)
- secondary or post‑primary (reactivation in adults)
- extrapulmonary (lymph nodes, pleura, bone‑joint, genitourinary, meninges, etc.)
morphology
- rod‑shaped (bacilli), 2–4 µm long, 0.3–0.6 µm wide
- gram‑positive‑appearing but acid‑fast because of thick, waxy cell wall
- cell wall rich in mycolic acids, arabinogalactan, lipids → resistant to decolorisation, gives “cording” appearance on culture
- non‑spore forming, non‑motile
pathogenesis – step‑wise sequence
- inhalation of droplet nuclei → bacilli reach alveolar spaces
- bacilli are phagocytosed by alveolar macrophages → survive by inhibiting phagolysosome fusion (mycolic acid barrier)
- → multiply inside macrophages → spread to regional hilar lymph nodes via lymphatics
- → formation of Ghon focus (primary lesion) and Ghon‑complex (focus + affected node)
- → cell‑mediated immunity (Th1, IFN‑γ, TNF‑α) activates macrophages → granuloma (caseating) formation
- → most bacilli are contained (latent infection) or killed (healed lesion)
- → if immunity wanes → reactivation → bacilli break granuloma, spread to apex of lung (high O₂) → caseous necrosis → cavitation (secondary TB)
memory rhyme – “Inhale → Alveoli → Macrophage → Multiply → Lymph → Granuloma → Reactivate → Cavity” → I A M L G R C (I am large, great, re‑cavities)
primary tuberculosis pathology
- Ghon focus – small peripheral subpleural granuloma (often asymptomatic)
- involvement of hilar/mediastinal lymph nodes → Ghon‑complex
- healing → fibrosis and calcification (Ranke’s nodule)
- possible lymph node enlargement → scrofula (cervical)
secondary (post‑primary) tuberculosis pathology
- reactivation of latent foci, usually in upper lobes (rich in O₂)
- caseous necrosis → soft, cheese‑like centre → liquefaction → cavity formation
- cavitary lesions → chronic cough, haemoptysis, weight loss, night sweats
- bronchogenic spread → multiple patchy infiltrates, “tree‑in‑bud” appearance on CT
- fibrosis and bronchiectasis may follow healing
clinical features – primary (children)
- low‑grade fever, malaise, mild cough
- hilar lymphadenopathy, possible mediastinal widening on X‑ray
- may be asymptomatic, discovered incidentally
clinical features – secondary (adults)
- productive cough with blood‑tinged sputum
- night sweats, fever, weight loss (constitutional)
- chest pain, dyspnoea if extensive involvement
- extrapulmonary signs if other organs involved
complications
- extensive fibrosis → restrictive lung disease
- calcified nodules (Ranke’s) → may mimic neoplasm
- bronchiectasis, chronic bronchitis
- spread to meninges → tubercular meningitis
- bone‑joint involvement → Pott’s disease (spine)
laboratory diagnosis
- sputum smear microscopy – Ziehl‑Neelsen stain → acid‑fast bacilli (AFB)
- culture – Lowenstein‑Jensen medium (3–8 weeks) or liquid MGIT system (faster)
- molecular – PCR (GeneXpert MTB/RIF) → detects DNA, rifampicin resistance in <2 h
- tuberculin skin test (Mantoux) – delayed‑type hypersensitivity, indicates exposure
- interferon‑γ release assays (IGRA) – blood test, useful in BCG‑vaccinated subjects
- chest X‑ray – primary: Ghon focus, hilar node; secondary: upper‑lobe cavitations, infiltrates
management (brief, exam‑oriented)
- DOTS (Directly Observed Treatment, Short‑course) – 2 months intensive phase (INH + RIF + PZA + EMB) → 4 months continuation (INH + RIF)
- monitor liver function (isoniazid, rifampicin) and visual acuity (ethambutol)
- treat drug‑resistant TB with second‑line agents (fluoroquinolones, injectables) as per WHO regimen
- adjunctive corticosteroids for TB meningitis, pericarditis, severe pleural effusion
exam tip – always write the arrow flow for pathogenesis and remember the “I A M L G R C” rhyme to retrieve steps quickly.