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Pathology 2 - Second Year BHMS

Contents

Pathology 2 - Second Year BHMS

Contents

CoursesBHMSPathology 2 - Second Year BHMSMYCOBACTERIUM TUBERCULOSIS

MYCOBACTERIUM TUBERCULOSIS

Content

**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)

  1. primary (first infection, usually in children)
  2. secondary or post‑primary (reactivation in adults)
  3. extrapulmonary (lymph nodes, pleura, bone‑joint, genitourinary, meninges, etc.)

morphology

  1. rod‑shaped (bacilli), 2–4 µm long, 0.3–0.6 µm wide
  2. gram‑positive‑appearing but acid‑fast because of thick, waxy cell wall
  3. cell wall rich in mycolic acids, arabinogalactan, lipids → resistant to decolorisation, gives “cording” appearance on culture
  4. non‑spore forming, non‑motile

pathogenesis – step‑wise sequence

  1. inhalation of droplet nuclei → bacilli reach alveolar spaces
  2. bacilli are phagocytosed by alveolar macrophages → survive by inhibiting phagolysosome fusion (mycolic acid barrier)
  3. → multiply inside macrophages → spread to regional hilar lymph nodes via lymphatics
  4. → formation of Ghon focus (primary lesion) and Ghon‑complex (focus + affected node)
  5. → cell‑mediated immunity (Th1, IFN‑γ, TNF‑α) activates macrophages → granuloma (caseating) formation
  6. → most bacilli are contained (latent infection) or killed (healed lesion)
  7. → 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

  1. Ghon focus – small peripheral subpleural granuloma (often asymptomatic)
  2. involvement of hilar/mediastinal lymph nodes → Ghon‑complex
  3. healing → fibrosis and calcification (Ranke’s nodule)
  4. possible lymph node enlargement → scrofula (cervical)

secondary (post‑primary) tuberculosis pathology

  1. reactivation of latent foci, usually in upper lobes (rich in O₂)
  2. caseous necrosis → soft, cheese‑like centre → liquefaction → cavity formation
  3. cavitary lesions → chronic cough, haemoptysis, weight loss, night sweats
  4. bronchogenic spread → multiple patchy infiltrates, “tree‑in‑bud” appearance on CT
  5. fibrosis and bronchiectasis may follow healing

clinical features – primary (children)

  1. low‑grade fever, malaise, mild cough
  2. hilar lymphadenopathy, possible mediastinal widening on X‑ray
  3. may be asymptomatic, discovered incidentally

clinical features – secondary (adults)

  1. productive cough with blood‑tinged sputum
  2. night sweats, fever, weight loss (constitutional)
  3. chest pain, dyspnoea if extensive involvement
  4. extrapulmonary signs if other organs involved

complications

  1. extensive fibrosis → restrictive lung disease
  2. calcified nodules (Ranke’s) → may mimic neoplasm
  3. bronchiectasis, chronic bronchitis
  4. spread to meninges → tubercular meningitis
  5. bone‑joint involvement → Pott’s disease (spine)

laboratory diagnosis

  1. sputum smear microscopy – Ziehl‑Neelsen stain → acid‑fast bacilli (AFB)
  2. culture – Lowenstein‑Jensen medium (3–8 weeks) or liquid MGIT system (faster)
  3. molecular – PCR (GeneXpert MTB/RIF) → detects DNA, rifampicin resistance in <2 h
  4. tuberculin skin test (Mantoux) – delayed‑type hypersensitivity, indicates exposure
  5. interferon‑γ release assays (IGRA) – blood test, useful in BCG‑vaccinated subjects
  6. chest X‑ray – primary: Ghon focus, hilar node; secondary: upper‑lobe cavitations, infiltrates

management (brief, exam‑oriented)

  1. DOTS (Directly Observed Treatment, Short‑course) – 2 months intensive phase (INH + RIF + PZA + EMB) → 4 months continuation (INH + RIF)
  2. monitor liver function (isoniazid, rifampicin) and visual acuity (ethambutol)
  3. treat drug‑resistant TB with second‑line agents (fluoroquinolones, injectables) as per WHO regimen
  4. 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.