Tuberculous Bronchopneumonia

Tuberculosis: (TB) is a chronic, communicable disease caused by Mycobacterium tuberculosis made distinctively a necrotizing (caseating) granulomatous tissue response to seeded organisms.

Transmission is usually by inhalation of infected droplets produced by the coughing or sneezing of infected individuals (open cases).

Predisposing factors are any debilitating or immunosuppressive condition (e.g. diabetes, alcoholism, malnutrition, chronic lung disease.)

Pathogenesis:

1. Macrophages phagocytose bacteria (multiplies in macrophages!)  transported to regional lymph nodes (via lymphatics)

The cell wall lipids and carbohydrates of M. tuberculosis appear to enhance virulence by interfering with phagolysosomal fusion. This interference allows the intracellular survival of mycobacteria (resists killing by macrophages).

2. Macrophages at site of infection transforms into epithelioid cells (ample eosinophilic cytoplasm) and multinucleate giant cells

3. Outer ring of fibroblasts and lymphocytes accumulates; forming the ‘hard’ tubercle

4. After 2-3 weeks central caseous necrosis occurs; forming the ‘soft’ tubercle (characteristic TB lesion)

5. Later still areas of caseation may coalesce to form larger granulomatous lesions ( smaller peripheral tubercles)

Tuberculosis bronchopneumonia: caused by the spread of the bacilli from primary focus in the lung or hilar lymph nodes, via the bronchi

Mantoux reaction:

Delayed hypersensitivity (type IV) to the tubercle bacillus develops in 2-4 weeks after initial infection. A sensitized individual shows increased induration (>5mm) at the site of intradermal injection of purified protein derivative of M. tuberculosis (PPD test). A positive test result indicates sensitivity, however, not active disease.

Once sensitization appears during infection, the non-specific inflammatory response becomes granulomatous (abundant epithelioid histiocytes [modified macrophages], occasional giant cells and peripheral mononuclear cells). There is often central, caseous necrosis of the granulomas. A concomitant increase in resistance – the ability to inhibit intracellular replication of bacilli – occurs.

Primary tuberculosis: first time infection…

• Usually settles in middle zone of lung, forms Ghon focus: small subpleural inflammation (1-1.5cm)

• After ~2 weeks (sensitization); lesions spread to regional lymph nodes forming the Ghon complex

• Majority of cases will heal by fibrosis with later calcification (therefore may pass unnoticed clinically)

• Even so, a few viable bacilli may persist in quiescent, apparently healed lesions or in other organs to which they may have spread

Secondary tuberculosis: reactivation of primary lesion or reinfection; when resistance is lowered as in immunocompromised or malnutrition (esp. AIDS, poverty)…

• Classically the lesions (~1-3cm) settles at the apices of the lungs

• Pre-existing hypersensitivity / immunity  organisms tend to be localised, with rapid granulomatous caseation and fibrous reaction

Category: Medicine Notes