Pulmonary tuberculosis

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"pulmonary tuberculosis"[MeSH Terms] AND "treatment"[MeSH Terms]

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I now have comprehensive pathology content from Robbins (the gold standard for pathology). Here is the complete 5-mark answer:

Pathology of Pulmonary Tuberculosis

1. Causative Organism and Route of Entry

Pulmonary TB is caused by Mycobacterium tuberculosis, an obligate aerobe transmitted by inhalation of infectious droplet nuclei. The bacilli are ingested by alveolar macrophages, where they block phagosome-lysosome fusion and resist acidification, allowing intracellular multiplication.

2. Primary Tuberculosis

The initial infection (primary TB) almost always begins in the lungs in adults. Key morphological events:

Inhaled bacilli implant in the distal airspaces of the lower upper lobe or upper lower lobe, close to the pleura
A 1-1.5 cm gray-white area of consolidation develops - the Ghon focus - with central caseous necrosis
Bacilli drain to regional hilar/mediastinal lymph nodes, which also caseate
The parenchymal lesion + lymphangitis + caseous lymphadenopathy = Ghon complex (Ranke complex)
In ~95% of immunocompetent individuals, cell-mediated immunity controls infection; the Ghon complex undergoes progressive fibrosis and calcification
Despite hematogenous seeding of other organs during this phase (liver, spleen, kidneys, lung apices), no lesions develop if immunity is adequate

3. The Tuberculous Granuloma (Hallmark Lesion)

The characteristic microscopic lesion is the caseating granuloma (tubercle):

Early tuberculous granuloma (H&E) showing a multinucleate giant cell surrounded by epithelioid cells and lymphocytes

Fig. A - Early granuloma: multinucleate giant cell surrounded by epithelioid cells and lymphocytes (Sherris Medical Microbiology)

Multiple granulomas surrounding a vein near the lung hilum with early central degeneration

Fig. B - Multiple granulomas with early caseous degeneration (Sherris Medical Microbiology)

Composition of a tubercle (from center outward):

Layer	Cell Type
Center	Caseous necrosis - cheesy, amorphous, acellular
Inner zone	Epithelioid cells (activated macrophages with abundant pink cytoplasm)
Middle	Langhans-type giant cells (fused macrophages, nuclei arranged in horseshoe/peripheral pattern)
Outer rim	Lymphocytes (CD4+ Th1, CD8+ CTLs) and fibroblasts

Individual granulomas are microscopic; they become macroscopically visible only when multiple coalesce
Caseous necrosis is the hallmark - named for the cheese-like, semisolid appearance grossly; it results from the destructive delayed-type hypersensitivity (DTH) response driven by IFN-γ
In immunocompromised individuals, granulomas fail to form; macrophages instead contain sheets of bacilli without organized reaction

4. Secondary (Postprimary/Reactivation) Tuberculosis

Reactivation occurs in 10% of latently infected persons, preferentially at aerobic high-oxygen-tension sites (lung apices, renal cortex):

Apical lesion: small (<2 cm), sharply circumscribed, firm, gray-white to yellow focus within 1-2 cm of apical pleura
Histology: coalescent caseating tubercles; acid-fast bacilli identifiable by Ziehl-Neelsen stain in early phases
Outcomes of progressive disease:

Pathway	Morphology
Cavity formation	Caseous center liquefies and drains into bronchus → ragged, irregular cavity with poorly walled fibrous tissue; erosion of vessels → hemoptysis
Bronchogenic spread	Spread to other lobar segments via airway secretions
Miliary TB	Lymphohematogenous spread → 1-2 mm yellow-white foci throughout lung parenchyma resembling millet seeds
Pleural involvement	Serous effusion, empyema, or obliterative fibrous pleuritis
Healing	Fibrosis, calcification, architectural distortion; sterile cavities may persist

5. Summary of Key Pathological Distinctions

Feature	Primary TB	Secondary TB
Site	Lower upper / upper lower lobe, subpleural	Apex of upper lobe
Ghon focus	Present	Absent
Lymphadenopathy	Prominent	Minimal
Cavitation	Rare	Common
Spread	Hematogenous	Bronchogenic
Granulomas	Yes (if immunocompetent)	Yes, coalescent

Sources: Robbins & Cotran Pathologic Basis of Disease (10th Ed.), Sherris & Ryan's Medical Microbiology (8th Ed.)

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