Clinical Pathology · MU Sofia

136. Secondary pulmonary tuberculosis – classification, organ site damage. Microscopic & gross pathomorphology.

Covers reactivation (secondary) pulmonary tuberculosis, its typical apical location, and how caseous lesions progress to cavitation, haemoptysis and miliary spread. Also describes microscopic caseating granulomas with an H&E micrograph, and extrapulmonary forms: cervical lymphadenitis, tuberculous meningitis with CSF changes, and bone involvement with the vertebral Pott disease example.

Inside: 1 section · 2 labelled pictures · 14 flashcards · 2 min

Topic 136 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 426 words (2 min of reading), with 14 flashcards.

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  1. Secondary pulmonary tuberculosis - classification, organ site damage. Microscopic & gross pathomorphology

Secondary pulmonary tuberculosis - classification, organ site damage. Microscopic & gross pathomorphology

Secondary TB, also known as reactivation TB, it is the pattern of disease that occurs in a previously sensitized host. It may be a new infection to someone who has already been affected, but more commonly it is reactivation of the dormant primary lesion decades after initial infection. Only 5% of primary TB sufferers get affected by secondary TB.

Secondary TB is initially confined to the upper lobes of the lung, with the lesion in the apical pleura, with central caseation and peripheral fibrosis. Localised apical secondary TB may heal with fibrosis or progress to progressive pulmonary TB (as mentioned above).

H&E, pulmonary TB: caseating granuloma - pink, granular, structureless caseous centre rimmed by epithelioid macrophages, with lymphocytes at the edge (lower left).

Image: “Pulmonary tuberculosis - Necrotizing granuloma (6545187509)” by Yale Rosen from USA, CC BY-SA 2.0, via Wikimedia Commons.

Remember: reactivation TB favours the apices, probably because oxygen tension is highest there. When an apical caseous focus erodes into a bronchus, the caseum is coughed up and a cavity forms; the patient now spreads bacilli in the sputum (open, infectious TB).

In progressive TB we see apical lesion enlarge, become cavitated, with the cavity lined by caseous material, with blood vessel erosion and hemoptysis. These cavities often remain many years after the event. Pulmonary Miliary TB then occurs when organisms drain through lymphatics into venous return and then into right sided pulmonary circulation, causing ‘millions’ of scattered lesions. We can also have systemic miliary TB, when we get scattering throughout the body (see above). Remember these miliary lesions contain lymphocytes, plasma cells and macrophages.

Lymphadenitis is the most frequent form of extrapulmonary TB, occuring in the cervical region. It tends to be unifocal, with no extranodal diseases associated.

Tuberculosis meningitis A type of meningitis that manifests with general CNS signs and symptoms. Moderate increase in CSF cellularity, with mononuclear cells, protein level is elevated. Can also cause tuberculoma in the brain which may trigger meningitis.

Tuberculosis osteomyelitis Mycobacterial infection of the bone is a significant problem in developing countries. Bone infections complicate 1-3% of all pulmonary TB cases, arriving from the bloodstream, organisms target long bones and vertebrae. Lesions can be focal or multifocal. TB of the vertebral bodies is clinically the most severe, causing vertebral deformity, collapse and can cause neurological disorders.

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