Tuberculous Pleurisy

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Abstract
MYCOBACTERIUM tuberculosis invades the pleural cavity chiefly through rupture of subpleural caseous foci within 6 to 12 weeks after a primary infection. Bacillus protein antigens seem to induce a delayed hypersensitivity reaction that stimulates lymphocytes, which in turn release certain lymphokines that (1) activate macrophages against the mycobacterium and (2) alter the permeability of pleural vessels and affect the formation of granulomas.1 Tuberculous pleural effusion (TPE) is an acute granulomatous pleurisy caused by recent infection by the mycobacterium. Patients with TPE invariably have a small subpleural nidus of tuberculosis showing fibrous and granulomatous inflammation and clear signs of leakage into the pleural space.2 Although TPE can resolve spontaneously within a few weeks or months, about one third of persons with untreated TPE subsequently develop a more serious form of tuberculosis.3 In our region (Galicia, in the northwest part of Spain), TPE chiefly affects young adults and children,4 radiologically has no preference for either the right or the left side,5 and is generally unaccompanied by pulmonary lesions.