The role of tuberculosis and other forms of bronchopulmonary necrosis in the pathogenesis of bronchiectasis.

The pathogenesis of bronchial dilatations which serve as foci for later pyogenic infection' is still debated among both clinicians and pathol~ ogists. The importance of bacterial and viral infections of childhood is undisputed as a major factor in the pathogenesis of bronchiectasis (1-6) but, beyond this, agreement is limited. Of other infections, the demonstration of bronchial dilatation accompanying granulomatous disease ( especially tuberculosis, both of the primary (7-13) and chronic adult types (7, 14-25)), and fungal infections (26) is recognized; yet, few works devoted to bronchiectasis per se even mention these as a possible cause of the original damage to the bronchial walls in cases of secondarily infected bronchiectasis (18, 25). Bronchial obstruction from any cause (16, 27, 28), is commonly mentioned as an important cause of chronic infection and bronchial dilatation. Allergic (29), mechanical traction (30, 31), neurogenic (32), and vascular (33) factors also have been mentioned occasionally. Finally, the influence of congenital and developmental abnormalities (34-37) of the bronchial structure is often invoked, either as a direct cause of the dilatation or in some manner, by making an area of the lung susceptible to bronchial infections. In general, this etiology must be considered as one of exclusion, despite the histopathologic evidence presented by Medlar (35) that the regular presence of columnar epithelium and smooth muscle in bronchiectatic lesions precludes an infectious pathogenesis, and, conversely, that even the absence of these structures need not imply Previous inflammatory changes in that they may never have been present. Even after all of these factors are considered, however, the pathogenesis