OBJECTIVE: The present study was designed to evaluate the process of cavity formation in Mycobacterium avium intracellulare complex (MAC) lung infection, pathologically and clinically. METHODS: Using resected lung specimens, we first evaluated the distribution of MAC as well as the distribution of myofibroblasts in MAC lung infection according to several pathological findings classified as bronchiectasis, centrilobular nodules, cavity, nodules, bronchiolitis, or consolidation. Resected lung specimens (9 cases) were evaluated by special staining: Ziehl-Neelsen's method and immunohistochemically for CD68 (stain for monocytes and macrophages) and alpha-smooth muscle actin (stain for myofibroblasts). Chest CT findings were also examined in these 9 patients. In addition, the serial chest CT scans were reviewed in another 3 patients to evaluate the process of cavity formation, radiologically. RESULTS: Although extensive granuloma formations were observed in every pathological classification, MAC was demonstrated only in the necrotic tissue of the inner surface of the cavitary wall, which was connected to the airway. Myofibroblasts which expressed alpha-smooth muscle actin were intensely demonstrated in the cavitary wall compared with other pathological classifications. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and the layer of myofibroblasts surrounded the layer of epithelioid cells. Chest CT findings demonstrated that the cavitary walls were relatively thick. The evaluation of serial chest CT scans demonstrated that cavities were formed from previously existing nodules. CONCLUSIONS: Detection of mycobacteria in the cavitary wall, massive infiltration of myofibroblasts compared with other pathological classifications, and connection to the drainage bronchus, were believed to be important in the process of cavity formation in MAC pulmonary infection.
OBJECTIVE: The present study was designed to evaluate the process of cavity formation in Mycobacterium avium intracellulare complex (MAC) lung infection, pathologically and clinically. METHODS: Using resected lung specimens, we first evaluated the distribution of MAC as well as the distribution of myofibroblasts in MAC lung infection according to several pathological findings classified as bronchiectasis, centrilobular nodules, cavity, nodules, bronchiolitis, or consolidation. Resected lung specimens (9 cases) were evaluated by special staining: Ziehl-Neelsen's method and immunohistochemically for CD68 (stain for monocytes and macrophages) and alpha-smooth muscle actin (stain for myofibroblasts). Chest CT findings were also examined in these 9 patients. In addition, the serial chest CT scans were reviewed in another 3 patients to evaluate the process of cavity formation, radiologically. RESULTS: Although extensive granuloma formations were observed in every pathological classification, MAC was demonstrated only in the necrotic tissue of the inner surface of the cavitary wall, which was connected to the airway. Myofibroblasts which expressed alpha-smooth muscle actin were intensely demonstrated in the cavitary wall compared with other pathological classifications. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and the layer of myofibroblasts surrounded the layer of epithelioid cells. Chest CT findings demonstrated that the cavitary walls were relatively thick. The evaluation of serial chest CT scans demonstrated that cavities were formed from previously existing nodules. CONCLUSIONS: Detection of mycobacteria in the cavitary wall, massive infiltration of myofibroblasts compared with other pathological classifications, and connection to the drainage bronchus, were believed to be important in the process of cavity formation in MAC pulmonary infection.