The present study was designed to evaluate the pathological and immunohistochemical findings of Mycobacterium avium intracellulare complex (MAC) lung infection.A retrospective study was performed in five cases with positive cultures for MAC in whom lung resections were performed between January 1989 and December 1996. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria defined by the American Thoracic Society. In addition, MAC was cultured from all of the five lung specimens. Pathological and immunohistochemical findings as well as chest computed tomography (CT) findings were evaluated in these five patients.Pathological findings of bronchiectasis, bronchiolitis, centrilobular lesion, consolidation, cavity wall and nodules were demonstrated, respectively, in relation to chest CT findings. Extensive granuloma formation throughout the airways was clearly demonstrated. Immunohistochemical staining demonstrated: 1) epithelioid cells and giant cells; 2) myofibroblasts extensively infiltrating the cavity wall; and 3) B-cells detected in aggregates in the vicinity of the epithelioid granulomas.This study identified pathological and immunohistochemical characteristics of Mycobacterium avium complex infection relative to chest computed tomography findings and allowed the conclusion that bronchiectasis and bronchiolitis were definitely caused by Mycobacterium avium complex infection. Eur Respir J 1999; 13: 535±540.

It has been argued whether bronchiectasis is truly caused by MAC infection or just a predisposed condition in which MAC colonizes. Our present study was designed to evaluate the pathological findings of bronchiectases caused by Mycobacterium avium intracellulare complex (MAC) lung infection and to demonstrate MAC in the lesion of bronchiectases. A retrospective study was performed in nine cases with positive cultures for MAC in whom lung resections were performed. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria required by the American Thoracic Society. In addition, MAC were cultured from all nine lung specimens. Pathological findings of bronchiectases were evaluated in these nine patients. Destruction of bronchial cartilage and smooth muscles layer, obstruction of airway by granulomas, and ulceration of bronchial mucosa were frequently observed. Our present study demonstrates that destruction of fundamental bronchial structure due to extensive granuloma formation throughout the airways was likely the main cause of bronchiectases in MAC infection.

The clinical features of 24 patients with non-specific interstitial pneumonia (NIP) were evaluated. The patients consisted of seven men and 17 women, with a median age of 60 years. In seven patients, the disease was idiopathic and eight had collagen vascular diseases. Cough, dyspnoea and fever were frequently observed. The time interval between the onset of symptoms and open lung biopsy was 3 months. Mild increases of IgG, CRP, and LDH were also frequently observed. The average per cent VC was 65.1 +/- 3.2% and the average PaO2 was 71.3 +/- 2.4 Torr. Bronchoalveolar lavage was done in 20 patients, and a moderate increase in lymphocytes (27.8 +/- 6.7%) with a low CD4/CD8 ratio (0.86 +/- 0.22) was observed. Multiple patchy infiltration or diffuse interstitial shadows, located predominantly in the lower fields of both lungs were the characteristic chest CT findings. Lung biopsies in this group were characterized by varying proportions of chronic interstitial inflammation and fibrosis which was temporarily uniform. Patients were given steroid pulse therapy or oral steroids. The results were mild to marked improvements in chest roentgenographic findings and lung functions. Four patients (16.7%) died because of respiratory failure caused by NIP. This is the first report to describe clinical features of NIP since the original report by Katzenstein and Fiorelli.

The aim of this study was to evaluate the changes in chest CT findings examined successively in patients with Mycobacterium avium-intracellulare complex (MAC) infection. We carried out a retrospective study of 25 patients with MAC infection who had serial CT scans. Patients included 18 women and seven men with a median age of 66 years. Mean (+/- SE) follow-up interval between the first and second CT was 27.5 +/- 4.2 months. The serial chest CT scans were reviewed with consensus reading by two observers. At the first chest CT examination, we found the following: bronchiectasis (in 133 of 250 fields), cavity formation (11 of 250 fields), centrilobular nodules (167 of 250 fields), air-space disease (30 of 250 fields) and nodules (81 of 250 fields). The middle lobe and lingula were frequently involved. Centrilobular nodule scores improved in seven patients; disease progressed in nine patients and was stable in nine patients. In addition, bronchiectasis scores improved in four patients; disease progressed in 15 patients and was stable in six patients. The score of bronchiectasis in the second CT was significantly higher than in the first CT. In conclusion, our data suggest that centrilobular nodules and bronchiectasis are frequent observations in patients with MAC. In addition, progression of bronchiectasis appeared to be caused by MAC infection.

The present study was designed to evaluate the distribution of epithelioid cells, myofibroblasts, and TGF‐β1 in the formation of granuloma caused by Mycobacterium avium intracellulare complex (MAC) lung infection. A retrospective study was performed for 9 cases of positive MAC culture in which lung resections were performed between January 1989 and August 1999. Resected lung specimens were evaluated histologically and immunohistochemically for CD68 (stain for monocytes and macrophages, and epithelioid cells) and α‐smooth muscle actin as well as vimentin (stain for myofibroblasts), and TGF‐β1 was performed. When granuloma was initially formed, no myofibroblasts were found, but as caseous necrosis appeared, the thin epithelioid cell layer was detected and the outer myofibroblast layer gradually became thick. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and was associated with the outer layer of myofibroblasts. In addition, the anti‐TGF‐β1 antibody stained the cytoplasm of epithelioid cells and multinucleated giant cells, preceding the advent of myofibroblasts. In summary, our present study evaluated distributions of epithelioid cells, myofibroblasts, and TGF‐β along with the morphogenesis of granuloma, and clearly demonstrated the immunohistochemical difference between granuloma with caseous necrosis and granulomas without caseous necrosis.