Bronchoscopic examination was performed using a 4.9-mm bronchoscope (LTF TYPE 260; Olympus, Tokyo, Japan). A large cavity was directly visible through both the posterior and the anterior segmental bronchi of the right upper lobe (Fig. 3A). The inner wall was almost completely covered with thick gray debris (Fig. 3B). Microscopy of biopsy specimens of the debris showed necrotic tissue, and a culture of the cavitary lavage was found to be positive for M. avium. The organism was found to be clarithromycin resistant.
The patient was treated with streptomycin 0.75 g 3 times a week and daily rifabutin 300 mg/d, levofloxacin 500 mg/d, and ethambutol 500 mg/d. Six months later, chest radiography showed improvement of the consolidated opacities around the cavities (Fig. 1C). High-resolution CT also showed decreased cavitary wall thickening and consolidation (Fig. 2C). Bronchoscopic examination demonstrated decrease in the gray debris of the inner wall (Fig. 3C). A culture of the cavitary lavage was negative. Three months after the last bronchoscopic examination, Aspergillus fumigatus was detected in the patient’s sputum culture. He was administered micafungin 150 mg/d; however, he suffered sudden death because of massive hemoptysis. An autopsy was performed.
The cavitary walls of the right lung consisted of collapsed lung parenchyma or fibrous tissue, and their inner surface were covered with either hemorrhages or granulation tissue along with aggregates of fungal hyphae (Fig. 4). A culture of the lung tissue obtained at autopsy was positive for A. fumigatus but not M. avium.
The cavities are predictors of poor response to treatment and have an important role in MAC infection.12 The mechanisms of cavity formation in MAC patients are not clear. Two hypotheses have been proposed: (1) a check-valve mechanism and (2) the discharge of the necrotic tissue containing MAC to the draining bronchus.13,14 Fujita et al14 reported the pathologic analysis of 9 patients with MAC infection. MAC existed predominantly in the caseating necrotic tissue of the inner walls of the cavities and not in the bronchus. In the patient in the present study, we could not find any bronchial stenosis or obstruction in the right upper lobe, suggesting that cavity formation was caused by a discharge of necrotic tissue to the draining bronchus and not by a check-valve mechanism. In addition, serial CT scans of our patient revealed growing cavitary lesions, with destruction of partitions, and pulmonary parenchyma.
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