PURPOSE: This study was designed to evaluate the mechanism of Mycobacterium avium extension in lung infection. STUDY DESIGN: Retrospective study. PARTICIPANTS: A 42-year-old man with acquired immune deficiency syndrome and immune reconstitution inflammatory syndrome. The patient developed mediastinal lymphadenopathy and a peripheral lesion in the right upper lobe within 2 weeks of starting highly active antiretroviral therapy. METHODS: Pulmonary tissue and lymph nodes were dissected under thoracoscopy and evaluated pathologically and immunohistochemically. RESULTS: Pulmonary pathologic examination revealed extensive granuloma formation throughout the acini. Mycobacterial antigens were found in the macrophages in the alveoli and in the alveolar septa. Some macrophages including mycobacterial antigens were surrounded by lymphatic endothelial cells in the interstitium. In addition, a proliferative granulomatous lesion was found under the intact epithelial layer of a bronchiole. Pathological examination of the lymph nodes revealed aggregated proliferative granulomas with few mycobacteria. Genetically closely related M. avium strains were isolated from both tissues. CONCLUSIONS: This study showed the mechanism involved in the progression of pulmonary M. avium infection from the pulmonary focus to the regional lymph nodes via the lymphatic vessels.
PURPOSE: This study was designed to evaluate the mechanism of Mycobacterium avium extension in lung infection. STUDY DESIGN: Retrospective study. PARTICIPANTS: A 42-year-old man with acquired immune deficiency syndrome and immune reconstitution inflammatory syndrome. The patient developed mediastinal lymphadenopathy and a peripheral lesion in the right upper lobe within 2 weeks of starting highly active antiretroviral therapy. METHODS: Pulmonary tissue and lymph nodes were dissected under thoracoscopy and evaluated pathologically and immunohistochemically. RESULTS: Pulmonary pathologic examination revealed extensive granuloma formation throughout the acini. Mycobacterial antigens were found in the macrophages in the alveoli and in the alveolar septa. Some macrophages including mycobacterial antigens were surrounded by lymphatic endothelial cells in the interstitium. In addition, a proliferative granulomatous lesion was found under the intact epithelial layer of a bronchiole. Pathological examination of the lymph nodes revealed aggregated proliferative granulomas with few mycobacteria. Genetically closely related M. avium strains were isolated from both tissues. CONCLUSIONS: This study showed the mechanism involved in the progression of pulmonary M. avium infection from the pulmonary focus to the regional lymph nodes via the lymphatic vessels.