Pathological Analysis of the Cavitary Wall in Mycobacterium Avium Intracellulare Complex Pulmonary Infection.

Abstract

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 MACas well as the distribution of myofibroblasts in MAClung 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 a-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, MACwas demonstrated only in the necrotic tissue of the inner surface of the cavitary wall, which was connected to the airway. Myofibroblasts which expressed a-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 CTscans demonstrated that cavities were formed from previously existing nodules. Conclusions Detection of mycobacteria in the cavitary wall, massive infiltration of myofibroblasts comparedwith other pathological classifications, and connection to the drainage bronchus, were believed to be important in the process of cavity formation in MACpulmonary infection. (Internal Medicine 41: 617-621, 2002)

Diagnostic utility and pitfalls of intraoperative pulmonary imprint cytology based on final pathological diagnoses

“…It is also important to note that five (41.7%) of our 12 cases for which the IC preparation was deemed inadequate were diagnosed as epithelioid granuloma with caseous necrosis, which is believed to occur in cases of tuberculosis and atypical mycobacteriosis and mycosis such as cryptococcosis . Nevertheless, tuberculosis is not readily recognised during surgery, making real‐time polymerase chain reaction‐based detection of causative bacteria essential for a differential diagnosis in such cases, and particularly because the post‐operative management of tuberculous infection is quite different from that of other diagnoses .…”

Risk factors and secondary care utilisation in a primary care population with non-tuberculous mycobacterial disease in the UK

“…Patients with a history of TB may be more likely to have their sputum cultured for mycobacteria, increasing NTMD identification; however, it has also been proposed that post-inflammatory bronchiectasis resulting from TB may account for some increased risk [24]. …”

The Role of Myofibroblasts in Granulomatous Lymphadenitis in Pigs Naturally Infected with M. Avium Subsp. Hominissuis

“…However, all immunophenotypic characteristics of effector cells in granulomas important for pathogenesis of swine mycobacteriosis are not well described. The ratio of myofibroblasts, epithelioid cells and occurrence of necrosis is controlled by various factors, but attention is paid mainly to TGF-β1 (18). It is believed that cytokines and growth factors which cause necrosis also lead to myofibroblast stimulation (TGF-β) supporting that that myofibroblasts have a significant role in formation of granulomas caused by mycobacterium (19).…”

“…When activated, myofibroblasts express adhesive molecules for lymphocytes, mast cells and neutrophil granulocytes. They also participate in formation of tissue granulomas and play a significant role in inflammatory reactions, having in mind that they produce important inflammatory mediators (18). It is assumed that TGF-β1 induces proliferation of myofibroblasts in granulomas, which changes interpretation of its role considering that this factor has been also ascribed an inhibitory role in activation of macrophages in granulomatous lesions in tuberculosis.…”