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dc.contributor.authorZota, Victor
dc.contributor.authorAngelis, Sheryn M.
dc.contributor.authorFraire, Armando E.
dc.contributor.authorMcNamee, Ciaran
dc.contributor.authorKielbasa, Shasta
dc.contributor.authorLibraty, Daniel H.
dc.date2022-08-11T08:09:38.000
dc.date.accessioned2022-08-23T16:38:34Z
dc.date.available2022-08-23T16:38:34Z
dc.date.issued2008-05-15
dc.date.submitted2009-11-30
dc.identifier.citationJ Med Case Reports. 2008 May 13;2:152. <a href="http://dx.doi.org/10.1186/1752-1947-2-152">Link to article on publisher's site</a>
dc.identifier.issn1752-1947 (Electronic)
dc.identifier.doi10.1186/1752-1947-2-152
dc.identifier.pmid18477401
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39277
dc.description.abstractABSTRACT: INTRODUCTION: Mycobacterium avium complex (MAC) is an increasingly recognized cause of pulmonary disease in immunocompetent individuals. An acute form of MAC lung disease, MAC-associated pneumonitis, has generally been associated with the use of hot tubs. There is controversy in the literature about whether MAC-associated pneumonitis is a classic hypersensitivity pneumonitis or is a direct manifestation of mycobacterial infection. CASE PRESENTATION: We report the second case in the literature of MAC-associated pneumonitis not related to the use of hot tubs. The source of MAC in a 52-year-old immunocompetent patient was an intrapulmonary cyst containing numerous acid-fast bacilli. The patient developed disseminated miliary nodules throughout both lung fields. Histological examination of resected lung tissue revealed well-formed, acid-fast negative granulomas composed predominantly of CD4+ T-cells and CD68+ histiocytes. The granulomas were strongly positive for tumor necrosis factor-alpha, a pro-inflammatory cytokine. CONCLUSION: The attempt to classify MAC-associated pneumonitis as either a classic hypersensitivity pneumonitis or a direct manifestation of mycobacterial infection is not particularly useful. Our case demonstrates that MAC-associated pneumonitis is characterized by a vigorous T-helper 1-like, pro-inflammatory, immune response to pulmonary mycobacterial infection. The immunopathology provides a rationale for clinical studies of anti-MAC therapy with the addition of anti-inflammatory agents (for example, corticosteroids) to hasten the resolution of infection and symptoms.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18477401&dopt=Abstract">Link to Article in PubMed</a>
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleLessons from Mycobacterium avium complex-associated pneumonitis: a case report
dc.typeJournal Article
dc.source.journaltitleJournal of medical case reports
dc.source.volume2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3077&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2078
dc.identifier.contextkey1074377
refterms.dateFOA2022-08-23T16:38:34Z
html.description.abstract<p>ABSTRACT: INTRODUCTION: Mycobacterium avium complex (MAC) is an increasingly recognized cause of pulmonary disease in immunocompetent individuals. An acute form of MAC lung disease, MAC-associated pneumonitis, has generally been associated with the use of hot tubs. There is controversy in the literature about whether MAC-associated pneumonitis is a classic hypersensitivity pneumonitis or is a direct manifestation of mycobacterial infection. CASE PRESENTATION: We report the second case in the literature of MAC-associated pneumonitis not related to the use of hot tubs. The source of MAC in a 52-year-old immunocompetent patient was an intrapulmonary cyst containing numerous acid-fast bacilli. The patient developed disseminated miliary nodules throughout both lung fields. Histological examination of resected lung tissue revealed well-formed, acid-fast negative granulomas composed predominantly of CD4+ T-cells and CD68+ histiocytes. The granulomas were strongly positive for tumor necrosis factor-alpha, a pro-inflammatory cytokine. CONCLUSION: The attempt to classify MAC-associated pneumonitis as either a classic hypersensitivity pneumonitis or a direct manifestation of mycobacterial infection is not particularly useful. Our case demonstrates that MAC-associated pneumonitis is characterized by a vigorous T-helper 1-like, pro-inflammatory, immune response to pulmonary mycobacterial infection. The immunopathology provides a rationale for clinical studies of anti-MAC therapy with the addition of anti-inflammatory agents (for example, corticosteroids) to hasten the resolution of infection and symptoms.</p>
dc.identifier.submissionpathoapubs/2078
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentCenter for Infectious Disease and Vaccine Research
dc.contributor.departmentDepartment of Medicine
dc.source.pages152


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