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Clinical and Vaccine Immunology, October 2008, p. 1580-1589, Vol. 15, No. 10
1071-412X/08/$08.00+0     doi:10.1128/CVI.00173-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Clinical and Immunologic Features of an Atypical Intracranial Mycobacterium avium Complex (MAC) Infection Compared with Those of Pulmonary MAC Infections{triangledown}

Mouhannad Sadek,2 Feng Yun Yue,1 Erika Yue Lee,1 Gabor Gyenes,1 R. Brad Jones,1 Victor Hoffstein,2 David G. Munoz,2 Ignatius Fong,2 and Mario Ostrowski1,2*

Clinical Sciences Division and Department of Immunology, University of Toronto, Toronto, Ontario, Canada,1 St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada2

Received 15 May 2008/ Returned for modification 4 June 2008/ Accepted 18 July 2008

Members of the Mycobacterium avium complex (MAC) may cause chronic pulmonary infections in otherwise healthy elderly persons but rarely invade parts of the body outside of the lungs in immunocompetent hosts. We present a case of an isolated intracranial MAC infection in an apparently immunocompetent individual and review previous reports. We studied the T-cell and monocyte responses in healthy volunteers, individuals with a pulmonary MAC infection, and one individual with an isolated intracranial MAC infection. Genomic DNA from the individual with the brain MAC infection was studied for gamma interferon (IFN-{gamma}) receptor mutations. Individuals with localized pulmonary MAC infections showed increased activation of monocytes and enhanced monocyte and T-cell tumor necrosis factor alpha (TNF-{alpha}) production in response to lipopolysaccharide and MAC antigens but defects in T-cell IFN-{gamma} secretion. The individual with an intracranial MAC infection showed a lack of monocyte activation and deficiencies in both monocyte and T-cell TNF-{alpha} production and monocyte interleukin-12 (IL-12) production but had preserved T-cell IFN-{gamma} production. Mutations or deletions in the IFN-{gamma} receptor were not detected in the individual with the intracranial MAC infection. Our data suggest that distinct immune defects characterize two different manifestations of MAC infection. A relative defect in IFN-{gamma} production in response to MAC may predispose an individual to localized but partially controlled lung disease, whereas defects leading to reduced IL-12 and TNF-{alpha} production may allow the dissemination of MAC. Further studies delineating the potential role of TNF-{alpha} in limiting the spread of MAC outside the lung are warranted.

* Corresponding author. Mailing address: Clinical Sciences Division, Rm. 6271, 1 King's College Circle, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Phone: (416) 946-5805. Fax: (416) 978-8765. E-mail: mario.ostrowski{at}gmail.com

{triangledown} Published ahead of print on 13 August 2008.

Clinical and Vaccine Immunology, October 2008, p. 1580-1589, Vol. 15, No. 10
1071-412X/08/$08.00+0     doi:10.1128/CVI.00173-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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