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Original Research: CHEST INFECTIONS |

Aging, COPD, and Other Risk Factors Do Not Explain the Increased Prevalence of Pulmonary Mycobacterium avium Complex in OntarioRisk Factors and Mycobacterium avium Complex

Mohammed Al-Houqani, MBBS; Frances Jamieson, MD; Mauli Mehta, BSc; Pamela Chedore, MLT; Kevin May, MLT; Theodore K. Marras, MD, FCCP
Author and Funding Information

From the Faculty of Medicine and Health Sciences (Dr Al-Houqani), United Arab Emirates University, Al-Ain, United Arab Emirates; TB and Mycobacteriology Laboratory (Dr Jamieson, Ms Chedore, and Mr May), Public Health Laboratories, Public Health Ontario; Department of Laboratory Medicine and Pathobiology (Dr Jamieson); and Division of Respirology, Department of Medicine (Ms Mehta and Dr Marras), University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada.

Correspondence to: Theodore K. Marras, MD, FCCP, Toronto Western Hospital, 7E-452, 399 Bathurst St, Toronto, ON, M5T 2S8, Canada; e-mail: ted.marras@uhn.ca


Funding/Support: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(1):190-197. doi:10.1378/chest.11-0089
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Background:  The cause of observed increases in pulmonary Mycobacterium avium complex (pMAC) isolation and disease is unexplained. To explore possible causes of the increase in pMAC isolation and disease prevalence in Ontario, Canada, we studied age and other population-level risk factors.

Methods:  We determined age and sex of patients with pMAC disease between 2003 and 2008. We then estimated whether the potential effect of population aging and changes in prevalence of HIV infection, solid organ transplant, COPD, and tumor necrosis factor-α (TNF-α) inhibition have contributed to the observed increase in pMAC disease.

Results:  During 2003 to 2008, pMAC isolation and disease prevalence (per 100,000) both increased (8.44 to 12.62 and 4.35 to 6.81, respectively). The total number of cases of disease increased by 348 (2.46 per 100,000). Based on actual contemporary population changes, aging could explain 70 additional cases (increase of 0.57 per 100,000). The increase in self-reported COPD prevalence could potentially explain 11 (95% CI, 0-42) additional cases (increase of 0.09 per 100,000 [95% CI, 0-0.34 per 100,000]). HIV infection, solid organ transplant, and TNF-α inhibition combined could potentially explain no more than 73 additional cases (increase of 0.60 per 100,000).

Conclusions:  Although population aging appears to be a major risk factor, the increase in pMAC disease in Ontario could be only partly explained by aging, increases in COPD, HIV, solid organ transplantation, and TNF-α inhibition therapy. The increase in pMAC is likely multifactorial and may be affected by environmental or pathogen factors not addressed in this study.

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