Published ahead of print on May 3, 2007, doi:10.1164/rccm.200703-417OC
American Journal of Respiratory and Critical Care Medicine Vol 176. pp. 356-361, (2007)
© 2007 American Thoracic Society
doi: 10.1164/rccm.200703-417OC
Airway Bacterial Concentrations and Exacerbations of Chronic Obstructive Pulmonary Disease
Sanjay Sethi1,2,
Rohin Sethi2,
Karen Eschberger2,
Phyllis Lobbins3,
Xueya Cai4,
Brydon J. B. Grant1,2 and
Timothy F. Murphy2,3
1 Division of Pulmonary and Critical Care and Sleep Medicine, Department of Medicine, University at Buffalo, State University of New York, Buffalo, New York; 2 Veterans Affairs Western New York Healthcare System, Buffalo, New York; and 3 Division of Infectious Diseases, Departments of Medicine and Microbiology, and 4 Department of Biostatistics, University at Buffalo, State University of New York, Buffalo, New York
Correspondence and requests for reprints should be addressed to Sanjay Sethi, M.D., Veterans Affairs Western New York Healthcare System (151), 3495 Bailey Avenue, Buffalo, NY 14215. E-mail: ssethi{at}buffalo.edu
Rationale: Increased bacterial concentration (load) in the lower airways and new bacterial strain acquisition have been posited as mechanisms for chronic obstructive pulmonary disease (COPD) exacerbations. Bacterial concentrations are higher during exacerbation than during stable disease; however, these studies are cross sectional and devoid of strain typing.
Objectives: To determine if the increased bacterial concentrations function as a separate mechanism for exacerbation induction independent of new strain acquisition.
Methods: In a prospective, longitudinal cohort of patients with COPD, the relationship between exacerbation occurrence, sputum bacterial concentrations, and new strain acquisition was examined.
Measurements and Main Results: Clinical information, quantitative sputum cultures, and molecular typing of potential bacterial pathogen isolates. Over 81 months, 104 subjects completed 3,009 clinic visits, 560 (19.6%) during exacerbations and 2,449 (80.4%) during stable disease. Among preexisting strains, sputum concentrations of Nontypeable Haemophilus influenzae and Haemophilus haemolyticus were not different in exacerbation versus stable disease. Moraxella catarrhalis (stable, 108.38 ± 0.13 [mean ± SEM] vs. exacerbation, 107.78 ± 0.26; p = 0.02) and Streptococcus pneumoniae (stable, 108.42 ± 0.21 vs. exacerbation, 107.76 ± 0.52; p = 0.07) concentrations were lower during exacerbations compared with stable periods. Concentrations of new strains of H. influenzae (stable, 107.28 ± 0.15 vs. exacerbation, 107.76 ± 0.17; p = 0.04) and M. catarrhalis (stable, 107.85 ± 0.15 vs. exacerbation, 108.37 ± 0.14; p = 0.02), were increased during exacerbations; however, the differences were small.
Conclusions: Change in bacterial load is unlikely to be an important mechanism for exacerbations. Better understanding of the host–pathogen interaction, rather than enumerating bacteria in respiratory samples, is required to provide new insights into bacterial infection in COPD.
Key Words: bacteria chronic obstructive pulmonary disease exacerbation
| AT A GLANCE COMMENTARY
Scientific Knowledge on the Subject
Bacterial concentrations in the lower airways are higher during exacerbations of chronic obstructive pulmonary disease; however, it is not known if the increased bacterial concentrations are independent of acquisition of new strains and function as a separate mechanism for exacerbation induction.
What This Study Adds to the Field
Sputum concentrations of preexisting bacterial strains were not higher during exacerbations. Among new strains, small increases were seen. These results demonstrate that change in bacterial load is unlikely to be an important mechanism for exacerbations of COPD.
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Copyright © 2007 American Thoracic Society
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