Published ahead of print on May 3, 2007, doi:10.1164/rccm.200703-417OC Am. J. Respir. Crit. Care Med., Volume 176, Number 4, August 2007, 356-361 A more recent version of this article appeared on August 15, 2007
Submitted on March 13, 2007 Airway Bacterial Concentrations and Exacerbations of Chronic Obstructive Pulmonary DiseaseSanjay Sethi1*,1 Division of Pulmonary and Critical Care and Sleep Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA; Veterans Affairs Western New York Healthcare System, Buffalo, NY, USA, 2 Veterans Affairs Western New York Healthcare System, Buffalo, NY, USA, 3 Division of Infectious Diseases, Department of Medicine and Department of Microbiology, University at Buffalo, State University of New York, Buffalo, NY, USA, 4 Department of Biostatistics, University at Buffalo, State University of New York, Buffalo, NY, USA, 5 Division of Infectious Diseases, Department of Medicine and Department of Microbiology, University at Buffalo, State University of New York, Buffalo, NY, USA; Veterans Affairs Western New York Healthcare System, Buffalo, NY, USA * To whom correspondence should be addressed. 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 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 COPD patients, the relationship between exacerbation occurrence, sputum bacterial concentrations and new strain acquisition was examined. Measurements: Clinical information, quantitative sputum cultures and molecular typing of potential bacterial pathogen isolates. Main Results: Over 81 months, 104 subjects completed 3009 clinic visits, 560 (19.6%) during exacerbations and 2449 (80.4%) stable visits. Among pre-existing strains, sputum concentrations of Nontypeable Haemophilus influenzae and Haemophilus haemolyticus were not different in exacerbation vs.stable disease. Moraxella catarrhalis (Stable 108.38±0.13 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 vs. 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: COPD, exacerbation, bacteria
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