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Previous Volume 347:465-471 August 15, 2002 Number 7 Next

	Full Text PDF PDA Full Text PowerPoint Slide Set Editorial by Anthonisen, N. R. Letters Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background The role of bacterial pathogens in acute exacerbations of chronic obstructive pulmonary disease is controversial. In older studies, the rates of isolation of bacterial pathogens from sputum were the same during acute exacerbations and during stable disease. However, these studies did not differentiate among strains within a bacterial species and therefore could not detect changes in strains over time. We hypothesized that the acquisition of a new strain of a pathogenic bacterial species is associated with exacerbation of chronic obstructive pulmonary disease.

Methods We conducted a prospective study in which clinical information and sputum samples for culture were collected monthly and during exacerbations from 81 outpatients with chronic obstructive pulmonary disease. Molecular typing of sputum isolates of nonencapsulated Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and Pseudomonas aeruginosa was performed.

Results Over a period of 56 months, the 81 patients made a total of 1975 clinic visits, 374 of which were made during exacerbations (mean, 2.1 per patient per year). On the basis of molecular typing, an exacerbation was diagnosed at 33.0 percent of the clinic visits that involved isolation of a new strain of a bacterial pathogen, as compared with 15.4 percent of visits at which no new strain was isolated (P<0.001; relative risk of an exacerbation, 2.15; 95 percent confidence interval, 1.83 to 2.53). Isolation of a new strain of H. influenzae, M. catarrhalis, or S. pneumoniae was associated with a significantly increased risk of an exacerbation.

Conclusions The association between an exacerbation and the isolation of a new strain of a bacterial pathogen supports the causative role of bacteria in exacerbations of chronic obstructive pulmonary disease.

Source Information

From the Divisions of Pulmonary and Critical Care Medicine (S.S., B.J.B.G.) and Infectious Diseases (T.F.M.), Department of Medicine, the Department of Microbiology (T.F.M.), and the Departments of Physiology and Biophysics and Social and Preventive Medicine (B.J.B.G.), State University of New York; and the Veterans Affairs Western New York Healthcare System (S.S., N.E., B.J.B.G., T.F.M.) — both in Buffalo, N.Y.

Address reprint requests to Dr. Sethi at the Veterans Affairs Western New York Healthcare System (151), 3495 Bailey Ave., Buffalo, NY 14215, or at ssethi{at}buffalo.edu.

Full Text of this Article

Related Letters:

New Strains of Bacteria and Exacerbations of COPD
Kureishi A., Hirschmann J. V., Bresser P., van Alphen L., Lutter R., Sethi S., Murphy T. F., Anthonisen N. R.
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N Engl J Med 2002; 347:2077-2079, Dec 19, 2002. Correspondence

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