© 2008 American Thoracic Society
Bacterial Load and Exacerbations of COPDTo the Editor:There has been longstanding debate concerning the role of bacteria in acute exacerbations of chronic obstructive pulmonary disease (COPD). In the classical study by Anthonisen and colleagues (1), it was shown that antibiotics do have a benefit, especially in type 1 exacerbations when patients have worsening of all three key symptoms (dyspnea, sputum volume, and sputum purulence). Studies from our own group have emphasized the importance of the latter symptom. Sputum neutrophils and hence purulent appearance relate to bacterial numbers (2) as do several markers of inflammation. During exacerbations, patients either become infected with bacteria, which disappear with treatment, or the numbers increase and then decrease with treatment in line with inflammation (3, 4). Why bacterial number increases in subjects already "colonized" when stable remains largely unknown, although the classical paper by Dr. Sethi and colleagues (5) highlighted epitopic changes that could potentially enable the bacteria to evade the controlling adaptive immunity. The same group has once again addressed this issue (6). However, in this study, while Sethi and coworkers found that the numbers of the commonly implicated organisms (H. influenzae and M. catarrhalis) increased during exacerbations when new strains were detected, they commented that this change was small and likely to be insignificant. We would like to point out that the change in number is larger than Sethi and coworkers stated (6). The average bacterial load rose from 107.28 to 107.76, which was said to represent a 7% increase (6). We believe this to be the comparison of the two log numbers (7.28, 7.76), which is incorrect. 107.28 is 19,054,607 bacteria/ml and 107.76 is 57,543,993 bacteria/ml, which represent a 202% increase or threefold change in bacterial numbers. Although numbers in our own studies showed slightly greater changes in bacterial load, this was based on careful selection of a purulent nature of the sputum, which may be the critical feature as bacterial numbers do not change when the sputum remains mucoid (3). Thus we feel that this further study by Sethi and coworkers (6) provides important data for understanding the changes of bacteria and load that occur during exacerbations, but we wish to emphasize that exacerbations can occur for reasons other than bacterial infection even when the sputum culture is positive, although in this scenario the sputum remains mucoid and bacterial load does not change (3).
The University of Birmingham FOOTNOTES Conflict of Interest Statement: H.A. has been sponsored to attend the European Respiratory Society meeting by Allen & Hanbury in 2006. R.A.S. has received funding to attend international conferences from Boehringer Ingelheim and Talecris and to speak at conferences organized by GlaxoSmithKline (GSK) and AstraZeneca (AZ); he has served on advisory panels for Roche, GSK, and Merck Sharpe and Dohme ($5,000 in 2006); he has received grants from AZ (£30,000 in 2006) and Talecris (£317,000 in 2006). REFERENCES
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