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Journal of Clinical Microbiology, December 2003, p. 5836-5837, Vol. 41, No. 12
0095-1137/03/$08.00+0 DOI: 10.1128/JCM.41.12.5836-5837.2003
| LETTER TO THE EDITOR |
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We read the paper by Pabst et al. in the June issue of the Journal of Clinical Microbiology (1) with great interest. The authors try to shed light on the role of diarrheagenic E. coli in Switzerland by using a case-control setup and molecular diagnostic methods for the identification of the different E. coli groups. However, the study has a couple of shortcomings that makes us wonder if all of the conclusions presented are correct.
Firstly, the authors do not take into account the potential bias of the travel history of the patients when comparing cases and controls. Travel may be an important confounder because none of the controls reported traveling, whereas travel was quite common among the patients; i.e., if a pathogen is more common in travelers than in patients with domestically acquired cases, it will not be possible to ascertain the relative importance of travel if the patients are compared with a group of controls who have not traveled in a univariate analysis. A way of circumventing the problem would be to exclude the travel-associated cases from the analysis. In the case of EAEC, the number of patients who had traveled was 9 or 47%; the total number of diarrheal patients who had traveled was 31. It is thus possible to compare the occurrence of EAEC in patients and controls with no travel history: The prevalence in patients was 9 of 156, and that in controls was 3 of 137. This difference is not statistically significant (P = 0.21; Fisher's two-tailed exact test).
Secondly, the authors did not find any difference in the prevalence of EPEC between cases and controls. This conclusion may be questioned too, because the EPEC definition used is based solely on detection of the intimin gene (eae). In the definition of EPEC, the serotype of the strains should also be taken into account (2). We performed a study similar to that of Pabst et al. and found a strong correlation between disease in infants less than 2 years of age and EPEC, defined as eae-positive strains belonging to the classical EPEC O groups, whereas other A/EEC showed no correlation to disease (B. Olesen, P. Schiellerup, M. Helms, J. Neimann, F. Scheutz, and P. Gerner-Smidt, Abstr. 12th Eur. Congr. Clin. Microbiol. Infect. Dis., abstr. P607, 2002). Classical EPEC is the most common bacterial cause of diarrhea in children less than 2 years old in Denmark. We wonder if Pabst et al. would have reached the same conclusion had they serotyped their eae-positive isolates.
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P. Gerner-Smidt* C. Jensen K. E. P. Olsen F. Scheutz Department of Gastrointestinal and Parasitic Infections
K. Mølbak
B. Olesen
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* Phone: 45 32683798 Fax: 45 32688238 E-mail: pgs{at}ssi.dk |
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The second point raised concerns the definition of EPEC. This has been debated for a long time, with particular serogroups and the presence of the intimin gene (eae) or the bundle-forming pilus gene (bfp) being among the factors considered to be important. In our study, as described in Materials and Methods, we did not check single colonies and thus were not able to do serotyping. We based our diagnosis of EPEC on the detection of eae and the absence of genes coding for verotoxins. When eae and genes coding for verotoxins could be detected in a single stool specimen, it was interpreted as containing EHEC. On the basis of this procedure, no significant difference was found between patients and controls. The serologic workup of eae-positive bacteria by Gerner-Smidt et al. shows very interesting results that point in the direction that the presence of the eae gene in E. coli is necessary but not sufficient to be regarded as EPEC. Possibly, we might have found differences in the prevalence of certain EPEC serotypes in our analysis, too. However, serotyping is no longer absolutely necessary to diagnose EPEC (2), nor is it practical in a diagnostic setting.
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Werner L. Pabst David Nadal* Division of Infectious Diseases University Children's Hospital of Zurich Zurich, Switzerland
Martin Altwegg
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* Phone: 41 1 266 7562 Fax: 41 1 266 7157 E-mail: David.Nadal{at}kispi.unizh.ch |
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