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Industry: Email Alert RSS FeedEscherichia coli and community-acquired gastroenteritis, Melbourne, Australia
Emerging Infectious Diseases, Oct, 2004 by Roy M. Robins-Browne, Anne-Marie Bordun, Marija Tauschek, Vicki R. Bennett-Wood, Jacinta Russell, Frances Oppedisano, Nicole A. Lister, Karl A. Bettelheim, Christopher K. Fairley, Martha I. Sinclair, Margaret E. Hellard
Together, atypical EPEC and EAEC accounted for 19.3% of all cases; 21% of cases were attributable to all other bacterial, viral, and parasitic causes combined. However, the frequency of EAEC in patients with gastroenteritis and that in the baseline group without diarrhea was the same when matched for the time of year when the sample of feces was collected. In contrast, atypical EPEC was isolated significantly more often from patients with gastroenteritis than from those without symptoms, regardless of when the sample was collected. A subset of 22 randomly selected atypical EPEC strains was examined and found to be highly heterogeneous, which indicates that the high frequency of atypical EPEC in the study population was not the result of one or more outbreaks attributable to a small number of strains.
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Despite the persuasive evidence of a volunteer study and reports of outbreaks of diarrhea with atypical EPEC (12,26,31), the role of atypical EPEC in disease is controversial. Originally, atypical EPEC were grouped with EPEC but were then segregated because they lack EAF. Justification for this division stemmed from the observation that EAF-bearing EPEC far outnumber atypical EPEC as the cause of infantile diarrhea in less-developed countries and of diarrhea outbreaks in general (3). In recent reports, however, from countries as diverse as Iran, Poland, South Africa, and the United Kingdom, atypical EPEC strains have outnumbered typical strains as a cause of gastroenteritis (32-35). Atypical EPEC were also more frequent than typical strains in aboriginal children hospitalized for diarrhea in the Northern Territory of Australia (36). These findings were reflected in the present study: 89 (94%) of eae-bearing strains identified in patients with gastroenteritis were atypical EPEC.
As for EPEC in general, atypical EPEC were originally incriminated as intestinal pathogens by virtue of their epidemiologic association with cases of diarrhea (2). Subsequently, these strains, which had been identified by serotype alone, were shown to be EPEC sensu stricto (37). Although atypical EPEC generally are serotypes which differ from EAF-positive EPEC (and other pathotypes of diarrheagenic E. coli), the 12 O-serogroups recognized by the World Health Organization as EPEC (i.e., serogroups O26, O55, O86, O111, O114, O119, O125, O126, O127, O128, O142, and O158) include both typical and atypical varieties (3). Some of the atypical EPEC strains within these serogroups carry accessory virulence-associated determinants such as the EHEC hemolysin (commonly found in serotypes O26:H11 and O111ac:H8). Some strains also carry astA, the gene for enteroaggregative heat-stable enterotoxin, EAST1, which is frequently found in serotypes O55:H7, O119:H2, and O128:H2 (3). Atypical EPEC strains of non-EPEC serogroups generally do not express these factors. In the present study, none of the 89 atypical strains was positive for ehxA, which is required for the production of EHEC hemolysin, and although two strains (both serogroup O55) tested positive for astA, both carried the previously described mutations in this gene, which would preclude the synthesis of biologically active enterotoxin (38).
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