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1 Universidad Peruana Cayetano Heredia, Lima, Peru;
2 U.S. Food and Drug Administration, Laurel, Maryland, USA;
3 4E. coli Reference Center, Pennsylvania State University;
4 Departamento de Salud Publica. Facultad de Medicina, Universidad Nacional Autnoma de Mexico;
5 Department of Medical Genetics, University of Antwerp, Antwerp, Belgium;
6 University of Maryland, Baltimore;
7 Instituto de Investigación Nutricional, Lima, Peru;
8 Instituto de Investigación Nutricional, Lima, Peru;
9 University of Texas School of Public Health
10 E-mail: theresa.j.ochoa{at}uth.tmc.edu
Received June 19, 2009
Accepted September 25, 2009
Enteropathogenic Escherichia coli (EPEC) are a leading cause of infantile diarrhea in developing countries. The aim of this study was to describe the allelic diversity of critical virulence EPEC genes and their association with clinical characteristics. 120 EPEC strains isolated from a cohort diarrhea study in Peruvian children were characterized for the allele type of eae (intimin), bfpA (bundlin pilin protein of bundle-forming pilus) and perA (plasmid encoded regulator) genes by PCR-restriction fragment length polymorphism. Atypical EPEC strains (eae+, bfp-) were the most common pathotype in diarrhea (54/74, 73%) and control samples from children without diarrhea (40/46, 87%). Overall there were 13 eae alleles; the most common were beta (34/120, 28%), theta (24/120, 20%), kappa (14/120, 12%) and mu (8/120, 7%). There were 5 bfpA alleles; the most common were beta1/7 (10/26), alpha3 (7/26) and beta5 (3/26). There were 3 perA alleles: beta (8/16), alpha (7/16) and gamma (1/16). The strains belonged to 36 distinct serogroups; O55 was the most frequent. The gamma-intimin allele was more frequently found in diarrhea episodes of longer duration (>7 days) than shorter (3/26, 12% vs. 0/48, 0%, p<0.05). The kappa-intimin allele had the highest clinical severity score in comparison to other alleles (p<0.05). In Peruvian children the virulence genes of EPEC strains are highly variable. Further studies are needed to evaluate additional virulence markers to determine whether relationships exist between specific variants and clinical features of disease.
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