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Journal of Clinical Microbiology, December 2006, p. 4528-4536, Vol. 44, No. 12
0095-1137/06/$08.00+0     doi:10.1128/JCM.01474-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Phylogenetic Comparisons Reveal Multiple Acquisitions of the Toxin Genes by Enterotoxigenic Escherichia coli Strains of Different Evolutionary Lineages ^,

Division of Immunity and Infection, The Medical School,¹ School of Biosciences, The University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom,² St. Luke's Episcopal Hospital, 6720 Bertner Avenue, MC 1-164, Houston, Texas 77083,³ University of Guelph, Guelph, Ontario, Canada⁴

Received 18 July 2006/ Returned for modification 29 August 2006/ Accepted 9 October 2006

Escherichia coli is a diverse bacterial species which is widely distributed in the environment but also exists as a commensal and pathogen of different host species. Human intestinal pathogenic E. coli causes over 160 million cases of diarrhea and an estimated 1 million deaths per year. The majority of deaths are attributable to one pathovar of E. coli, namely, enterotoxigenic E. coli. The pathogenesis of enterotoxigenic E. coli is dependent on the production of a colonization factor to promote adhesion to the intestinal epithelium and the elaboration of heat-labile or heat-stable toxins which induce a secretory diarrhea. Despite the high morbidity and mortality associated with enterotoxigenic E. coli infection, little is known of the genetic background of this global pathogen. Here we demonstrate by multilocus sequence typing that enterotoxigenic E. coli isolates are present in all phylogenetic lineages of E. coli, indicating that acquisition of the toxin genes may be sufficient to generate an enterotoxigenic E. coli strain. In addition, screening of diarrheal isolates for the presence of additional genes previously associated with the virulence of enterotoxigenic E. coli revealed that they were not abundant. These observations have significant implications for disease epidemiology and for the design of effective vaccines.

Published ahead of print on 18 October 2006.

Supplemental material for this article may be found at http://jcm.asm.org/.

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