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Molecular Analysis as an Aid To Assess the Public Health Risk of Non-O157 Shiga Toxin-Producing Escherichia coli Strains ^,

Brian K. Coombes,^1,2*, Mark E. Wickham,^3,, Mariola Mascarenhas,² Samantha Gruenheid,⁴ B. Brett Finlay,³ and Mohamed A. Karmali²

Department of Biochemistry and Biomedical Sciences and Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada,¹ Laboratory for Foodborne Zoonoses, Public Health Agency of Canada, Guelph, Ontario, Canada,² Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, Canada,³ Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada⁴

Received 14 November 2007/ Accepted 21 January 2008

Shiga toxin-producing Escherichia coli (STEC) strains are commensal bacteria in cattle with high potential for environmental and zoonotic transmission to humans. Although O157:H7 is the most common STEC serotype, there is growing concern over the emergence of more than 200 highly virulent non-O157 STEC serotypes that are globally distributed, several of which are associated with outbreaks and/or severe human illness such as hemolytic-uremic syndrome (HUS) and hemorrhagic colitis. At present, the underlying genetic basis of virulence potential in non-O157 STEC is unknown, although horizontal gene transfer and the acquisition of new pathogenicity islands are an expected origin. We used seropathotype classification as a framework to identify genetic elements that distinguish non-O157 STEC strains posing a serious risk to humans from STEC strains that are not associated with severe and epidemic disease. We report the identification of three genomic islands encoding non-LEE effector (nle) genes and 14 individual nle genes in non-O157 STEC strains that correlate independently with outbreak and HUS potential in humans. The implications for transmissible zoonotic spread and public health are discussed. These results and methods offer a molecular risk assessment strategy to rapidly recognize and respond to non-O157 STEC strains from environmental and animal sources that might pose serious public health risks to humans.

Published ahead of print on 1 February 2008.

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

B.K.C. and M.E.W. contributed equally to this study.

Present address: Phillips, Ormonde, and Fitzpatrick, Melbourne, Australia.