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Applied and Environmental Microbiology, April 2008, p. 2153-2160, Vol. 74, No. 7
0099-2240/08/$08.00+0     doi:10.1128/AEM.02566-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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

Brian K. Coombes,1,2*,{dagger} Mark E. Wickham,3,{dagger},§ 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.

* Corresponding author. Mailing address: Department of Biochemistry and Biomedical Sciences, McMaster University, Health Sciences Centre 4H17, 1200 Main St. West, Hamilton, Ontario L8N 3Z5, Canada. Phone: (905) 525-9140, ext. 22159. Fax: (905) 522-9033. E-mail: coombes{at}mcmaster.ca

{triangledown} Published ahead of print on 1 February 2008.

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

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

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

Applied and Environmental Microbiology, April 2008, p. 2153-2160, Vol. 74, No. 7
0099-2240/08/$08.00+0     doi:10.1128/AEM.02566-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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