IAI Accepts, published online ahead of print on 29 June 2009

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Infect. Immun. doi:10.1128/IAI.00198-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Analysis of the genome of the Escherichia coli O157:H7 2006 spinach-associated outbreak isolate indicates candidate genes that may enhance virulence

Bridget R. Kulasekara, Michael Jacobs, Yang Zhou, Zaining Wu, Elizabeth Sims, Channakhone Saenphimmachak, Laurence Rohmer, Jennifer M. Ritchie, Matthew Radey, Matthew McKevitt, Theodore Larson Freeman, Hillary Hayden, Eric Haugen, Will Gillett, Christine Fong, Jean Chang, Viktoriya Beskhlebnaya, Matthew K. Waldor, Mansour Samadpour, Thomas S. Whittam, Rajinder Kaul, Mitchell Brittnacher, and Samuel I. Miller^*

Molecular and Cellular Biology Program, University of Washington, Seattle, Washington; Department of Immunology, University of Washington, Seattle, Washington; University of Washington Genome Center, University of Washington, Seattle, Washington; Howard Hughes Medical Institute, Channing Laboratories, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Institute for Environmental Health, Lake Forest Park, Washington; Microbial Evolution Laboratory, National Food Safety and Toxicology Center, Michigan State University, East Lansing, MI; Department of Genome Sciences, University of Washington, Seattle, Washington; Department of Microbiology, University of Washington, Seattle, Washington; Department of Medicine, University of Washington, Seattle, Washington

^* To whom correspondence should be addressed. Email: millersi{at}u.washington.edu.

In addition to causing diarrhea, Escherichia coli O157:H7 infection can lead to hemolytic uremic syndrome (HUS), a severe disease characterized by hemolysis and renal failure. Differences in HUS frequency among E. coli O157:H7 outbreaks have been noted, but there is incomplete understanding of bacterial factors that promote HUS. In 2006, an outbreak of E. coli O157:H7, caused by consumption of contaminated spinach, occurred with a notably high frequency of HUS. We sequenced the genome of this strain (TW14359) with the goal of identifying candidate genetic factors that contribute to an enhanced ability to cause HUS. The TW14359 genome contains 70-kb of DNA segments not present in either of the two reference O157:H7 genomes. We identified seven putative virulence determinants, including two putative Type III secretion system effector proteins, candidate genes that could result in increased pathogenicity or, alternatively, adaptation to plants, and an intact anaerobic nitric oxide reductase gene, norV. We surveyed one hundred O157:H7 isolates for the presence of these putative virulence determinants. A norV deletion was found in over half of strains surveyed and correlates strikingly with the absence of stx₁. The other putative virulence factors were found in eight to thirty-five percent of O157:H7 isolates surveyed and their presence also correlates with the presence of norV and absence of stx₁ indicating the presence of norV may serve as a marker of greater propensity for HUS similar to the correlation between the absence of stx₁ and HUS propensity.