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Molecular Characterization Reveals Similar Virulence Gene Content in Unrelated Clonal Groups of Escherichia coli of Serogroup O174 (OX3)

Enteric Diseases Laboratory Branch, National Center for Zoonotic, Vectorborne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30329,¹ Microbial Evolution Laboratory, National Food Safety and Toxicology Center, Michigan State University, East Lansing Michigan 48824,² National Reference Laboratory for Escherichia coli, Federal Institute for Risk Assessment (BfR), D-12277 Berlin, Germany,³ Statens Serum Institut, Copenhagen, Denmark⁴

Received 14 August 2007/ Accepted 17 November 2007

Most severe illnesses that are attributed to Shiga toxin-producing Escherichia coli are caused by isolates that also carry a pathogenicity island called the locus of enterocyte effacement (LEE). However, many cases of severe disease are associated with LEE-negative strains. We characterized the virulence gene content and the evolutionary relationships of Escherichia coli isolates of serogroup O174 (formerly OX3), strains of which have been implicated in cases of hemorrhagic colitis and hemolytic uremic syndrome. A total of 56 isolates from humans, farm animals, and food were subjected to multilocus virulence gene profiling (MVGP), and a subset of 16 isolates was subjected to multilocus sequence analysis (MLSA). The MLSA revealed that the O174 isolates fall into four separate evolutionary clusters within the E. coli phylogeny and are related to a diverse array of clonal groups, including enteropathogenic E. coli 2 (EPEC 2), enterohemorrhagic E. coli 2 (EHEC 2), and EHEC-O121. Of the 15 genes that we surveyed with MVGP, only 6 are common in the O174 strains. The different clonal groups within the O174 serogroup appear to have independently acquired and maintained similar sets of genes that include the Shiga toxins (stx₁ and stx₂) and two adhesins (saa and iha). The absence of certain O island (OI) genes, such as those found on OI-122, is consistent with the notion that certain pathogenicity islands act cooperatively with the LEE island.

Published ahead of print on 14 December 2007.