title: Genomic O island 122, locus for enterocyte effacement, and the evolution of virulent verocytotoxin-producing Escherichia coli.
abstract: The locus of enterocyte effacement (LEE) and genomic O island 122 (OI-122) are pathogenicity islands in verocytotoxin-producing Escherichia coli (VTEC) serotypes that are associated with outbreaks and serious disease. Composed of three modules, OI-122 may occur as "complete" (with all three modules) or "incomplete" (with one or two modules) in different strains. OI-122 encodes two non-LEE effector (Nle) molecules that are secreted by the LEE type III secretion system, and LEE and OI-122 are cointegrated in some VTEC strains. Thus, they are functionally linked, but little is known about the patterns of acquisition of these codependent islands. To examine this, we conducted a population genetics analysis, using multilocus sequence typing (MLST), with 72 VTEC strains (classified into seropathotypes A to E) and superimposed on the results the LEE and OI-122 contents of these organisms. The wide distribution of LEE and OI-122 modules among MLST clonal groups corroborates the hypothesis that there has been lateral transfer of both pathogenicity islands. Sequence analysis of a pagC-like gene in OI-122 module 1 also revealed two nonsynonymous single-nucleotide polymorphisms that could help discriminate a subset of seropathotype C strains and determine the presence of the LEE. A nonsense mutation was found in this gene in five less virulent strains, consistent with a decaying or inactive gene. The modular nature of OI-122 could be explained by the acquisition of modules by lateral transfer, either singly or as a group, and by degeneration of genes within modules. Correlations between clonal group, seropathotype, and LEE and OI-122 content provide insight into the role of genomic islands in VTEC evolution.
authors.affiliation: Laboratory for Foodborne Zoonoses, Public Health Agency of Canada, 110 Stone Rd. West, Guelph, Ontario, Canada N1G 3W4.
authors.forename: Paulina
authors.initials: P
authors.lastname: Konczy
authors.forename: Kim
authors.initials: K
authors.lastname: Ziebell
authors.forename: Mariola
authors.initials: M
authors.lastname: Mascarenhas
authors.forename: Aileen
authors.initials: A
authors.lastname: Choi
authors.forename: Corinne
authors.initials: C
authors.lastname: Michaud
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Kropinski
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Whittam
authors.forename: Mark
authors.initials: M
authors.lastname: Wickham
authors.forename: Brett
authors.initials: B
authors.lastname: Finlay
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: Karmali
mesh_terms: D000818:Animals; D002417:Cattle; D004926:Escherichia coli / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity; D019143:Evolution, Molecular; D022761:Gene Transfer, Horizontal; D005798:Genes, Bacterial / Q000235:genetics; D044404:Genomic Islands / Q000235:genetics*; D006801:Humans; D008957:Models, Genetic; D017422:Sequence Analysis, DNA; D022603:Shiga Toxins / Q000378:metabolism*; D014774:Virulence / Q000235:genetics
chemical_list: D022603:Shiga Toxins