Evolutionary context of non–sorbitol-fermenting shiga toxin–producing Escherichia coli O55:H7

Kyle Schutz, Lauren A. Cowley, Sharif Shaaban, Anne Carroll, Eleanor McNamara, David L. Gally, Gauri Godbole, Claire Jenkins*, Tim Dallman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

In July 2014, an outbreak of Shiga toxin–producing Escherichia coli (STEC) O55:H7 in England involved 31 patients, 13 (42%) of whom had hemolytic uremic syndrome. Isolates were sequenced, and the sequences were compared with publicly available sequences of E. coli O55:H7 and O157:H7. A core-genome phylogeny of the evolutionary history of the STEC O55:H7 outbreak strain revealed that the most parsimonious model was a progenitor enteropathogenic O55:H7 sorbitol-fermenting strain, lysogenized by a Shiga toxin (Stx) 2a–encoding phage, followed by loss of the ability to ferment sorbitol because of a non-sense mutation in srlA. The parallel, convergent evolutionary histories of STEC O157:H7 and STEC O55:H7 may indicate a common driver in the evolutionary process. Because emergence of STEC O157:H7 as a clinically significant pathogen was associated with acquisition of the Stx2a-encoding phage, the emergence of STEC O55:H7 harboring the stx2a gene is of public health concern.

Original languageEnglish
Pages (from-to)1958-1965
Number of pages8
JournalEmerging Infectious Diseases
Volume23
Issue number12
DOIs
Publication statusPublished - Dec 2017

Bibliographical note

Funding Information:
This work was supported by the National Institute for Health Research Health Protection Research Unit in Gastrointestinal Infections. D.L.G., T.J.D., and S.S. were supported by a Food Standards Scotland/Food Standards Agency study grant (FS101055).

Publisher Copyright:
© 2017, Centers for Disease Control and Prevention (CDC). All rights reserved.

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