Pathogenic Potential to Humans of BovineEscherichia coliO26, Scotland

Margo E Chase-Topping,David L Gally,Emily Courcier,Mark E.J Woolhouse,Tracy Rosser,Alfredo Caprioli,Judith Evans,Iain J Mckendrick,Kevin G.J Pollock,Mary F Hanson,J Chris Low,Ian Handel,Helge Karch,Michael C Pearce,Lesley J Allison,Mary E Locking,Louise Matthews

doi:10.3201/eid1803.111236

Abstract

Escherichia coli O26 and O157 have similar overall prevalences in cattle in Scotland, but in humans, Shiga toxin-producing E. coli O26 infections are fewer and clinically less severe than E. coli O157 infections. To investigate this discrepancy, we genotyped E. coli O26 isolates from cattle and humans in Scotland and continental Europe. The genetic background of some strains from Scotland was closely related to that of strains causing severe infections in Europe. Nonmetric multidimensional scaling found an association between hemolytic uremic syndrome (HUS) and multilocus sequence type 21 strains and confirmed the role of stx(2) in severe human disease. Although the prevalences of E. coli O26 and O157 on cattle farms in Scotland are equivalent, prevalence of more virulent strains is low, reducing human infection risk. However, new data on E. coli O26-associated HUS in humans highlight the need for surveillance of non-O157 enterohemorrhagic E. coli and for understanding stx(2) phage acquisition.

Highlights

The pathogenesis of EHEC strains is associated with production of Shiga toxins expressed from lysogenic bacteriophages in the EHEC genome
There are 2 predominant classes of Shiga toxins (1 and 2), each encoded from 2 genes, stxAB, with the genotypes simplified to stx1 or stx2 in this study
The T3S system is central to the formation of attaching and effacing lesions on the intestinal epithelium that requires the bacterial outer membrane protein intimin and the secreted bacterial protein—the translocated intimin receptor (Tir)— that is injected into the host cell

Summary

Introduction

The pathogenesis of EHEC strains is associated with production of Shiga toxins expressed from lysogenic bacteriophages in the EHEC genome. EPEC and EHEC express a type III secretion (T3S) system that translocates multiple effector proteins into host cells and manipulate host innate responses, which are needed for colonization [5,6,7]. Among non-O157 EHEC, Stx-producing E. coli O26 causes human disease [13,14,15] and has been isolated from livestock [16]. Most identified EHEC infections are associated with serogroup O157, and incidence rates in Scotland are among the highest, compared with rates in countries with comparable surveillance [23]. Our first objective was to identify the cause of the disparity between the incidence of E. coli O157 and O26 infections among humans in Scotland by examining the natural heterogeneity among serogroup O26 strains and reexamining their prevalence in cattle. We used different molecular techniques to compare the relationships between E. coli O26 isolates recovered from humans and cattle

Methods

Results

Conclusion