Abstract

Shiga toxin-producing Escherichia coli (STEC) is a foodborne pathogen, and serotype O157:H7 is typically associated with severe disease. Australian STEC epidemiology differs from many other countries, as severe outbreaks and HUS cases appear to be more often associated with non-O157 serogroups. It is not known why Australian strains of O157 STEC might differ in virulence to international strains. Here we investigate the reduced virulence of Australian strains. Multiple genetic analyses were performed, including SNP-typing, to compare the core genomes of the Australian to the international isolates, and accessory genome analysis to determine any significant differences in gene presence/absence that could be associated with their phenotypic differences in virulence. The most distinct difference between the isolates was the absence of the stx2a gene in all Australian isolates, with few other notable differences observed in the core and accessory genomes of the O157 STEC isolates analyzed in this study. The presence of stx1a in most Australian isolates was another notable observation. Acquisition of stx2a seems to coincide with the emergence of highly pathogenic STEC. Due to the lack of other notable genotypic differences observed between Australian and international isolates characterized as highly pathogenic, this may be further evidence that the absence of stx2a in Australian O157 STEC could be a significant characteristic defining its mild virulence. Further work investigating the driving force(s) behind Stx prophage loss and acquisition is needed to determine if this potential exists in Australian O157 isolates.

Highlights

  • Shiga toxin-producing Escherichia coli (STEC) is a foodborne human pathogen that causes a wide spectrum of disease varying in severity from asymptomatic carriage, to haemorrhagic colitis, through to life threatening disease such as haemolytic uremic syndrome (HUS) (Paton and Paton, 1998; Castro et al, 2017; Kim et al, 2020)

  • To determine the genetic characteristics associated with this contrasting epidemiology, core genome comparisons were made between 164 O157 isolates (76 Australian, 20 international, and 68 United Kingdom 2015 outbreak isolates), analyzing regions of the genome that are shared amongst all 164 O157 isolates

  • The most distinct difference in relation to virulence between the Australian STEC isolates was the absence of stx2a, with other notable differences including the presence of many type IV secretion system genes and differences in bacteriophagederived genes observed in the core and accessory genomes of the O157 STEC isolates analyzed in this study

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Summary

Introduction

Shiga toxin-producing Escherichia coli (STEC) is a foodborne human pathogen that causes a wide spectrum of disease varying in severity from asymptomatic carriage, to haemorrhagic colitis, through to life threatening disease such as haemolytic uremic syndrome (HUS) (Paton and Paton, 1998; Castro et al, 2017; Kim et al, 2020). Shiga toxin-producing Escherichia coli was first recognized as an emerging pathogen following the investigation of two haemorrhagic colitis outbreaks in 1982, leading to the identification of E. coli serotype O157:H7 as the cause (Riley et al, 1983) This led to the association of the O157:H7 serotype of E. coli with STEC. It is not known why there are differences in virulence between the Australian O157 STEC and international strains but studies have demonstrated some genotypic differences, notably the absence of stx2a (Mellor et al, 2012; Ingle et al, 2019)

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