Abstract
The disease caused by Shiga toxin-producing Escherichia coli (STEC) remains a significant public health challenge globally, but the incidence of human STEC infections in Australia remains relatively low. This study examined the virulence characteristics and diversity of STEC isolates in the state of New South Wales between December 2017 and May 2020. Utilisation of both whole and core genome multi-locus sequence typing (MLST) allowed for the inference of genomic diversity and detection of isolates that were likely to be epidemiologically linked. The most common STEC serotype and stx subtype detected in this study were O157:H7 and stx1a, respectively. A genomic scan of other virulence factors present in STEC suggested interplay between iron uptake system and virulence factors that mediate either iron release or countermeasures against host defence that could result in a reduction of stx1a expression. This reduced expression of the dominant stx genotype could contribute to the reduced incidence of STEC-related illness in Australia. Genomic surveillance of STEC becomes an important part of public health response and ongoing interrogation of virulence factors in STEC offers additional insights for the public health risk assessment.
Highlights
Escherichia coli is a bacterial commensal in humans, but some strains have evolved to be pathogens by the acquisition of virulence factors
We examined genomic diversity and pathogenic potential of Shiga toxin-producing Escherichia coli (STEC) isolates recovered from human cases of gastroenteritis and haemolytic uraemic syndrome (HUS) between December 2017 and May 2020 in New South Wales (NSW), Australia using Whole genome sequencing (WGS) and downstream analysis
We developed a virulence barcode to be used with WGS data, which tracks the subtypes of prominent STEC virulence factors eae and stx, and allows for the inference of multiple, isogenic stx copies derived from short read sequencing data
Summary
Escherichia coli is a bacterial commensal in humans, but some strains have evolved to be pathogens by the acquisition of virulence factors. Shiga toxin-producing Escherichia coli (STEC) is a group of predominantly food-borne pathogens that can cause acute gastroenteritis and sometimes haemolytic uraemic syndrome (HUS), neurological complications, and even death (Tarr et al, 2005). This progression to HUS has been linked to the production of Shiga toxin (Stx) encoded by the stx operon consisting of two genes encoding the enzymatically active subunit A and a receptor binding pentameric subunit B of the A1B5 holotoxin, respectively (Melton-Celsa, 2014). This switch to the lytic life cycle via prophage induction releases infectious phage virions, which can disseminate the stx genes to other E. coli cells at the expense of its current host (Allison, 2007)
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