Abstract
Signs and symptoms of Shiga toxin–producing Escherichia coli (STEC) serogroup O157:H7 infection range from mild gastrointestinal to bloody diarrhea and hemolytic uremic syndrome (HUS). We assessed the association between Shiga toxin gene (stx) subtype and disease severity for »3,000 patients with STEC O157:H7 in England during 2009–2019. Odds of bloody diarrhea, HUS, or both, were significantly higher for patients infected with STEC O157:H7 possessing stx2a only or stx2a combined with other stx subtypes. Odds of severe signs/symptoms were significantly higher for isolates encoding stx2a only and belonging to sublineage Ic and lineage I/II than for those encoding stx2a only and belonging to sublineage IIb, indicating that stx2a is not the only driver causing HUS. Strains of STEC O157:H7 that had stx1a were also significantly more associated with severe disease than strains with stx2c only. This finding confounds public health risk assessment algorithms based on detection of stx2 as a predictor of severe disease.
Highlights
Signs and symptoms of Shiga toxin–producing Escherichia coli (STEC) serogroup O157:H7 infection range from mild gastrointestinal to bloody diarrhea and hemolytic uremic syndrome (HUS)
Descriptive National Enhanced Surveillance System for STEC (NESSS) clinical data were available for 3,241 STEC O157:H7 case-patients with genomic strain data in England during 2009–2019
1,889 (58.3%) case-patients in the dataset were categorized as having severe disease, this proportion varied by Shiga toxin (Stx) subtype (Table 1)
Summary
Signs and symptoms of Shiga toxin–producing Escherichia coli (STEC) serogroup O157:H7 infection range from mild gastrointestinal to bloody diarrhea and hemolytic uremic syndrome (HUS). Strains of STEC O157:H7 that had stx1a were significantly more associated with severe disease than strains with stx2c only This finding confounds public health risk assessment algorithms based on detection of stx as a predictor of severe disease. Previous studies have demonstrated an association between Stx subtype and disease severity; strains producing Stx, the Stx2a subtype, are more associated with severe disease and HUS [12,13,14,15,16] These findings have led to the development and implementation of differential case management and public health management of cases based on Stx profile–derived STEC pathotypes in England and elsewhere [17,18,19]. The emergence of each clade appears to coincide with the acquisition of phage encoding the stx2a gene, which, if causing more severe disease, increases the likelihood that those cases will be detected [20]
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