Abstract

We evaluated clinical Shiga toxin-producing Escherichia coli O157 infections in England and Wales during 1983-2012 to describe changes in microbiological and surveillance methods. A strain replacement event was captured; phage type (PT) 2 decreased to account for just 3% of cases by 2012, whereas PT8 and PT21/28 strains concurrently emerged, constituting almost two thirds of cases by 2012. Despite interventions to control and reduce transmission, incidence remained constant. However, sources of infection changed over time; outbreaks caused by contaminated meat and milk declined, suggesting that interventions aimed at reducing meat cross-contamination were effective. Petting farm and school and nursery outbreaks increased, suggesting the emergence of other modes of transmission and potentially contributing to the sustained incidence over time. Studies assessing interventions and consideration of policies and guidance should be undertaken to reduce Shiga toxin-producing E. coli O157 infections in England and Wales in line with the latest epidemiologic findings.

Highlights

  • We evaluated clinical Shiga toxin–producing Escherichia coli O157 infections in England and Wales during 1983– 2012 to describe changes in microbiological and surveillance methods

  • Shiga toxin–producing Escherichia coli (STEC) serogroup O157 emerged as a pathogen of public health concern during the early 1980s and was first isolated in the United Kingdom in July 1983 (Figure 1) from 3 cases linked to an outbreak of hemolytic uremic syndrome (HUS) [1]

  • Case Ascertainment, 1983–2012 Beginning in 1983, only fecal specimens from patients with HUS or hemorrhagic colitis were referred for STEC O157 testing; before 1989, few specimens were referred for testing

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Summary

Introduction

We evaluated clinical Shiga toxin–producing Escherichia coli O157 infections in England and Wales during 1983– 2012 to describe changes in microbiological and surveillance methods. We describe changes in the epidemiology of STEC O157 in England and Wales during a 30-year period (1983–2012) against a background of changing microbiological and surveillance methods over time. Local PHE units report standardized epidemiologic data on all outbreaks of gastrointestinal diseases, including source of infection and microbiological data.

Results
Conclusion
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