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Web Content Viewer (JSR 286)

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Web Content Viewer (JSR 286)

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Web Content Viewer (JSR 286)

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2015-2017 Subcommittee: Virulence Factors and Attributes that Define Foodborne Shiga Toxin-producing Escherichia coli (STEC) as Severe Human Pathogens

Subcommittee Members

  • Dr. Alison O’Brien and Dr. Carolyn Hovde: Working Group Chairs
  • MAJ Barbara Cloutier
  • Ms. Vanessa Coffman
  • Dr. Peter Feng
  • Dr. David Gombas
  • Dr. Larry Goodridge
  • Dr. Mohammad Koohmaraie
  • Dr. Richard Linton
  • Dr. Peter Muriana
  • Dr. Wilfredo Ocasio
  • Dr. Tiffiani Onifade
  • Dr. Laurie Post
  • Dr. John Ruby
  • Dr. Robert Tauxe

Executive Summary

Shiga toxin-producing Escherichia coli (STEC) are a large, diverse group of bacteria that are characterized by the production of Shiga toxins (Stx). There are two main Stx types, designated Stx1 and Stx2 and within each are many subtypes. Currently, there are 3 known Stx1 (Stx1a, Stx1c and Stx1d) and 7 known Stx2 (Stx2a, Stx2b, Stx2c, Stx2d, Stx2e, Stx2f and Stx2g) subtypes, but some of these are produced mostly by environmental or animal associated strains. Thus far, Stx1a, Stx2a, Stx2c and Stx2d are the subtypes most frequently been implicated in human illness. There are estimated to be ~300-400 known STEC serotypes that can produce any of the Stx types, subtypes or combination of subtypes. However, only a subset of these types have been associated with human illness. Furthermore, the production of Stx alone without other virulence factors, such as intimin, has been deemed to be insufficient to cause severe human illness.

Background

Many STEC serotypes have been isolated from various foods, including ground meats, fresh produce and dairy products. Of the 300 to 400 known STEC serotypes, ~100 serotypes have reportedly caused human illnesses. Some of these, such as various serotypes in the serogroups O26, O111, O103, O121, O145 and O45 that also include the adherence factor intimin, which are commonly referred to as the “big 6”, are well recognized pathogens and are of human health concern. The virulence potential of other STEC strains is more difficult to determine due to the lack of a clear understanding of STEC pathogenesis. In addition to the previously mentioned adherence factor, there may be additional virulence determinants required for a particular STEC strain to be fully virulent. Recent FDA investigations on STEC in fresh produce showed that multiple STEC serotypes, including members of the “big 6”, can be found in many types of fresh produce. These STEC seem to be more prevalent in spinach and cilantro. Conversely, a majority of the produce-derived STEC strains lacked at least one virulence factor and were of serotypes not associated with human illness. Furthermore, the methods that are used to isolate STEC from foods are inefficient and too time consuming. The confirmatory tests used for assessing the risk potential of STEC strains are limited and lastly, these algorithms are unable to provide timely health risk information, especially for products like fresh produce that has an average shelf-life of 2 weeks.

The Food and Drug Administration (FDA), the Centers for Disease Control and Prevention (CDC), The Food Safety and Inspection Service (FSIS), the National Marine Fisheries Service (NMFS), and the Department of Defense Veterinary Service Activity (DoDVSA) believe that enhancing the scientific information available on STECs and improved detection and identification methodology will assist in reducing illness from STEC. For this reason they provide the following charge questions to NACMCF.

Charge Questions for the Subcommittee

  1. What is currently known about the virulence and pathogenicity of STECs and how they cause illness in humans? Address data generated within and outside of the U.S.
  • What defines or differentiates an STEC as a human pathogen from other STEC that are under represented in severe illnesses?
  • Please discuss all combinations of virulence attributes that contribute to human illness and the probable severity associated with certain combinations. Are there specific attributes that can be identified as associated with STEC virulence in humans and the colonization and persistence on fresh produce, in lieu of colonization of environmental or host animal niches?
  • In terms of pathogenicity and virulence, please discuss what is known empirically and what has been clearly defined.
  1. What methods are available to detect STEC and their specific virulence factors, either separately or in combination?
  • What data gaps exist and what research is required to improve the effectiveness of these methods? For example, please discuss the strengths and weaknesses of using molecular subtyping/genotyping approaches for characterization any genetic markers that contribute to STEC virulence, including specific toxin gene subtypes (i.e., stx1, 1c, 1d and stx2, 2b, 2c, 2d, etc.).
  1. What are the principal attributes that can be exploited to rapidly detected STEC that are a high probability of causing severe human illness?
  • If such attributes exists, can they be implemented in a high through-put tool to ensure public health and help industry rapidly decide to hold or release product?
  • What data gaps exist and what research is required to determine an accepted set of attributes for virulence and pathogenicity determination?
  • What are the limitations to establishing such a rapid, high-throughput method for this determination?
  • Are there a collection of SNPs, or other molecular identifiers that can be used in these methods (i.e. virulent lineages)?
  1. If the attributes critical for differentiating pathogenic STEC from non-pathogenic STEC can be identified, what concerns and confounding issues do you foresee in the need to determine whether those attributes are expressed or not?
  • What data gaps exist and what research is required to support methods development in relation to gene expression? For example, is there a need for a national research effort to establish a STEC full “transcriptome” multi-lab collaborative project on a strain-to-strain basis?
  1. What data gaps exist and what research is required to conduct a “molecular risk assessment” to determine the probability that a particular STEC isolate is highly virulent to humans?
  • Can we refine our understanding of the required genetic repertoir for STEC virulence and how that translates into the “risk” posed by a particular organism?
  • Will there always be a degree of uncertainty associated with such an assessment?
  • Is it more appropriate in the short term, or long term, to assess collections of virulence genes present in the genome or SNPs of virulent lineages?

 

Last Modified Apr 13, 2016