The Evolution of Virulence in Non-O157 Shiga Toxin-Producing Escherichia Coli

Abstract

Shiga toxin-producing Escherichia coli (STEC) are zoonotic foodborne and waterborne pathogens that are a serious public health concern because they cause outbreaks and the potentially fatal hemolytic uremic syndrome (HUS). The most common STEC serotype associated with human disease is O157:H7, but there is a growing recognition of over 100 non-O157 serotypes that also may result in human illness. Some of these non-O157 STEC strains cause outbreaks and severe disease such as HUS and hemorrhagic colitis, whereas others are associated with only mild diarrhea or with no human disease at all. The relative scarceness of whole genome sequence data for non-O157 STEC has limited the scientific discovery into the genetic basis of these differences in virulence. Uncovering the scope of genetic diversity and phylogeny of the non-O157 STEC through targeting sequencing of clinically relevant isolates will offer new biological insight to the pathogenic behavior of these emerging pathogens. These approaches would also enable molecular risk assessment strategies to rapidly identify and respond to emerging non-O157 STEC that pose a serious public health risk to humans.

Distribution of Pathogenicity Islands OI-122, OI-43/48, and OI-57 and a High-Pathogenicity Island in Shiga Toxin-Producing Escherichia coli

“…Estimations indicate that non-O157 STEC strains cause 112,752 illness each year in the United States, almost twice the number of O157:H7 illnesses (63,153) (3). Although some non-O157 STEC strains have been associated with disease symptoms indistinguishable from O157:H7, not all STEC serotypes can cause HUS and outbreaks, and some STEC serotypes have never been reported to be related to any human illness (4). The scientific basis for this difference, however, is poorly understood.…”

“…Several PAIs have been identified and characterized in STEC. A chromosomal pathogenicity island termed the locus of enterocyte effacement (LEE) was identified in E. coli O157:H7 strain EDL933, which encodes a type III secretion system, as well as virulence genes (eae and tir) associated with the intimate attachment of bacteria to intestinal epithelial cells (4). LEE appears to confer enhanced virulence, since LEE-positive STEC are much more commonly associated with HUS and outbreaks than LEEnegative STEC (5).…”

Escherichia coli Serotype O55:H7 Diversity Supports Parallel Acquisition of Bacteriophage at Shiga Toxin Phage Insertion Sites during Evolution of the O157:H7 Lineage

“…The latter serotype has been established as a recent precursor to the virulent enterohemorrhagic E. coli (EHEC) serotype O157:H7 (18,71), which can cause disease in all age groups. Extensive analysis of the diversity of the O157:H7 serotype has provided insight into its continued evolution (15,34,42,75,76) and has led to a search to define genetic properties that could identify more virulent strains of related O157:H7, nonmotile O157, and non-O157 EHEC (3,4,5,8,32,63,74).…”

Novel Repressor of Escherichia coli O157:H7 Motility Encoded in the Putative Fimbrial Cluster OI-1

“…higa toxin-producing Escherichia coli (STEC) is a zoonotic food-borne and waterborne pathogen that has been implicated in outbreaks worldwide and can cause hemorrhagic colitis and the potentially fatal hemolytic-uremic syndrome (7,14,16,17,24). The O157:H7 serotype of enterohemorrhagic STEC (EHEC), classified as a seropathotype A strain, is one of the most prevalent and is recognized for its high virulence in human populations (10,13,24).…”