A Brief Overview of Escherichia coli O157:H7 and Its Plasmid O157

Abstract

Enterohemorrhagic Escherichia coli O157:H7 is a major foodborne pathogen causing severe disease in humans worldwide. Healthy cattle are a reservoir of E. coli O157:H7, and bovine food products and fresh produce contaminated with bovine waste are the most common sources for disease outbreaks in the United States. E. coli O157:H7 also survives well in the environment. The abilities to cause human disease, colonize the bovine gastrointestinal tract, and survive in the environment require that E. coli O157:H7 adapt to a wide variety of conditions. Three major virulence factors of E. coli O157:H7 have been identified including Shiga toxins, products of the pathogenicity island called the locus of enterocyte effacement, and products of the F-like plasmid pO157. Among these virulence factors, the role of pO157 is least understood. This review provides a board overview of E. coli O157:H7 with an emphasis on pO157.

Routes of Transmission in the Food Chain

“…Cattle are the primary reservoir for E. coli O157:H7, a bacterium that is distributed worldwide and is most often transmitted by contaminated water or food (Ahmed and Shimamoto, 2015;Bell et al, 1994;Jensen et al, 2015;King et al, 2014;Marder et al, 2014;Riley, 2014;Soon et al, 2011;Wendel et al, 2009). Infection with E. coli O157:H7 may be asymptomatic (Griffin et al, 1988;Rahal et al, 2012;Su and Brandt, 1995) and it may cause mild disease or nonbloody diarrhea (Lim et al, 2010;Rodrigue et al, 1995), but the pathogen is feared for the more severe outcomes, which include bloody diarrhea, hemolytic-uremic syndrome, thrombocytic thrombocytopenic purpura, and death (see Chapter 7).…”

“…Healthy cattle harbor E. coli O157:H7 in their gastrointestinal tract (see Chapter 7), with the terminal rectum and the rectoanal junction being some of the main colonization sites, from where the bacteria are shed into the feces (Gansheroff and O'Brien, 2000;Naylor et al, 2003;Low et al, 2005;Robinson et al, 2009;Lim et al, 2010;Cote et al, 2015;Munns et al, 2015). The bovine rectoanal junction is located between the descending colon and the anal canal, and marks the abrupt transition between two cell types, the follicle-associated columnar epithelium toward the distal colon and the nonkeratinized stratified squamous epithelium toward the anal canal (Kudva and Dean-Nystrom, 2011;Kudva et al, 2012).…”

Pathogen–host–environment interplay and disease emergence

“…59,60 For example, E. coli O157:H7 obtained the large virulence plasmid pO157 and a bacteriophage expressing Shiga toxin leading to an emerging disease challenge in the food chain. 61 The plasmid containing New Delhi metallo-beta-lactamase forms another example; this plasmid is easily transferable by horizontal gene transfer and has conferred carbapenem resistance to many different Enterobacteriaceae species. 62 In fact, genes conferring antimicrobial resistance are ancient and known to circulate also in places out of reach of human and veterinary medicine.…”

“…[66][67][68] Examples of aggressive pathogens featuring environmental robustness include the H5N1 HPAI virus, E. coli bacteria including E. coli O157:H7 and the infectious bursal disease virus. 61,[69][70][71][72] Drivers of emergence of a pathogen with novel traits Drivers of the evolution of pathogens emerging with novel traits comprise the rise in food animal populations, the process of agricultural intensification and global food supply dynamics as well as the extensive use of antimicrobials and vaccines. 27,59,66,73 Food animal production, processing, marketing and distribution have intensified progressively in most industrial countries since the 1950s.…”

Multilocus sequence typing and virulence factors analysis of Escherichia coli O157 strains in China

“…The ability of E. coli O157:H7 strains to cause severe diseases in human is primarily related to their capacities to secrete shiga toxin (Stx) and other toxins and to induce attaching and effacing lesion (A/E lesion) (Pradel et al, 2001;Lim et al, 2010). Stx mainly form two subgroups, Stx1 and Stx2, both of which are toxic to humans and animals for their ability to inhibit protein synthesis (O'Brien and Holmes, 1987;Sandvig et al, 2004).…”