Genomic comparison of Escherichia coli serotype O103:H2 isolates with and without verotoxin genes: implications for risk assessment of strains commonly found in ruminant reservoirs

摘要

Pathogenic Escherichia coli have evolved by the acquisition of mobile genetic elements containing virulence and fitness factors through horizontal gene transfer (1). Enteropathogenic E. coli (EPEC) are characterized by variants of the locus of enterocyte effacement (LEE), a genetic element that encodes intimin and components for a type III secretion system as well as several other virulence factors. These factors allow EPEC to cause attaching and effacing (A/E) lesions in the human intestinal epithelium (2). Most human-pathogenic verotoxigenic E. coli (VTEC, also known as STEC) originate from populations of EPEC lysogenized by one or more phages carrying genes encoding verotoxin 1 and/or verotoxin 2 (vtx1, vtx2) (1). Although typical human-pathogenic EPEC carry the EPEC adherence factor plasmid, this plasmid is frequently absent in VTEC-like EPEC. Therefore, these strains are considered ‘atypical’ EPEC (aEPEC) (2). Ruminants are the natural reservoir of many forms of aEPEC and VTEC (2) and are colonized with a high prevalence and great diversity of these bacteria, but rarely develop symptoms as a result. Both VTEC and the different types of EPEC can cause diarrhea in infected humans, but VTEC can also cause more severe forms of bloody diarrhea and occasionally fatal complications like hemolytic uremic syndrome (HUS) (3). The E. coli O157:H7 serotype is the most common cause of human VTEC infection in Sweden as well as in many countries worldwide, but non-O157 serogroups including O26, O103, and O121 also cause a significant number of cases every year (4). A major outbreak of enteroaggregative VTEC O104:H4 in 2011 caused more than 4,000 cases in several European countries, including Sweden (5),and led to an increased interest in the role of verotoxin-encoding phages in the emergence of new VTEC types.