Abstract

Shiga toxin-producing Escherichia coli (STEC) are foodborne pathogens associated with outbreaks and hemolytic-uremic syndrome. Cattle and meat foods are the main reservoir and infection source, respectively. Pathogenicity islands (PAIs) play an important role in STEC pathogenicity, and non-locus of the enterocyte effacement(LEE) effector (nle) genes present on them encode translocated substrates of the type III secretion system. A molecular risk assessment based on the evaluation of the nle content has been used to predict which STEC strains pose a risk to humans. The goal was to investigate the distribution of the PAIs OI (O-island)-36 (nleB2, nleC, nleH1-1, nleD), OI-57 (nleG2-3, nleG5-2, nleG6-2), OI-71 (nleA, nleF, nleG, nleG2-1, nleG9, nleH1-2) and OI-122 (ent/espL2, nleB, nleE, Z4321, Z4326, Z4332, Z4333) among 204 clinical, food and animal isolates belonging to 52 non-O157:H7 serotypes. Differences in the frequencies of genetic markers and a wide spectrum of PAI virulence profiles were found. In most LEE-negative strains, only module 1 (Z4321) of OI-122 was present. However, some unusual eae-negative strains were detected, which carried other PAI genes. The cluster analysis, excluding isolates that presented no genes, defined two major groups: eae-negative (determined as seropathotypes (SPTs) D, E or without determination, isolated from cattle or food) and eae-positive (mostly identified as SPTs B, C, or not determined).

Highlights

  • Shiga toxin-producing Escherichia coli (STEC) are heterogeneous foodborne pathogens associated with outbreaks and hemolytic-uremic syndrome (HUS) [1]

  • The distribution of 16 nle genes and four putative virulence genes encoded in four genomic pathogenicity islands (PAIs) (OI-36, OI-57, OI-71, OI-122) among non-O157 STEC strains were analyzed

  • The presence of nle genes and the number of genes carried by an E. coli strain are important

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Summary

Introduction

Shiga toxin-producing Escherichia coli (STEC) are heterogeneous foodborne pathogens associated with outbreaks and hemolytic-uremic syndrome (HUS) [1]. E. coli O157:H7 is the serotype most associated with diseases; more current studies have shown that the number of non-O157 STEC infections sometimes surpasses the number of STEC O157 infections [2]. A large number of these determinants are located within pathogenicity islands (PAIs), and can be exchanged among different bacterial species, and assembled and stabilized by selective pressure, leading to emerging pathogenic variants [3]. Increasing evidence shows that differences in virulence between pathogenic and non-pathogenic bacterial strains can be attributed in part to virulence genes located in PAIs [4,5]

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