Abstract
Shiga toxin-producing Escherichia coli (STEC) cause infections in humans ranging from asymptomatic carriage to bloody diarrhoea and haemolytic uremic syndrome (HUS). Here we present whole genome comparison of Norwegian non-O157 STEC strains with the aim to distinguish between strains with the potential to cause HUS and less virulent strains. Whole genome sequencing and comparisons were performed across 95 non-O157 STEC strains. Twenty-three of these were classified as HUS-associated, including strains from patients with HUS (n = 19) and persons with an epidemiological link to a HUS-case (n = 4). Genomic comparison revealed considerable heterogeneity in gene content across the 95 STEC strains. A clear difference in gene profile was observed between strains with and without the Locus of Enterocyte Effacement (LEE) pathogenicity island. Phylogenetic analysis of the core genome showed high degree of diversity among the STEC strains, but all HUS-associated STEC strains were distributed in two distinct clusters within phylogroup B1. However, non-HUS strains were also found in these clusters. A number of accessory genes were found to be significantly overrepresented among HUS-associated STEC, but none of them were unique to this group of strains, suggesting that different sets of genes may contribute to the pathogenic potential in different phylogenetic STEC lineages. In this study we were not able to clearly distinguish between HUS-associated and non-HUS non-O157 STEC by extensive genome comparisons. Our results indicate that STECs from different phylogenetic backgrounds have independently acquired virulence genes that determine pathogenic potential, and that the content of such genes is overlapping between HUS-associated and non-HUS strains.
Highlights
Shiga toxin producing E. coli (STEC) are important human pathogens known to cause infections ranging from diarrhoea and haemorrhagic colitis to haemorrhagic uremic syndrome (HUS) [1]
Sequencing and whole genome comparison of the 95 non-O157 STEC strains included in this study revealed high degree of variation in gene content as well as diversity in whole genome phylogeny
Of the stx1 subtypes, stx1c was significantly associated with Locus of Enterocyte Effacement (LEE) negative STEC
Summary
Shiga toxin producing E. coli (STEC) are important human pathogens known to cause infections ranging from diarrhoea and haemorrhagic colitis to haemorrhagic uremic syndrome (HUS) [1]. Since the first reports of disease caused by O157:H7 in 1982 [2,3], this serotype has been the most frequently reported cause of severe STEC disease and outbreaks worldwide [1]. Several non-O157 STEC serogroups (e.g. O26, O45, O103, O111, O121 and O145) have been recognized to be responsible for severe disease and outbreaks [4,5]. The adherence factor intimin, encoded by the eae gene located in the Locus of Enterocyte Effacement (LEE) pathogenicity island, is important for STEC pathogenicity. LEE encodes several genes responsible for the attaching and effacing nature of STEC, a feature that these bacteria share with the closely related enteropathogenic E. coli (EPEC). The LEE encodes additional associated regulators, translocators, effector proteins and chaperones [22,23]
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