Abstract
BackgroundEnteropathogenic E. coli (EPEC) is a prominent cause of diarrhoea, and is characterised in part by its carriage of a pathogenicity island: the locus for enterocyte effacement (LEE). EPEC is divided into two subtypes according to the presence of bundle-forming pili (BFP), a fimbrial adhesin that is a virulence determinant of typical EPEC (tEPEC), but is absent from atypical EPEC (aEPEC). Because aEPEC lack BFP, their virulence has been questioned, as they may represent LEE-positive Shiga toxin-producing E. coli (STEC) that have lost the toxin-encoding prophage, or tEPEC that have lost the genes for BFP. To determine if aEPEC isolated from humans in Australia or New Zealand fall into either of these categories, we undertook phylogenetic analysis of 75 aEPEC strains, and compared them with reference strains of EPEC and STEC. We also used PCR and DNA hybridisation to determine if aEPEC carry virulence determinants that could compensate for their lack of BFP.ResultsThe results showed that aEPEC are highly heterogeneous. Multilocus sequence typing revealed that 61 of 75 aEPEC strains did not belong to known tEPEC or STEC clades, and of those that did, none expressed an O:H serotype that is frequent in tEPEC or STEC strains associated with disease. PCR for each of 18 known virulence-associated determinants of E. coli was positive in less than 15% of strains, apart from NleB which was detected in 30%. Type I fimbriae were expressed by all aEPEC strains, and 12 strains hybridised with DNA probes prepared from either bfpA or bfpB despite being negative in the PCR for bfpA.ConclusionOur findings indicate that clinical isolates of aEPEC obtained from patients in Australia or New Zealand are not derived from tEPEC or STEC, and suggest that functional equivalents of BFP and possibly type I fimbriae may contribute to the virulence of some aEPEC strains.
Highlights
Enteropathogenic E. coli (EPEC) is a prominent cause of diarrhoea, and is characterised in part by its carriage of a pathogenicity island: the locus for enterocyte effacement (LEE)
This overall heterogeneity was confirmed by multi-locus sequence typing (MLST) analysis, which showed that 56 of the 79 atypical EPEC (aEPEC) strains of human origin investigated in the study belonged to one of 11 different clades and that 23 strains could not allocated to a clade (Figure 1)
Five of 11 clades which contained aEPEC strains in this study were clades that include either typical EPEC (tEPEC) or Shiga toxin-producing E. coli (STEC) strains, whereas six clades were apparently distinct for aEPEC
Summary
Enteropathogenic E. coli (EPEC) is a prominent cause of diarrhoea, and is characterised in part by its carriage of a pathogenicity island: the locus for enterocyte effacement (LEE). EPEC is divided into two subtypes according to the presence of bundle-forming pili (BFP), a fimbrial adhesin that is a virulence determinant of typical EPEC (tEPEC), but is absent from atypical EPEC (aEPEC). 90-kb EPEC adherence factor plasmid (pEAF) that encodes type IV-like bundle-forming pili (BFP) [7]. The latter facilitate the adherence of bacteria to the intestinal mucosa and to each other, allowing them to form micro-colonies on epithelial cells in vitro and in vivo [8,9]. There is evidence that a subset of EPEC strains, known as atypical EPEC (aEPEC), which lack pEAF and BFP, are pathogenic [2]
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