Escherichia coli strains that cause diarrhoea in humans have been divided into different pathotypes according to their virulence attributes and the mechanisms involved in the disease process [1, 2]. Five major groups of intestinal pathogenic strains have been established, such as enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enteroaggregative E. coli (EAEC), enterotoxigenic E. coli (ETEC) and enteroinvasive E. coli (EIEC).
While EPEC is a major cause of infantile diarrhoea in the developing world, EHEC is associated with foodborne outbreaks in the developed world and can cause bloody diarrhoea, haemorrhagic colitis (HC) and the Haemolytic Uraemic Syndrome (HUS) due to the elaboration of Shiga toxin (Stx). More than 400 E. coli serotypes that produce Shiga toxins (STEC) have been described . A small number of these have been shown to be implicated in severe disease such as HC and HUS in humans. A classification scheme has been established to group STEC strains into the five seropathotype groups A-E depending on the severity of disease, the incidence of human infections and the frequency of their involvement in outbreaks .
Strains belonging to the EPEC group have been subdivided into typical and atypical EPEC as these differ from each other in their adherence mechanisms to human epithelial cells  and in their evolutionary lineages . Typical EPEC adhere in a localized manner mediated by bundle-forming pili that are encoded by EAF (EPEC adherence factor) type plasmids harboured by these strains [5, 6]. Atypical EPEC do not carry EAF plasmids and most of these adhere in a localized adherence-like pattern to epithelial cells . Some EPEC strains share similarities with certain EHEC strains in terms of their O:H serotypes, virulence genes and other phaenotypical traits [5, 7, 8].
The chromosomally encoded locus of enterocyte effacement (LEE) which is present in both, EPEC and EHEC strains plays a major role in their pathogenesis. The LEE carries genes for the attaching and effacing phenotype promoting bacterial adhesion and the destruction of human intestinal enterocytes [2, 7, 9, 10]. Besides LEE encoded genes, a large number of non-LEE effector genes have been found on prophages and on integrative elements in the chromosome of the typical EPEC strains B171-8 (O111:NM)  and 2348/69 (O127:H6) . In a homology-based search, all non-LEE effector families, except cif, found in the typical EPEC strains were also present in EHEC O157:H7 Sakai strain [11, 12]. On the other hand, some strain specific effectors were only present in EHEC O157:H7 (EspK, EspX) and not in the EPEC strains. Moreover, EPEC O111 and O127 strains were different from each other regarding the presence of some effector genes (EspJ, EspM, EspO, EspV, EspW, NleD, OspB and EspR) [11, 12].
It has been shown that EHEC O157:H7 has evolved stepwise from an atypical EPEC O55:H7 ancestor strain [13, 14]. Atypical EPEC and EHEC strains of serotypes O26, O103, O111 and O145 have been found to be similar in virulence plasmid encoded genes, tir-genotypes, tccP genes, LEE and non-LEE encoded genes indicating that these are evolutionarily linked to each other [8, 15–19]. The classification of these strains into the EPEC or the EHEC group is merely based on the absence or presence of genes encoding Shiga toxins (Stx) 1 and/or 2. In EHEC strains, stx-genes are typically harboured by transmissible lambdoid bacteriophages and the loss of stx-genes has been described to be frequent in the course of human infection with EHEC [20, 21]. On the other hand, it has been demonstrated that stx-encoding bacteriophages can convert non-toxigenic O157 and other E. coli strains into EHEC [22, 23].
A molecular risk assessment (MRA) concept has been developed to identify virulent EHEC strains on the basis of non-LEE effector gene typing  and a number of nle genes such as nleA, nleB, nleC, nleE, nleF, nleG2, nleG5, nleG6, nleH1-2 and ent/espL2 have been found to be significantly associated with EHEC strains causing HUS and outbreaks in humans [4, 16, 17, 24].
We recently investigated 207 EHEC, STEC, EPEC and apathogenic E. coli strains for the presence of nle genes and EHEC virulence plasmid-associated genes. By statistical analysis, two clusters of strains were obtained. OI-122 encoded genes ent/espL2, nleB and nleE were most characteristic for Cluster 1, followed by OI-71 encoded genes nleH1-2, nleA and nleF. EHEC-plasmid encoded genes katP, etpD, ehxA, espP, saa and subA showed only medium to low influence on the formation of clusters. Cluster 1 was formed by all EHEC (n = 44) and by eight of twenty-one EPEC strains investigated, whereas Cluster 2 gathered all LEE-negative STEC (n = 111), apathogenic E. coli (n = 30) and the remaining thirteen EPEC strains . These findings indicate that some EPEC strains share non-LEE encoded virulence properties with O157:H7 and other EHEC strains. Such EPEC strains could be derivatives of EHEC which have lost their stx-genes but could also serve as a reservoir for the generation of new EHEC strains by uptake of stx-phages [16, 20, 25, 26].
To classify strains of the EPEC group according to their relationship to EHEC we have investigated 308 typical and atypical EPEC strains for the presence of nle-genes of O-islands OI-57, OI-71 and OI-122, as well as prophage and EHEC-plasmid-associated genes. OI-122 encoded genes were found to be significantly associated with atypical EPEC strains that showed close similarities to EHEC regarding their serotypes and other virulence traits. In typical EPEC, the presence of O-island 122 was significantly associated with strains which are frequently the cause of outbreaks and severe disease in humans.