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
LY411575 [5, 6]. Atypical EPEC do not carry EAF plasmids and most of these adhere in a localized adherence-like pattern to epithelial cells [5]. 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 this website chromosome of the typical EPEC strains B171-8 (O111:NM) [11] and 2348/69 (O127:H6) [12]. 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, Tideglusib 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 ISRIB assessment (MRA) concept has been developed to identify virulent EHEC strains on the basis of non-LEE effector gene typing [24] 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.