JW helped in statistical analyses, selleck chemicals contributed to interpretation of data and preparation of the manuscript. AKK performed the statistical analysis. MMK collected rhizobial strains and helped with Rlt plasmid analyses. AS provided scientific guidance and discussion and prepared final version of manuscript. All authors have read and approve of this final manuscript.”
“Background Enteropathogenic (EPEC) and enterohaemorrhagic (EHEC) Escherichia coli represent two important classes of enteric pathogens. EPEC strains belonging to different serogroup (e.g. 026, 055, 086, 0111, O128) are a major cause of infant diarrhoea in many countries and are also associated

with diarrhoea in most domestic animal species [1, 2]. These

strains can be classified into two groups: typical-EPEC strains (t-EPEC), harbouring a specific plasmid named EPEC Adherence Factor (EAF plasmid), and atypical-EPEC strains (a-EPEC), which do not carry this specific EAF plasmid. EHEC strains have been responsible for individual cases, and small to large outbreaks in developed Geneticin datasheet countries [3–8]. O157:H7 is the main serotype responsible for human illness in several countries. Nevertheless non-O157 serogroups can also be associated frequently with severe disease in humans and O26 serogroup represent the second more important serogroup in Europe [9–11]. Syndromes caused in humans are diverse: undifferentiated diarrhoea, haemorrhagic colitis (HC), haemolytic uremic syndrome (HUS) and thrombotic thrombocytopaenic

purpura (TP) [12]. Transmission often occurs via consumption of foodstuffs contaminated by faeces Thalidomide from ruminants (mainly cattle), which can be asymptomatic healthy carriers [13, 14]. Nevertheless, several serogroups of EHEC strains (e.g. O26, O111, O118) are also associated with diarrhoea in calves [15–18]. EPEC and EHEC share four Dorsomorphin in vivo stages in their pathogenicity: (1) colonisation of the intestine by specific adhesins, (2) translocation of a signal into the enterocyte by the type III secretion system (T3SS) of the bacteria and integration of the Translocated intimin receptor (Tir) into the host cell membrane, (3) intimate adhesion of bacteria to eukaryote cells by specific adhesins (intimins) that bind to Tir, and (4) actin polymerization after Tir phosphorylation. These four stages allow the bacteria to produce a specific lesion called an “”attaching and effacing (A/E) lesion”" [1]. Furthermore, as well as using the Tir phosphorylation pathway, some strains (EPEC 2 strains and the vast majority of non-O157 EHEC strains) are able to utilize the T3SS effector TccP2 (Tir-cytoskeleton coupling protein 2) to trigger actin polymerization, which leads to the formation of a pedestal characteristic of the A/E lesion [19].