“…The ExPEC pathotype differs from commensals by the presence of functional genes which enable the colonization of a specific host organism. Within the pathogenicity islands present in the ExPEC reference strains (serotypes: O6: K2: H1, O6: K15: H31, O18: K1: H7, OR: K5: H, and O1: K1: H7), various iron uptake systems are coded, the most often mentioned being: ent (enterobactin), iro (salmochelin), chu (hemin uptake system), sie (iron and manganese transport), iutA (aerobactin), fyuA (yersiniabactin), adhesins: fimbriae fim (type 1), pap (P), sfa (S), foc (F1C), or toxins: hly (α-haemolysin), CNF1 (cytotoxic necrosis factor), vat (vacuolating autotransporter toxin), or sat (autotransporter), but the spectrum of virulence genes detected for these isolates is much wider and varies with the isolate [ 7 , 8 , 9 ]. In turn, the most common APEC virulence genes determine the production of colicins ( cva ), aerobactin ( iut ), hemagglutinin ( tsh ), envelope antigens ( kps ), the irp2 gene associated with iron transport genes, the pap operon encoding P-type fimbria, and the Iss protein associated with bactericidal resistance to the serum, encoded by the iss gene located within the plasmid pColV-I-K94 [ 10 , 11 , 12 ].…”