Virulence-associated genes in avian pathogenic Escherichia coli (APEC) isolated from internal organs of poultry having died from colibacillosis

Escherichia coli infections are responsible for significant losses in the p oultry industry in many parts of the world. The pathogenesis and the role o f virulence factors are not yet totally elucidated. We, therefore, examined 150 E. coli strains isolated from visceral organs of poultry having died f rom colibaciliosis for the presence of virulence-associated genes by PCR. T he E. coli strains were investigated for the presence of a total of 17 viru lence-associated genes described for diarrheagenic (stx1/2, eae, hlyEHEC, e stI, eltl, astA, cdtb), septicemic (hlyA, papC, cnf1/2, fyuA, irp2) and avi an pathogenic E. coli (APEC; iucD, tsh, fimC, and hlyE as well as stx2f) Se ven genes were significantly distributed among APEC strains, while most of the other investigated genes could be demonstrated only sporadically or not at all. FimC (Type I fimbriae) was detected with the highest prevalence in 92.7% of the isolates. Most of the strains harboring iucD (88.7%) also gav e positive results for tsh (85.3%). Genes fyuA (ferric yersiniabactin uptak e) (66.0%) and irp2 (iron-repressible protein) (68.0%), necessary for Yersi nia to acquire iron in the mouse infection model, were regularly detected i n combination. Moreover, we found papC (pyelonephritis-associated pili) in 30.0% and astA (enteroaggregative heat stable toxin) in 17.3% of the field strains. A significant amount of strains (57.3%) harbored a combination of iucD, tsh, fimC, fyuA and irp2 virulence-associated genes, presumably rende ring these strains particularly virulent. These findings provide novel insights into the presence and distribution of virulence-associated genes in avian pathogenic E. coli field strains, whic h will help to more comprehensively characterize APEC in future epidemiolog ical studies. It is assumed that the existence of two iron acquisition syst ems points towards their important role in virulence. Furthermore, we sugge st that characterization of the respective phenotypes in infection models w ill provide substantial information to better understand the pathogenesis o f colibacillosis in poultry.