Potential for colonization of O111:H25 atypical enteropathogenic E. coli

Abstract

Using clonal phylogenetic methods, it has been demonstrated that O111:H25 atypical enteropathogenic E. coli (aEPEC) strains belong to distinct clones, suggesting the possibility that their ability to interact with different hosts and abiotic surfaces can vary from one clone to another. Accordingly, the ability of O111:H25 aEPEC strains derived from human, cat and dogs to adhere to epithelial cells has been investigated, along with their ability to interact with macrophages and to form biofilms on polystyrene, a polymer used to make biomedical devices. The results demonstrated that all the strains analyzed were able to adhere to, and to form pedestals on, epithelial cells, mechanisms used by E. coli to become strongly attached to the host. The strains also show a Localized-Adherence-Like (LAL) pattern of adhesion on HEp-2 cells, a behavior associated with acute infantile diarrhea. In addition, the O111:H25 aEPEC strains derived either from human or domestic animals were able to form long filaments, a phenomenon used by some bacteria to avoid phagocytosis. O111:H25 aEPEC strains were also encountered inside vacuoles, a characteristic described for several bacterial strains as a way of protecting themselves against the environment. They were also able to induce TNF-α release via two routes, one dependent on TLR-4 and the other dependent on binding of Type I fimbriae. These O111:H25 strains were also able to form biofilms on polystyrene. In summary the results suggest that, regardless of their source (i.e. linked to human origin or otherwise), O111:H25 aEPEC strains carry the potential to cause human disease.

Differences of Escherichia coli isolated from different organs of the individual sheep: molecular typing, antibiotics resistance, and biofilm formation

“…The presence of 15 virulence genes in all isolates was detected by PCR as analyzed previously (Ewers et al, 2005;Meng et al, 2014;Lorenz et al, 2013;Domingos et al, 2016;Johnson et al, 2008). The genes encoding aerobactin (iucD), iron-repressible protein (irp2), vacuolating autotransporter toxin (vat), outer membrane protein (ompA), invasion of brain endothelium (yijP), type mbriae ( mC), invasion of brain endothelium (ibeB), meningitis-associated and temperature-regulated mbriae (mat), autotransporter gene A (aatA), shiga toxin (sxt1 and sxt2), hemolysin (sheA and hlyA), curli mbriae (csgA), and serum resistance genes (bor) were ampli ed by PCR.…”