Journal of Microbiology

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Wild birds and urban pigeons as reservoirs for diarrheagenic Escherichia coli with zoonotic potential: Clarissa A. Borges , Marita V. Cardozo , Livia G. Beraldo , Elisabete S. Oliveira , Renato P. Maluta , Kaline B. Barboza , Karin Werther , Fernando A. Ávila; J. Microbiol. 2017;55(5):344-348. Published online March 9, 2017; DOI: https://doi.org/10.1007/s12275-017-6523-3

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In order to describe the role of wild birds and pigeons in the transmission of shiga toxigenic Escherichia coli (STEC) and enteropathogenic Escherichia coli (EPEC) to humans and other animals, samples were collected from cloacae and oropharynx of free-living wild birds and free-living pigeons. Two STEC (0.8%) and five EPEC strains (2.0%) were isolated from wild birds and four EPEC strains (2.0%) were recovered from pi-geons. Serogroups, sequence types (STs) and virulence genes, such as saa, iha, lpfAO113, ehxA, espA, nleB and nleE, detected in this study had already been implicated in human and ani-mal diseases. Multidrug resistance (MDR) was found in 25.0% of the pigeon strains and in 57.0% of the wild bird strains; the wild birds also yielded one isolate carrying extended-spec-trum β-lactamases (ESBLs) gene blaCTX-M-8. The high varia-bility shown by PFGE demonstrates that there are no preva-lent E. coli clones from these avian hosts. Wild birds and pi-geons could act as carriers of multidrug-resistant STEC and EPEC and therefore may constitute a considerable hazard to human and animal health by transmission of these strains to the environment.

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Potential for colonization of O111:H25 atypical enteropathogenic E. coli: Marta O. Domingos , Keyde C.M. Melo , Irys Viana Neves , Cristiane M. Mota , Rita C. Ruiz , Bruna S. Melo , Raphael C. Lima , Denise S.P.Q. Horton , Monamaris M. Borges , Marcia R. Franzolin; J. Microbiol. 2016;54(11):745-752. Published online October 29, 2016; DOI: https://doi.org/10.1007/s12275-016-6015-x

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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.

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Amino acid residues in the Ler protein critical for derepression of the LEE5 promoter in enteropathogenic E. coli: Su-Mi Choi , Jae-Ho Jeong , Hyon E. Choy , Minsang Shin; J. Microbiol. 2016;54(8):559-564. Published online August 2, 2016; DOI: https://doi.org/10.1007/s12275-016-6027-6

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Abstract

Enteropathogenic E. coli causes attaching and effacing (A/E) intestinal lesions. The genes involved in the formation of A/E lesions are encoded within a chromosomal island comprising of five major operons, LEE1-5. The global regulator H-NS represses the expression of these operons. Ler, a H-NS homologue, counteracts the H-NS–mediated repression. Using a novel genetic approach, we identified the amino acid residues in Ler that are involved in the interaction with H-NS: I20 and L23 in the C-terminal portion of α-helix 3, and I42 in the following unstructured linker region.

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Regulation of the Locus of Enterocyte Effacement in Attaching and Effacing Pathogens
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