Molecular characterization of Escherichia coli O157:H7 strains isolated from different sources and geographic regions.
10.4142/jvs.2012.13.2.139
- Author:
Adriana Hamond REGUA-MANGIA
1
;
Alice Goncalves M GONZALEZ
;
Aloysio M F CERQUEIRA
;
Joao Ramos C ANDRADE
Author Information
1. Departamento de Ciencias Biologicas, Fundacao Oswaldo Cruz, CEP 21041-210, Rio de Janeiro, Brazil. regua@ensp.fiocruz.br
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
enterohemorrhagic Escherichia coli;
molecular characterization;
O157:H7;
virulence
- MeSH:
Animals;
Argentina/epidemiology;
Brazil/epidemiology;
Cattle;
Cattle Diseases/epidemiology/*microbiology;
Enterohemorrhagic Escherichia coli/genetics/*isolation & purification/pathogenicity;
Escherichia coli O157/*genetics/*isolation & purification/pathogenicity;
Food Microbiology;
Gene Expression Regulation, Bacterial/physiology;
Genetic Markers;
Humans;
Polymerase Chain Reaction/veterinary;
Shiga Toxin 1/genetics/metabolism;
Shiga Toxin 2/genetics/metabolism;
Virulence
- From:Journal of Veterinary Science
2012;13(2):139-144
- CountryRepublic of Korea
- Language:English
-
Abstract:
Escherichia (E.) coli serotype O157:H7 is a globally distributed human enteropathogen and is comprised of microorganisms with closely related genotypes. The main reservoir for this group is bovine bowels, and infection mainly occurs after ingestion of contaminated water and food. Virulence genetic markers of 28 O157:H7 strains were investigated and multilocus enzyme electrophoresis (MLEE) was used to evaluate the clonal structure. O157:H7 strains from several countries were isolated from food, human and bovine feces. According to MLEE, O157:H7 strains clustered into two main clonal groups designated A and B. Subcluster A1 included 82% of the O157:H7 strains exhibiting identical MLEE pattern. Most enterohemorrhagic E. coli (EHEC) O157:H7 strains from Brazil and Argentina were in the same MLEE subgroup. Bovine and food strains carried virulence genes associated with EHEC pathogenicity in humans.