title: Genotypic and phenotypic changes in the emergence of Escherichia coli O157:H7.
abstract: Escherichia coli O157:H7 is a foodborne pathogen distinguished from typical E. coli by the production of Shiga toxins (Stx) and the inability to ferment sorbitol (SOR) and to express beta-glucuronidase (GUD) activity. An allele-specific probe for the GUD gene (uidA) and multilocus enzyme electrophoresis were used to elucidate stages in the evolutionary emergence of E. coli O157: H7. A point mutation at +92 in uidA was found only in O157:H7 and its nonmotile relatives, including a SOR+ O157:H clone implicated in outbreaks of hemolytic-uremic syndrome in Germany. The results support a model in which O157:H7 evolved sequentially from an O55:H7 ancestor, first by acquiring the Stx2 gene and then by diverging into two branches; one became GUD- SOR- , resulting in the O157:H7 clone that spread worldwide, and the other lost motility, leading to the O157:H clone that is an increasing public health problem in Europe.
authors.affiliation: Center for Food Safety and Applied Nutrition, US Food and Drug Administration, Washington, DC, USA.
authors.forename: P
authors.initials: P
authors.lastname: Feng
authors.forename: K A
authors.initials: KA
authors.lastname: Lampel
authors.forename: H
authors.initials: H
authors.lastname: Karch
authors.forename: T S
authors.initials: TS
authors.lastname: Whittam
mesh_terms: D004927:Escherichia coli Infections / Q000382:microbiology*; D019453:Escherichia coli O157 / Q000145:classification / Q000201:enzymology / Q000235:genetics; D005838:Genotype; D005966:Glucuronidase / Q000235:genetics; D006801:Humans; D010641:Phenotype
chemical_list: D005966:Glucuronidase