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Fifty Escherichia coli strains belonging to nine classic EPEC (enteropathogenic E. coil) O:H serotypes from infantile diarrhea were examined for enzyme polymorphism and typed according to their multilocus genotypes. They were further examined for lipopolysaccharide (LPS) patterns by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by silver staining, for localized adhesion to HEp2 cells, and for their outer membrane protein (OMP) pattern. A very close relationship was detected among electrophoretic type, O:H serotype, biotype, LPS type, and OMP pattern. Most likely these characteristic EPEC groups (all type I) each represented bacterial clones, and furthermore they could begrouped into two genetically closely related clusters. In each cluster the only phenotypic character that differed among strains was the 0 antigen, which might suggest that the genetic background for the LPS side chains can be transferred horizontally among EPEC strains. The results support the idea that O:H serotyping is useful for studies of epidemiologic linkages between cases of EPEC diarrhea.

Eighty-eight Escherichia coli strains of the enteropathogenic (EPEC) group 0114 that were isolated from humans and animals in geographically different places and over more than 30 years were examined for virulence markers, O:H serotypes, and for electrophoretic types by multilocus enzyme electrophoresis. Four major genetically tightly related clusters of strains showed close correlation between electrophoretic types and other phenotypic characters. Cluster I contained 35 EPEe class II strains of serotypes 0114:H9 and 0114:H− and 5 enterotoxigenic E. coli belonging to 0114:H21 and 0114:H49. Clusters II and III comprised 36 0114:H4, 0114:H32, and 0114:H− strains; most were of doubtful pathogenicity except one Verotoxin-positive 0114:H4 strain isolated from a human with diarrhea. Cluster IV contained 9 classic EPEC strains of serogroup 0114:H2 that were characterized by localized adherence to HEp-2 cells and by the EPEC adherence factor.

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 α-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.