Richard A. Wilson

TL;DR: It is proposed that the new pathogen emerged when an O55:H7-like progenitor, already possessing a mechanism for adherence to intestinal cells, acquired secondary virulence factors (Shiga-like cytotoxins and plasmid-encoded adhesins) via horizontal transfer and recombination.

TL;DR: The hypothesis that isolates of E. coli O157:H7 obtained from geographically separate outbreaks and sporadic cases of hemorrhagic colitis and hemolytic uremic syndrome belong to a pathogenic clone that occurs throughout North America is strongly supported.

TL;DR: Coliform colonies from children whose stools were submitted for microbiologic analysis were studied prospectively to determine the frequency of shedding of enteropathogenic Escherichia coli (EPEC), and adherence and actin-aggregating phenotypes were determined.

TL;DR: In the United States, the hemolytic–uremic syndrome of childhood typically follows gastrointestinal infection with Escherichia coli O157:H7, and it is presumed that the absorption from the gastrointestinal tract of Shiga toxins 1, 2, or both produces microangiopathic hemolytics anemia as a result of endothelial-cell injury.