Escherichia coli strains that carry genes encoding for specific virulence attributes cause diarrhea and edema disease in swine. Enterotoxigenic E. coli (ETEC) have genes for enterotoxins that stimulate secretion of electrolytes and water by the small intestine. To colonize the small intestine and cause diarrhea, ETEC must also produce fimbriae (pili). Escherechia coli strains that cause edema disease produce E. coli Shiga toxin (Verotoxin) and are designated as STEC.Shiga toxin is absorbed from the intestine into blood and causes systemic vascular damage resulting in edema disease. STEC must also produce fimbriae to colonize the small intestine and cause disease. Some E. coli strains are designated as attaching/effacing E. coli (AEEC) because of their ability to attach intimately to the surface of intestinal epithelial cells and efface microvilli.10 The attaching/effacing attribute is encoded by a series of chromosomal genes located in a pathogenicity island called the locus of enterocyte effacement. ETEC, STEC, and AEEC are considered to be different pathotypes of E. coli. However, some of the virulence genes that characterize them can be located on mobile genetic elements (plasmids, transposons, bacteriophages), and combinations of pathotypes occur. For example, some AEEC such as the human pathogen E. coli O157:H7 also have genes for Shiga toxin production, and some strains associated with edema disease of swine have genes for both Shiga toxin and enterotoxin production.