Of 519 E. coli strains and of 10 Pseudomonas aeruginosa strains, 68 and 6, respectively, produced toxins acting on African green monkey kidney Vero cells (VT+); all of 63 Salmonella, Shigella, Klebsiella, Enterobacter and Proteus strains were VT-. Most VT+ E. coli strains were from weaned pigs suffering from edema disease and/or diarrhea and belonged to serogroups O141:K85,88, O141:K85, O138:K81 and O139:K82; 6 VT+ E. coli strains were from diarrheic human babies, 4 of serogroup O26 and 2 of serogroup O128. The VT genes in 2 of the O26 strains and in the O128 strains were located in the genome of the phages with which they were lysogenized. One O141:K85,88 pig E. coli strain transferred its VT genes, probably by conjugation, to E. coli K12. The VT of the human E. coli strains, the pig E. coli strains and the P. aeruginosa strains were antigenically different from each other; unlike the others, the P. aeruginosa VT was heat-resistant. Cell-free preparations of cultures of E. coli K12 to which the VT genes of the 4 human E. coli strains were transferred caused fluid accumulation in ligated segments of rabbit intestine. Inoculated i.v., they were lethal for mice and rabbits; similar preparations of E. coli K12 to which the VT genes of the pig E. coli strain were transferred produced a disease in pigs that clinically and pathologically resembled edema disease.