Abstract
Escherichia coli K12 strains TB1(pCG5), with the genes for Shiga-like toxin IIv from an edema disease isolate of E. coli and TB1(pCG5-1), with the toxin genes inactivated by transposon mutagenesis, were used to test the hypothesis that Shiga-like toxin IIv was the same as edema disease principle. Ammonium sulfate precipitated culture supernatants from the pair of E. coli K12 strains and from a wild edema disease isolate of E. coli (E145) were tested for their ability to induce signs and lesions of edema disease in intravenously inoculated weaned pigs. Similar preparations from E. coli which produce Shiga-like toxins I and II were also tested. Preparations from E. coli TB1 (pCG5) and E145 contained high levels of Shiga-like toxin IIv and induced signs and lesions similar to those seen in edema disease, whereas preparations from E. coli TB1 (pCG5-1) failed to induce signs or lesions of edema disease. All Shiga-like toxin preparations produced delayed neurological signs, fibrinoid necrosis of arterioles and hemorrhages in the cerebellum of pigs. High doses of Shiga-like toxin IIv were associated with superficial necrosis of the colonic epithelium and vasculitis. Shiga-like toxins I and II resulted in kidney lesions but no enteric pathology. Shiga-like toxin II preparations had the lowest median lethal dose for pigs, Shiga-like toxin IIv was intermediate and Shiga-like toxin I was the least toxic.
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