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.