Experimental edema disease of swine (E. coli enterotoxemia). I. Dectection and preparation of an active principle.

Freeze-thaw lysates prepared from strains of Escherichia coli belonging to serogroups O138, O139, and O141 contained a principle (edema disease principle) which induced edema disease in swine. All freeze-thaw lysates contained endotoxic activity that tended to obscure the edema disease syndrome and methods were developed to reduce such activity. Freeze-thaw lysates prepared from E. coli O139 induced the most characteristic edema disease syndrome. Partially purified edema disease principle prepared from O139 freeze-thaw lysates by sequential precipitation with ammonium sulphate and streptomycin sulphate had increased specific activity with markedly reduced endotoxic activity. This material was insoluble at acidic pH but readily soluble at alkaline pH. The effective molecular weight of edema disease principle, based on retention and filtration properties of diaflo membranes, appeared to be greater than 50,000 and less than 100,000. The biological activity of edema disease principle was thermolabile. Sodium deoxycholate treatment of edema disease principle further reduced endotoxic activity. A thermolabile, ammonium sulphate precipitable material was prepared from E. coli O139 that induced a predictable syndrome which resembled edema disease clinically and pathologically following intravenous inoculation in pigs.

Experimental edema disease of swine (E. coli enterotoxemia). II. The development of hypertension after the intravenous administration of edema disease principle.

The intravenous inoculation of edema disease principle induced profound hypertension in pigs. The increase in blood pressure occurred approximately 40 hours after inoculation and coincided with the development of the characteristic neurological disturbance of edema disease. Therefore hypertension may play a pathogenetic role in the neuropathy of experimental edema disease.

Experimental edema disease of swine (E. coli enterotoxemia). 3. Pathology and pathogenesis.

Experimental colibacillary (Escherichia coli) enterotoxemia as described in this report mimics natural edema disease both clinically and in gross pathology. The histopathology is characterized by accumulations of non-inflammatory edema and by arteriopathy. The smaller arterial and arteriolar changes recorded here are similar to those described in natural edema disease. The vascular changes described in recovered cases of experimental colibacillary enterotoxemia concur with those reported in so-called subacute and chronic edema disease. The arteriolar changes that occur in colibacillary enterotoxemia of swine are comparable to those associated with hypertension. Thin sections of cerebral cortex from four pigs with acute experimental edema disease were examined by electron microscopy in an attempt to demonstrate brain edema. Sections from one pig taken during the convulsive phase of disease revealed dilatation of perivascular glial processes. However, examination of sections taken from three other pigs during an earlier phase of the neurological disturbance revealed no significant lesions. We were unable to ascertain the role of brain edema in the pathogenesis of the nervous system disturbance in these experiments.