Abstract

Salmonella species cause gastroenteritis and enteric fever in human beings. The former syndrome frequently includes vomiting and diarrhea. While the pathogenesis of salmonellosis is believed to involve penetration of the intestinal epithelium by the bacteria and the production of an inflammatory reaction in the lamina propria [1-3], substantial evidence has accrued that Salmonella strains may also elaborate an enterotoxin-like factor. Peterson and his associates [4-8] reported that Salmonella produce a delayed permeability factor which, like cholera enterotoxin (chloleragen or CT) and the heat-labile enterotoxins (LTs) of Escherichica coli, causes distinctive morphological alterations and increases cyclic AMP in cultured Chinese hamster ovary (CHO) cells. The activity is neutralized by cholera antitoxin and by gangliosides. Immunization with procholeragenoid, an immunogenic high M r polymer formed by heating pure choleragen [9,10], protected rabbits against fluid accumulation in intestinal loops infected with live Salmonella [6]. According to Jiwa, similar activity is widely distributed among the Salmonellae [11]. However, despite considerable effort, the enterotoxin has not previously been isolated to

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