Vibrio cholerae enterotoxin and its mode of action.

The probability that clinical cholera results from the interaction of a toxin produced by Vibrio cholerae with the intestine was proposed by Koch (59) and by other early investigators of the disease. Many subsequent studies support this conclusion. The nature of this toxin and its mode of action, however, remained obscure until recent years when the development of animal models closely resembling human cholera and purification of the diarrheagenic product of V. cholerae have permitted major advances in our understanding of the toxin and its mechanism of action. V. cholerae produces a number of enzymes and other products which have at times been implicated as participating in the diarrheaproducing process (9). These have been described in recent reviews (10, 11) and will not be considered here. This review will deal only with the diarrhea-producing moieties recently isolated in various degrees of purity by several investigators. These have been referred to as choleragen (34), skin permeability factor (73), vascular permeability factor (18), type-2 cholera toxin (16), cholera enterotoxin, and cholera exotoxin. Although different techniques have been employed to prepare and isolate these agents, the weight of present evidence strongly suggests that they contain the same diarrheagenic enterotoxin and that this enterotoxin is responsible for the production of the clinical cholera syndrome. In this review we have elected to employ the term cholera enterotoxin to describe this agent because its most important clinical effect is on the gut.