Pig-bel--a zoonosis?

Abstract

It is postulated that the combination of a very low protein diet, with low pancreatic tryptic activity, plus the continual consumption of sweet potato trypsin inhibitors leads to inadequate proteolysis when a meal containing meat contaminated with C. perfringens type C and its beta toxin is consumed. The necrotizing pathogenic process concluding as segmental gangrene is set in motion by toxin produced under altered dietary conditions first by motor paralysis via beta toxin, followed by villous attachment and colonisation by ingested or resident C. perfringens type C in the gut. Necrobiosis is maintained by further toxin production which may be blocked in immune individuals. The endemicity of the disease is governed by the amount of C. perfringens type C in both the general and gut environments, the latter determined by dietary influences and the protein nutrition of the host. A hypothesis put forward is that the organism is carried and dispersed by the domestic pig and man becomes an incidental host. Infectivity only occurs when critical ecological factors exist in the small gut of humans. Prevention in the short term is possible with a toxoided vaccine using three injections given at one month and twelve month intervals.