Experimental pigbel: the production and pathology of necrotizing enteritis due to Clostridium welchii type C in the guinea-pig.
An animal model for pigbel in man was developed using guinea-pigs. Intragastric dosing with growing cultures of Clostridium welchii Type C only produced necrotic lesions if protease inhibitors were given as well. beta toxin, which is made by the Type C organism, causes the intestinal damage and is very easily destroyed by proteases. Protease inhibitors in soybean and aprotinin were effectively in inducing disease in animals on a normal diet, while inhibitors in sweet potato, which inhibit only trypsin, were only effective in animals on a low-protein diet. In experiments using intragastric dosing, and in those where cultures and toxic filtrates were injected directly into the jejunum, the animals could be protected with an excess of pancreatic enzymes or by active or passive immunization against beta toxin. The pathology off Type C necrotizing enteritis in guinea-pigs had the macroscopic and microscopic features of pigbel in man. These experiments suggested the basic importance of a low-protein diet and dietary trypsin inhibitors in the pathogenesis of pigbel in man.
D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity; D003015:Clostridium Infections / Q000473:pathology; D003016:Clostridium perfringens; D004032:Diet / Q000009:adverse effects; D004195:Disease Models, Animal; D004761:Enterocolitis, Pseudomembranous / Q000209:etiology* / Q000473:pathology; D006168:Guinea Pigs; D006801:Humans; D007421:Intestine, Small / Q000473:pathology; D011480:Protease Inhibitors / Q000633:toxicity
D001427:Bacterial Toxins; D011480:Protease Inhibitors