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Clostridium perfringens Type A is one of the most common causes of food‐borne disease in the USA. Diarrheal and cramping symptoms associated with this illness are caused by a protein enterotoxin (abbreviated as CPE). Recently, diagnosis of C. perfringens food poisoning has been improved by the development of direct assays to detect CPE in feces or CPE production by food or fecal isolates of C. perfringens. The enterotoxin has a membrane‐active action which appears to involve four early steps: (1) binding of CPE to a mammalian receptor, (2) insertion of CPE into membranes, (3) formation of a complex between CPE and mammalian membrane proteins and (4) onset of toxin‐induced ion and water permeability changes. CPE has a unique amino acid sequence, and recent studies have indicated that the receptor‐binding region of enterotoxin is localized at the extreme C‐terminus. Further studies of the CPE structure versus function relationship may facilitate development of vaccines for human or veterinary usage.
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Bruce A. McClane (1991) studied this question.
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