Clostridium perfringens type C has been the cause of both sporadic and epidemic cases of necrotizing enteritis. Clinical entities such as Darmbrand ("bowel gangrene") in postwar Germany during the 1940s and pigbel97 in the Papua New Guinea highlands have been attributed to this organism, which elicits alpha and beta toxins capable of causing the enteritis. Poor nutrition and episodic dietary indulgence have been associated with these entities, with investigators suggesting that a low level of digestive enzymes in people with low protein dietary intake may prevent normal inactivation of bacterial toxins.98 Clinically, previously healthy patients present with a necrotizing enteritis syndrome that may include anorexia, nausea, vomiting, abdominal pain, and hematochezia and may progress to sepsis. Complications are common and include peritonitis secondary to bowel perforation, ileus, and chronic scarring leading to malabsorption, obstruction, or fistulas.
Multiple lines of evidence in animal and human models suggest that it is the beta toxin of C. perfringens type C that is responsible for clinical disease.98-100 Serum beta antitoxin titers were significantly increased after illness with pigbel in 12 of 21 cases in Papua New Guinea, and administration of type C antiserum resulted in a 30% decrease in the need for surgery, reducing mortality from 43% to 19%.97,101 Finally, active immunization against the beta toxin has proved to be effective in preventing pigbel.99,100
Therapy for these enteritides includes bowel decompression, supportive care, and surgical resection of involved bowel in patients who have perforation, sepsis, or a palpable mass lesion. Antiserum to C. perfringens type C containing beta antitoxin can be administered. The active beta toxin vaccine can be used prophylactically in areas where disease is likely to occur.
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