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Clostridial Necrotizing Enteritis
(Enteritis Necroticans; Pigbel)
Clostridial necrotizing enteritis is necrotizing inflammation of the jejunum and ileum caused by Clostridium perfringens.
C. perfringens occasionally causes severe inflammatory disease in the small bowel (primarily, the jejunum). Inflammation is segmental, involving small or large patches with varying degrees of hemorrhage and necrosis. Perforation may occur.
Disease is caused by clostridial β-toxin, which is very sensitive to proteolytic enzymes and is inactivated by normal cooking. Disease occurs primarily in populations with multiple risk factors, including protein deprivation (causing inadequate synthesis of protease enzymes), poor food hygiene, episodic meat feasting, staple diets containing trypsin inhibitors (eg, sweet potatoes), and Ascaris infestation (these parasites secrete a trypsin inhibitor). These factors are typically present collectively only in the hinterlands of New Guinea and parts of Africa, Central and South America, and Asia. In New Guinea, the disease is known as pigbel and is usually spread through contaminated pork, other meats, and perhaps peanuts.
Severity varies from mild diarrhea to a fulminant course of severe abdominal pain, vomiting, bloody stool, and sometimes death within 24 h.
Treatment is with antibiotics (penicillin G, metronidazole). Perhaps 50% of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to antibiotics. An experimental toxoid vaccine has been used successfully in endemic areas but is not available commercially.
This similar life-threatening syndrome develops in the cecum of neutropenic patients (eg, those with leukemia or receiving cancer chemotherapy). It may be associated with sepsis due to C. septicum. Symptoms are fever, abdominal pain, GI bleeding, and diarrhea.
Treatment is with antibiotics, but surgery may be necessary.
Neonatal necrotizing enterocolitis (see Necrotizing Enterocolitis), which occurs in neonatal ICUs, may be caused by C. perfringens, C. butyricum, or C. difficile, although the role of these organisms needs further study.
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