infectious diseases
Clostridial Necrotizing Enteritis
Introduction
Clostridial necrotizing enteritis is necrosis of the jejunum and ileum caused byClostridium perfringens. Symptoms can range from mild diarrhea to septic shock and sometimes death. Diagnosis is by identifyingC. perfringenstype C toxin in stool. Treatment is with antibiotics and sometimes surgery. (See also Overview of Anaerobic Bacteria and Clostridial necrotizing enteritis is a mild to severe clostridial infection, which can be fatal if not treated promptly. C. perfringenstype C occasionally causes severe necrosis in the small bowel (primarily the jejunum). Disease is mostly caused by clostridial beta-toxin, which is very sensitive to proteolytic enzymes and is inactivated by normal cooking. Necrosis is segmental, involving small or large patches with varying degrees of hemorrhage and intramural gas; necrosis ranges from mucosal injury to full-thickness necrosis and perforation. Clostridial necrotizing enteritis occurs primarily in populations with multiple risk factors, including the following: Protein deprivation (causing inadequate synthesis of protease enzymes) Poor food hygiene Episodic meat feasting Staple diets containing trypsin inhibitors (eg, sweet potatoes) Ascariasis (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, septic shock, and sometimes death within 24 hours. Diagnosisof clostridial necrotizing enteritis is based on clinical presentation plus the presence ofC. perfringenstype C toxin in stool. Treatmentof clostridial necrotizing enteritis is with parenteral antibiotics (penicillin G,metronidazole). Perhaps 50% of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to antibiotics. Experimental toxoid vaccine and antiserum containing beta antitoxin have been used successfully in endemic areas but are not available commercially. 