Clostridial necrotizing enteritis

[Britney]

Clostridial necrotizing enteritis is necrosis of the jejunum and ileum caused by Clostridium perfringens. Symptoms can range from mild diarrhea to septic shock and sometimes death. Diagnosis is by identifying C. perfringens type C toxin in stool. Treatment is with antibiotics and sometimes surgery.
(See also Overview of Anaerobic Bacteria and Overview of Clostridial Infections.)
Clostridial necrotizing enteritis is a mild to severe clostridial infection, which can be fatal if not treated promptly.
C. perfringens type C occasionally causes severe necrosis in the small bowel (primarily the jejunum). Disease is 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)
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, septic shock, and sometimes death within 24 hours.
Diagnosis of clostridial necrotizing enteritis is based on clinical presentation plus the presence of C. perfringens type C toxin in stool.
Treatment of 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. An experimental toxoid vaccine has been used successfully in endemic areas but is not available commercially.