Clostridial necrotizing enteritis

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Clostridial necrotizing enteritis (CNE) is a severe and potentially fatal type of food poisoning caused by a β-toxin of Clostridium perfringens,^[1] Type C. It occurs in some developing regions, particularly in New Guinea, where it is known as pig-bel.^[2] The disease was also documented in Germany following World War II, where it was called Darmbrand (literally "bowel fire," or bowel necrosis). The toxin is normally inactivated by certain proteolytic enzymes and by normal cooking, but when these protections are impeded by diverse factors, and high protein is consumed, the disease can emerge.

Sporadic and extremely rare cases occur in diabetics. In New Guinea, where people generally have-low protein diets apart from tribal feasts, a number of factors—diet and endemic helminth infections among them—compound to result in pig-bel.^[3]

Signs and symptoms[]

CNE is a necrotizing inflammation of the small bowel (especially the jejunum but also the ileum). Clinical results may vary from mild diarrhea to a life-threatening sequence of severe abdominal pain, vomiting (often bloody), bloody stool, ulceration of the small intestine with leakage (perforation) into the peritoneal cavity and possible death within a single day due to peritonitis. Many patients exhibit meteorism (swelling of the abdomen due to excess gas) and fever. Fluid can enter the peritoneum.

Sepsis can occur, with one case having 28,500 white blood cells per cubic milliliter.^[4]

Cause[]

All the factors collectively causing CNE are generally only present in the hinterlands of New Guinea and parts of Africa, Latin America, and Asia. These factors include protein deprivation (causing inadequate synthesis of the enzyme trypsin protease, to which the toxin is very sensitive), poor food hygiene, episodic meat feasting, staple diets containing trypsin inhibitors (sweet potatoes), and infection by Ascaris parasites, which secrete a trypsin inhibitor. In New Guinea (origin of the term "pig-bel"), the disease is usually spread through contaminated meat (especially pork) and perhaps by peanuts. CNE was also diagnosed in post-World War II Germany, where it was known as Darmbrand or "bowel fire," and reached epidemic proportions. The causative agents of these CNE cases have since been described as Type C isolates of C. perfringens, which possessed genes for β-toxins and enterotoxins.^[5]

In developed countries, CNE can also occur in people with diabetes, including children.^[6] This form of CNE is extremely rare: to demonstrate its scope, only three such cases have been reported in the United States up to 2002.^[7]

Diagnosis[]

An abdominal x-ray shows multiple dilated loops of small bowel and gas. The abdomen can be tender, distended, and soft. A differential diagnosis can be an intussusception.

Treatment[]

Treatment involves suppressing the toxin-producing organisms with antibiotics such as penicillin G or metronidazole. About half of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to the antibiotics. An investigational toxoid vaccine has been used successfully in some developing countries but is not available outside of research.

Other clostridial toxemias[]

• Leukemia patients, cancer chemotherapy recipients and others suffering from suppressed white blood cells (neutropenia) can be afflicted by a similar syndrome, neutropenic enterocolitis, in which the cecum is targeted by Clostridium septicum in much the same way.
• In neonatal intensive-care units, the syndrome of neonatal necrotizing enterocolitis may be caused in a similar way by C. perfringens, C. butyricum, and C. difficile, but this has not been proved.

See also[]

• Protein poisoning refers to a different diet-induced phenomenon.

References[]

External links[]