1887

Abstract

An Epidemic form of enteritis necroticans, locally known as pig-bel, occurs in children in the highlands of Papua New Guinea (Murrell and Roth, 1963; Murrell , 1966). The disease is a serious public-health problem with an annual mortality of about 14 per 10,000 population (Murrell , 1966). It is now the commonest cause of death in Eastern Highland Hospitals among children over 1 year of age and it is estimated that approximately 750 children die from pig-bel each year. Evidence suggests that the condition is precipitated by the growth of strains of type C (Egerton and Walker, 1964) present in small numbers in the normal intestinal flora or ingested with contaminated meat during pig feasting, with subsequent production of β toxin leading to segmental paralysis, inflammation and necrosis of the small intestine. The normal low-protein diet, the staple sweet potato, a dietary change to meat particularly during pig feasting, and low levels of β antitoxin in those at risk are thought to be predisposing factors in the pathogenesis of this gangrenous enteritis (Lawrence and Walker, 1976). Only small amounts of pancreatic protease, particularly trypsin which is known to destroy β toxin, are produced by children on a low-protein diet; this, coupled with the presence of trypsin inhibitors in semi-cooked sweet potato, may be of particular importance (Lawrence, 1974, 1975).

Pig-bel may present in several ways. In the acute toxic form, with toxaemia and shock, abdominal symptoms may be prominent; in the acute surgical form there is obstruction of the small bowel and severe pain, and surgery is life-saving; and in the subacute surgical form there is a degree of small-bowel obstruction with subsequent malabsorption resulting from scarring and fibrosis. The most common form is mild and there is usually complete recovery.

How the toxin penetrates the jejunal mucosa is not clearly understood. According to Lawrence (1974), the clinical course of pig-bel reflects the amount of damage done by large amounts of toxin produced in a short period after the meat meal that invariably precedes the disease. This process is localised in time, the damage done to the gut by absorption of toxin early in the

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/content/journal/jmm/10.1099/00222615-13-3-445
1980-08-01
2019-10-20
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