Enterolith ileus and jejunal diverticulitis from jejunal diverticulosis: the complications of a rare gastrointestinal entity

Small bowel diverticulosis is rare. False diverticula form in the jejunum, and less commonly, the ileum. As with their large bowel counterparts, these diverticula provide a pocket for stasis of bowel content, leading to the formation of enteroliths. This case report highlights two complications from jejunal diverticulosis: jejunal diverticulitis and a small bowel obstruction as a result of enterolithiasis; the latter being a rare entity which should be a differential diagnosis for any individual presenting with gastrointestinal obstructive symptoms and radiological evidence of small bowel diverticulosis.

RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION

Determinations of pH, Eh, and concentrations of acetic, butyric and lactic acids were made on the content of cecum and transverse colon of groups of mice killed 1, 3, and 5 days after oral administration of 50 mg streptomycin. Control observations on untreated mice are reported in the preceding communication. Heat-killed supenatants of suspensions of bowel content were tested in vitro for their ability to inhibit multiplication of our standard streptomycin-resistant strain of Salmonella enteritidis during aerobic and anaerobic incubation. Also tested in like fashion were series of cultures in broth buffered at various pH levels and containing acetic, butyric, and lactic acids in varying concentrations. In colon content of mice on the 1st day after streptomycin treatment, the pH had risen and the concentrations of the fatty acids fallen, a combination of effects which adequately accounts for its inability to inhibit multiplication of Salmonella in vitro and in vivo. By the 3rd day after streptomycin treatment, pH and fatty acid concentrations had returned to normal levels. The susceptibility of mice to oral challenge on the 3rd day was explained by the finding that lactic acid had accumulated in colon content to levels which, in broth, effectively counteracted the activity of inhibitory concentrations of the fatty acids. Other cocarboxylic acids also antagonized the inhibitory activity of the fatty acids; glucose did not.