Formula diet is a preventive factor in experimentally induced ideal ulcers in rats. A bacteriological study.

We earlier described an experimental model to create recurring chronic ileal inflammation with ulceration in the rat. A 2 cin segment of the distal ileum is excised but left attached to its intact mesentery; the ileum is reanastomosed. The ileal segment will seal off its open ends and a cyst-like structure of varying size will be formed, containing mucus, cell debris and bacteria. Approximately two thirds of the animals develop chronic inflammation with ulceration proximal to the ileal anastomosis. The ileal cyst and the surgical procedure on the distal ileum were shown to be prerequisites of the rat model for the development of lesions. We recently described that, in contrast to rats fed a standard diet, rats fed a hydrolyzed formula diet never developed inflammation or ulceration when subjected to the experimental procedure. In the present study we confirmed these observations and showed that the normal ileal flora (NIF) and the ileal cyst flora (ICF) were significantly influenced by the diets. The bacterial counts of both the aerobic and anaerobic NIF were 2 10log lower, i.e. greater-than-or-equal-to 99%, in rats fed the formula diet as compared to in those fed standard rat pellets. The NIF of the former group was represented by more aerobic species than the NIF of rats on the standard diet. Compared to the NIF there was a parallel increase in the bacterial counts of the ICF by approximately 2 10log CFU values in both groups of rats. The mean number of anaerobic species, mainly Gram-negative rods of the ICF, increased by approximately 70% in the rats on the standard diet that developed ileal ulceration, whereas identified aerobic species of the ICF decreased by 61% in rats on the formula diet and by 46% in those on the standard diet that did not develop ileal ulceration. The number of anaerobes in those groups of rats remained unchanged. The signficant bacteriological differences between the rats that developed ileal ulcers and those which did not indicate that bacteria may be involved, directly or indirectly, in the development of chronic ileal ulceration.