There is now much worldwide evidence that Campylobacter pylori plays a pathogenic role in the aetiology of
gastritis rather than colonizing an already inflamed gastric mucosa. 1) There is a very close association between the presence of C. pylori on the gastric mucosa and histologically confirmed Type B chronic active
gastritis. Ninety percent of patients with C. pylori
infection have
gastritis whereas less than 5% of patients with normal mucosa are colonized. 2) C. pylori only colonizes gastric type mucosa; it is not found colonizing intestinal type mucosa in the stomach. 3) Two volunteer studies have confirmed Koch's third and fourth postulates. Ingestion of C. pylori led to the development of histologically proven
gastritis. 4) Outbreaks of hypochlorhydric C. pylori
gastritis have occurred. In one such epidemic 17 of 37 volunteers developed C. pylori hypochlorhydric
gastritis after
acid secretion studies were undertaken with an unsterilized pH
electrode. 5) Susceptible animal models (gnotobiotic piglets and the macacus monkey) inoculated with a
suspension of C. pylori have developed histologically proven
gastritis. 6) Clearance of C. pylori with
antimicrobial agents (
amoxicillin or
nitrofurantoin) or
bismuth salts (
colloidal bismuth subcitrate or
bismuth salicylate), alone or in combination, leads to rapid resolution of the histologically confirmed
gastritis. If relapse occurs the
gastritis returns.