Pathogenicity of Campylobacter pylori – A Causative Factor in Gastritis?

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Abstract
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. S) 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.