Campylobacter pylori associated acute gastritis in a child.

The results accord with the suggestion that C pylori is able to neutralise bactericidal gastric acid very rapidly by buffering H+ ions. The rapid alkalinisation ofthe microenvironment around Cpylori seems likely to be mediated by the great amount of active urease available in the outer membrane of the bacterium. Thus urease of C pylori is a highly active enzyme that may be associated with virulence by different means: first, the urease activity protects the bacterium from the gastric acid; and secondly, the generated ammonia may then cause cytopathic effects like cell damage and possibly inflammation.