Abstract
Much attention has recently been focused on Helicobacter pylori (formerly Campylobacter pylori). It is strongly implicated as the causative agent in chronic gastritis, and may be involved in gastric and duodenal ulcers, although the latter has not been confirmed. Several virulence factors have been documented, although their involvement in the pathogenes is of H pylori is not proven. H pylori would appear to have one natural reservoir, ie, the gastric mucosa of humans. To avoid this harsh environment, it is postulated that H pylori possesses several characteristics which enhance survival. Strong urease enzymes produced by these organism reduce urea to ammonia and appear to create a locally elevated environment with respect to pH. The spiral shape of the cells and their flagellar motility allow them to wind themselves into the mucous layer of the stomach. Some evidence exists for the production of strong proteolytic activity, hence degrading the mucous barrier and increasing permeability for the organism. Cyroroxin excreted by the bacteria may have some effect on the surrounding cells, with the possible lysis and release of bacterial growth factors. There is evidence that a chemotactic response is present due to these growth factors and their higher concentration in the intracellular spaces. The presence of specific and nonspecific adhesion has also been demonstrated, thus allowing the bacterium, once at the epithelial cell surface, to attach and avoid being washed off by movement within the stomach. Although treatment with antimicrobials eradicates the organism and improves symptoms of peptic ulcer patients, there is no indication that the same occurs in nonulcer dyspepsia patients. Further work is essential to describe the virulence mechanisms of H pylori and the possible pathogenic role of the organism.