Until recently, chronic gastritis as well as duodenal and gastric ulcers were thought to be a result of imbalances in factors such as acid secretion and pepsin secretion brought on by high stress and dietary causes. In 1975, a bacteris was isolated from numerous peptic tumors. Yet the concept that gastritis and ulcer formation could be the result of bacterial infection was too advanced for that time, and the discovery was ignored. This all changed in 1982 with the work of Robin Warren and Barry Marshall in their laboratories in Perth, Western Australia. These to researchers were able to isolate the spiral, unease producing bacteria once again in mucosal specimens of patients suffering with gastric and duodenal ulcers. This bacteria made its home between the gastric epithelial cell surfaces and the mucus layer above them. This new bacteria was named Campylobacter pyloridis based on various similarities it shared with that species. Yet upon further rRNA analysis, key differences were noted between the new bacteria and those of he Campylobacter species, resulting in the formation of the Helicobacter family. Renamed Helicobacter pylori, this bacteria is one of eight gastric species. Also included in the Helicobacter family are three intestinal, and 2 hepatic species.
Early studies yielded evidence implicating the role of H. pylori in the formation of gastric and duodenal ulcers as well as antral gastritis. The correlation between the presence of H. pylori and these conditions was quite high. In addition, it was found that these gastroenterological condition could be cure by simply eradicating the bacteria. The studies done by Warren and Marshall have revolutionized the field of gastroenterology, as H. pylori is seen as the cause of almost 90% of all duodenal ulcers and 80% of all gastric ulcers.
Diagnosis / Symptoms of Infection