A bacterial species that produces urease and causes gastritis and nearly all peptic ulcer disease of the stomach and duodenum. Infection with this organism also plays an etiologic role (probably along with dietary cofactors) in dysplasia and metaplasia of gastric mucosa, distal gastric adenocarcinoma, and non-Hodgkin lymphoma of the stomach. Syn: Campylobacter pylori.
The organism was first observed in 1982 by Robin Warren and Barry J. Marshall at Royal Perth Hospital in Western Australia in biopsy specimens from patients with chronic gastritis. Originally believed to be a species of Campylobacter, the organism was reclassified as Helicobacter pylori in 1989. A curved or spiral, flagellated gram-negative bacillus, H. pylori colonizes the gastric mucosa, attaching itself to the surface of mucus-secreting columnar cells. The ability of the organism to survive in an acid medium is due to its production of urease, which converts urea to ammonia and alkalinizes the film of mucus in which it resides. Infection with H. pylori is common worldwide, and the prevalence of infection increases with age, reaching about 50% among people 60 and older. Transmission is believed to be from person to person by the fecal-oral route. Familial clustering of infection and a higher incidence among blacks and Hispanics have been attributed to social rather than genetic factors. After infection occurs, it typically remains for life unless treated with antibiotics. Newly acquired infection results in transitory acute gastritis with extensive damage to parietal cells accompanied by impairment of acid production. Most people have no symptoms (possibly because some strains of H. pylori do not produce cytotoxins) but each year about 1% of H. pylori-infected adults develop peptic ulcer. The risk of progression to peptic ulcer disease is increased by cigarette smoking and long-term use of nonsteroidal antiinflammatory agents. About 70% of all patients with gastric ulcers and 90% of those with duodenal ulcers are found to be infected with H. pylori. In the U.S., about 500,000 new cases of peptic ulcer disease occur each year. The disease is responsible for 3–4 million physician visits and approximately 16,000 deaths annually. H. pylori infection has not been associated with nonulcer dyspepsia or inflammatory disorders of the digestive tract other than peptic ulceration. However, incidence of both gastric adenocarcinoma and gastric lymphoma is higher in those infected. In addition, the organism has been implicated in some cases of cholecystitis and autoimmune thyroiditis, and some studies have suggested that gastric infection with H. pylori may be a factor, by an unknown mechanism, in some cases of sudden infant death syndrome (SIDS). Diagnosis of H. pylori infection can be confirmed by identification of the organism in stained sections of gastric biopsy material, by culture from biopsy material, by testing biopsy material for urease activity, by identification of bacterial antigen in stool, by finding IgG antibody to the organism in the serum (the method of choice to confirm infection in a previously untreated patient), or by detection of urease activity with various biochemical tests. The urea breath test is more useful than serologic testing to confirm eradication of H. pylori after a course of treatment because IgG antibody may remain elevated for 1–5 years after eradication. Antibiotic therapy does not yield faster healing of a peptic ulcer than treatment with antisecretory agents, but it greatly reduces the likelihood of ulcer recurrence. Recommended regimens for eradication of H. pylori include combinations of bismuth subsalicylate with two antibiotics (metronidazole or clarithomycin and tetracycline or amoxicillin). Acquired resistance of H. pylori to the macrolide and imidazole antibiotics is a growing problem. It is estimated that 30% of strains of the organism in the U.S. are resistant to metronidazole and that 10% are resistant to macrolides. A major factor in the emergence of resistant strains appears to be an inadequate or failed first course of treatment. Active vaccination by oral administration of an enzymatically inactive recombinant subunit of H. pylori urease combined with a mucosal adjuvant (labile toxin of Escherichia coli) has elicited microbiologic and clinical cure of H. pylori infection in animal studies and limited human trials.
Reference: Stedman's Medical Dictionary