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Helicobacter Pylori for the General Physician

the alkali ammonium hydroxide, which effectively neutralises the acid. It also possesses a proton pump which removes excess hydrogen ions from the bacterium. Finally, its flagellae allow the bacterium to be highly motile in the mucus gel layer. H. pylori attaches itself to the gastric cells via bacterial adhesins, for example, Lewis B blood group antigen which might explain why individuals who are secretors are less likely to have H. pylori clinging to their cells and this influences the course of disease. H. pylori exists in many strains, some of which appear to be more associated with disease than others. The possession of a gene cagA is highly correlated with disease, as is the ability to produce a toxin called 'vacuolating toxin' (vacA).

organism from the human stomach. This organism, Helicobacter pylori, was then demonstrated to be associated with gastritis, duodenal and gastric ulcers1. Few discoveries in recent years have so completely revolutionised our understanding of the aetiology and management of these common diseases.
The bacterium H. pylori is a curved microaerophilic Gram-negative rod with 4-6 flagellae at one end. It was initially thought to belong to the genus Campylobacter, and underwent a series of name changes before 16S  importantly, produces a urease which catalyses the breakdown of urea into ammonia and carbon dioxide. The ammonia dissolves in water to form the alkali ammonium hydroxide, which effectively neutralises the acid.
It also possesses a proton pump which removes excess hydrogen ions from the bacterium. Finally, its flagellae allow the bacterium to be highly motile in the mucus gel layer.
H. pylori attaches itself to the gastric cells via bacterial adhesins, for example, Lewis B blood group antigenwhich might explain why individuals who are secretors are less likely to have H. pylori clinging to their cells and this influences the course of disease. H. pylori exists in many strains, some of which appear to be more associated with disease than others. The possession of a gene cagA is highly correlated with disease, as is the ability to produce a toxin called 'vacuolating toxin' (vacA).
How is Helicobacter pylori spread?
The route of infection by H. pylori remains unclear, and may vary in different countries. The organism has been demonstrated in the water supply of developing countries, and is found more commonly in the lower socio-economic classes. It has also been cultured from faeces, which may suggest an oral-faecal route of infection. The opposing view of an oraloral route is probably less likely.
Helicobacter pylori and gastritis When H. pylori infects the stomach, it causes a gastritis. The initial infection is often asymptomatic but can cause nausea, vomiting and abdominal pain. The stomach is rendered temporarily achlorhydric, though it may remain so for some months before acid secretion recovers.
H. pylori has evolved mechanisms to thrive in the hostile gastric environment. It is not cleared by the host, and thus causes a chronic infection. Most     pylori. These agents were combined with antibiotics in various combinations: for example, 'classical triple therapy' was bismuth subcitrate (DeNol) 120 mg bd, metronidazole 400 mg tds and tetracycline 500 mg qds for two weeks. It was often poorly tolerated and complex to take; it is contraindicated in renal failure. Proton pump inhibitors (PPI) have a modest bactericidal effect and, by increasing the pH in the stomach, allow for maximum bioavailability of some antibiotics. Hence 'duotherapy' with omeprazole and amoxycillin for two weeks was developed, but the combination is of low efficacy and has now been abandoned.
The most consistently effective regimens in terms of eradication rates and low adverse reactions are based on triple therapy with a PPI and two antibiotics for seven days5.  Fig 3). The physician must, however, remain vigilant in looking for gastric carcinomas, and any sinister symptoms such as weight loss, dysphagia or vomiting should prompt endoscopy. He must also be alert for alternative diagnoses, particularly gastro-oesophageal reflux and biliary disease.

Asymptomatic subjects
Screening the whole population for H. pylori and treating all who are positive would be expected to prevent almost all duodenal ulcer disease and most stomach cancers. The pros and cons of treating asymptomatic subjects have been argued by Axon and Forman8. The side effects of therapy, including pseudomembranous colitis, are a weightier consideration when treating those without symptoms. The risk of producing antibiotic-resistant strains of H. pylori and other intestinal organisms is a major deterrent. There is even the possibility that some strains of H. pylori, which have coevolved with Homo sapiens, confer some benefit. Several controlled trials are in progress or planned which should demonstrate the cost benefit of this eradication strategy, but they are unlikely to continue long enough to give decisive information on cancer. A long-term alternative, which has stimulated much interest in recent years, would be the development of a safe effective vaccine against H. pylori.