Are Helicobacter pylori differences important in the development of Helicobacter pylori-related diseases?

Helicobacter pylori colonises the stomach of man and induces a strong mucosal inflammation and a local and systemic immune response. Differences in virulence characteristics of Helicobacter pylori isolates can account for different clinical outcomes of infection. Most determinants of Helicobacter pylori pathogenicity factors are present in all isolates examined; some are present only in or expressed more intensively by certain strains. Many enzymes, i.e., urease, mucinase, phospholipases, alcohol dehydrogenase, neuraminidase, etc. could promote tissue erosion and ulceration by destroying the integrity of mucous, by inducing lipid peroxidation, etc. Strains which express the vacuolating toxin VacA and the associated protein CagA are called Type I and are considered endowed with increased ulcerogenic and inflammatory potential. Type I Helicobacter pylori strains carry a 40 kb genomic fragment called cag which is absent in Type II strains (VacA and CagA negative), and which contains numerous genes encoding for protein homologues to virulence factors expressed by other bacterial pathogens. CagA positive strains are more likely to be isolated from patients with duodenal ulcer and other severe digestive diseases. A simple serological test can help to detect patients at increased risk of developing severe gastroduodenal diseases, which can, therefore, possibly be prevented.