To aid research investigations on the putative role of H. pylori infection in the etiopathogenesis of gastric ulcer and/or gastric adenocarcinoma/lymphoma, Advanced Biotechnologies Inc (ABI) offers H. pylori (Strain J 99: vacA +/ s1m1 and cagA+) quantitated PCR control DNA. In 1983, J. R. Warren and B. J. Marshall of Australia isolated and characterized Helicobacter pylori (formerly Campylobacter pylori) and suggested its association with gastritis/gastric ulcer. Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped (helical) rod, microaerophilic- and urease-producing bacteria that colonizes in the gastric epithelial surface. This infection is chiefly acquired in childhood, probably from parents or siblings (person-to-person transmission), and is prevalent throughout the world. In developing countries, >80% of adults and >50% of children are infected with H. pylori as compared to ~30% of adults and ~10% of children in developed countries.

$ba H. pylori colonization usually persists throughout life

  • 10% of infected persons suffer from symptoms like vomiting, epigastric or recurrent abdominal pain, and overt disease like chronic gastritis, duodenal or gastric ulcer

  • the bacteria is linked to mucosa-associated lymphoid tissue lymphoma and considered a risk factor for the development of distal gastric adenocarcinoma, and

  • is classified as a human carcinogen by the International Agency for Research on Cancer (1994).

    Gastric carcinoma is the second most common cause of cancer in developing countries; those infected with H. pylori have a higher risk of developing gastric cancer (3-8 times greater) and gastric lymphoma (6 times greater) (WHO). A recent study indicated that during chronic inflammation caused by H. pylori infection, gastric epithelial cells display sialyl Lewis x (sLex), a carbohydrate that is a marker for gastric dysplasia. Normal gastric epithelial cells do not display sLex. H. pylori strains exhibit a very high level of intraspecies genetic diversity. Strains possessing the cagA gene (cytotoxin-associated gene product A), secrete vacuolating cytotoxin that increases the production of the proinflammatory cytokine interleukin 1-beta, leading to tissue inflammation. H. pylori strains that carry the s1m1 mosaic combination of the vacA gene (vacA+/s1m1) usually also carry a 40 kb pathogenicity island with a cagA marker gene and are associated with disease more significantly than those that do not. The Cag pathogenicity island also encodes factors that activate a proinflammatory signal transduction pathway in epithelial cells, which probably contribute to enhanced inflammatory responses in the gastric mucosa.

    VacA+/s1m2 strains of H. pylori secrete a lower level of vacuolating cytotoxin than vacA+/s1m1 strains, while vacA+/s2m2 strains do not secrete the cytotoxin.

    The following assays can be performed for the diagnosis of H. pylori infection with varying degrees of sensitivity and specificity:

  • microbiologic culture

  • direct antigen detection in stool samples

  • histologic examination of gastric biopsy tissues

  • serology (ELISA, immunoblot assay)

  • rapid urease test or 14 C-urea breath test

  • fluorescent in situ hybridization test on gastric biopsy tissue specimens (snap frozen or paraffin embedded) using rRNA targeted fluorescence-labeled oligonucleotide probes, and

  • nucleic acid amplification tests.

    PCR assays have been developed for the detection and strain differentiation of H. pylori based on the gene sequences encoding urease structural genes, vacA and cagA genes, and 16s rRNA sequences. The detection of H. pylori by PCR assay in fresh gastric biopsy tissues obtained by endoscopy and gastric aspirates has a sensitivity of 93% and 85% respectively, with a specificity of 100% when compared to microbiologic culture and histologic examination of the corresponding biopsy tissues.

    Both prophylactic and curative treatment of H. pylori infection include the combination of broad spectrum antibiotics (e.g., amoxicillin, tetracycline, metronidazole, and clarithromycin) and proton pump inhibitors or bismuth salts. More than 90% of H. pylori infection can be eradicated with this treatment regimen.

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