In 1983 two Australian doctors discovered a spiral bacterium in the human stomach which was called Campylobacter pylori (or pyloridis) to be re-named (Helicobacter pylori) in 1990. Carried by half the global population it was first believed exclusive to Human causing chronic gastritis, peptic and duodenal ulcer, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. This discovery revolutionized peptic ulcer treatment with antibiotics instead of surgery. H.pylori is the only bacterial agent classified as Class 1 carcinogen. In 1997 genetic advances allowed genome sequencing and detailed research particularly on genomic pathogenesis. Genome printing methods revealed that H.pylori was transmitted from domesticated animals to pre-stone-age man probably of African ancestry. New non-pylori Helicobacter species were found in farm, small, wild, and non-human primate animals. Some cause chronic gastritis and vomiting, occasionally lymphocytic gastric tissue proliferation and cancer. Some animal and avian species are contagious to human, sometimes sharing genomic similarities with H.pylori. There are currently about 35 Helicobacter species. In pathogenic strains, certain genes function as virulence factors making proteins responsible for chronic inflammatory reactions and carcinogenesis in variable degrees. This is called (genomic polymorphism), it create diverse species and strains with variable degrees of pathogenicity. Genomic heterogeneity is the result of Helicobacter adaptation in various environmental, geographic, and host circumstances. Helicobacter strains with diverse virulence may exist in different ethnic and geographic groups. Both H.pylori in human and non-pylori species in animal may co-exist mixed in one host. Sheep is believed the reservoir for H.pylori and H.canis.
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