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Abstract Spiral bacteria were originally observed in human tissue many years ago, but early investigations to confirm these observations and to examine its significance yielding conflicting results. Therefore, these observations were ignored for many years until the investigations of Marshall and Warren (1984). They found a significant association between the occurence of gastritis, peptic ulcers and the presence of these bacteria, suggesting that these organisms might participate in causing these diseases. Thee most probable pathogenic mechanism on gastric mucosal epithelial cells is damage of the microvilli and the cytoskeletal web with disruption of intercellular junctions and bulging of cells with severe associated mucus depletion (Wyatt et al.,1987). Hypergastrinaemia is anther pathogenic mechanism through which the increased gastrin release through H. pylon infection might cause gastric hypersecretion predisposing to peptic ulcerations (Oderda et a!., 1989). The urease activity of II. pylon is another pathogenic mechanism, through which H+ back diffusion predisposes to ulcer formation (Hazel! and Lee, 1986). The urease, catalase and protease enzymes elaborated by H. pylon are important virulance factors and enable the organism to disintegrate the polymeric structure of gastric mucosa, and may be the important pathogenic mechanism of gastritis and peptic ulcer (Stewart et at. , 1988). |