N. F. Tanih1, L. M. Ndip2, A. M. Clarke1, R. N. Ndip1,2*
Helicobacter pylori induces chronic gastritis, the strongest known risk factor for peptic ulcer disease, distal gastric cancer and a number of extra gastric related morbidity. More than 50% of the world’s population is infected with this organism lifelong without effective bacterial eradication. Clinical sequelae are dependent upon bacterial virulence factors and host genetic diversity, particularly within immune response genes. The organism is able to evade the harsh acidic environment in the gastric mucosa and host immune response by elaborating a number of factors that aid in the achievement of its persistent colonization. H. pylori possess numerous virulence proteins (cagA, vacA and iceA) and enzymes (urease, catalase, lipase, phospholipase and proteases) with substantial genotypic diversity, which engenders differential host inflammatory responses that influence the pathologic outcome. The hallmark of H. pylori infection is a marked inflammatory response with the infiltration of various immune cells into the infected gastric mucosa; with a polarized Th1 immune response which further attracts inflammatory cells to the gastric mucosa leading to damage. Knowledge on H. pylori reservoirs and transmission remains elusive. However, studies have described the gastro-oral, oral-oral and faecal-oral as possible routes of acquisition and transmission. This paper provides an understanding of H. pylori persistence and pathogenesis as well as its route of transmission.
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