Pathogenicity and Antimicrobial Resistance of Helicobacter Pylori Review: Article

Abstract

Helicobacter pylori is a leading cause of peptic ulcer disease and gastric cancer comprising a major global health concern ana public health threat because of its persistent colonization, multiple pathogenic mechanisms, and the rapid rise in antimicrobial resistance. The bacterium is supplied with several virulence factors, such as urease, adhesins, CagA and VacA that allow it to survive in the acidic gastric environment and attach to gastric epithelial cells, modulate host immune responses and induce chronic gastric inflammation. In susceptible hosts, persistent infection can play a role in the development of gastritis, peptic ulcer disease, gastric mucosal atrophy and gastric adenocarcinoma. Furthermore, increasing resistance rates to widely used antimicrobial agents, including clarithromycin, metronidazole and fluoroquinolones are compromising the efficacy of standard eradication regimens resulting in treatment failure. Chromosomal mutations (e.g. of antibiotic targets or drug activation) ultimately lead to H. pylori antimicrobial resistance, but this has been engrained by prior exposure to a number of antimicrobials and/or suboptimal antibiotic regimens leading to selection for more resistant strains. Recent advancements in molecular diagnostics, antimicrobial susceptibility testing, resistance monitoring, and alternative eradication strategies has offered additional perspectives on this transforming therapeutic landscape of H. pylori treatment. This review summarizes the pathogenicity and major virulence mechanisms of H. pylori, highlights the molecular and epidemiological features of antimicrobial resistance, and outlines current challenges to effective eradication and control of H. pylori-associated diseases along with novel concepts for appropriate solutions.