H. pylori causes chronic gastritis, peptic ulcers, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. Eradication success rates have fallen in recent years, largely due to antimicrobial resistance. International consensus guidelines recommend that regional treatment strategies are determined by the prevalence of H. pylori antibiotic resistance in a given population. As culture-based antimicrobial susceptibility testing (AST) for H. pylori is time-consuming and challenging, it is not routinely performed in the majority of hospitals. Molecular methods offer a more rapid alternative and do not require the culture of H. pylori from stomach tissue samples. However, the current commerically available molecular diagnostics approved for clinical use are limited to detecting only the most common H. pylori resistance-associated DNA mutations. Emerging evidence supports a role for additional DNA mutations and alternative resistance mechanisms in H. pylori antimcrobial resistance. Using state-of-the-art methodology and a multidisciplinary approach involving microbiologists, molecular biologists and consultant gastroenterologists, the overall aim of this research is to define the involvement of (i) additional resistance-mediating mutations, (ii) efflux pumps and (iii) biofilm formation in H. pylori antimicrobial resistance, with a view to identifying new targets for more accurate diagnostic tools for resistance detection, resistance surveillance and tailoring therapy. In the long-term, this approach will encourage more prudent antimicrobial usage and improve patient outcomes by enhancing H. pylori eradication rates.
