Antimicrobial resistance in Helicobacter pylori

Helicobacter pylori is associated with chronic gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Triple treatment consisting of a proton pump inhibitor and two antibiotics out of amoxycillin, clarithromycin and metronidazole is the eradication therapy of choice. The clinical relevance of H. pylori resistance is still controversial, but resistance is generally assumed to be a major obstacle to effective eradication of this microorganism – in particular resistance to clarithromycin and, to a lesser extent, metronidazole. Clarithromycin resistance is caused by point mutations in the peptidyl transferase domain of the 23S rRNA ribosomal subunit whereas metronidazole resistance generally involves mutational inactivation of the rdxA gene, which encodes a NADPH nitroreductase that reduces nitroimidazole to active metabolites. Resistance to both antibiotics may vary between countries and populations. In Europe, clarithromycin resistance has reached 12–15 % in the Mediterranean area whereas in northern countries it is less than 3 %. Metronidazole resistance is higher in developing than in developed countries, reaching 80–90 % in Africa. Tetracycline resistance is still rare and the resistance mechanism has not yet been characterised. Amoxycillin resistance in H. pylori is an emerging problem. Resistant strains are tolerant to this antibiotic and show modification in the penicillin-binding protein profile. Most resistance in H. pylori occurs by mutation and resistant strains may be selected under inappropriate antimicrobial pressure. Knowledge of the susceptibility profile of H. pylori would allow the selection of adequate antimicrobial treatment.