Antibiotic resistance of Helicobacter pylori

Peptic ulcer disease due to infection with Helicobacter pylori is an extremely common chronic and disabling disease, which in the past was attributed to factors such as stress, genetics and personality. Reports of an association with flagellated bacilli had already appeared in the late 19th century, but this association was considered to be due to bacterial overgrowth in the presence of delayed gastric emptying and the significance of this observation was not realized. For decades, patients with ulcer disease were treated with rest, various diets, and finally, often with surgery. The recognition that chronic ulcer disease can result from infection with H. pylori turned it into a curable and preventable infectious disorder. Only a few antibiotics can be used successfully for eradication of H. pylori; these are metronidazole, tetracycline, amoxycillin, clarithromycin and azithromycin. Other drugs with some in vitro antimicrobial effect are bismuth salts and proton pump inhibitors. Successful eradication of H. pylori infection requires a combination of two or three antibiotics and an antacid drug. The increased prevalence of antibiotic-resistant H. pylori strains has serious implications as, apart from patient compliance, antimicrobial resistance is the most important factor determining the outcome of antibiotic treatment. Resistance against clarithromycin and metronidazole is of particular clinical importance as these two drugs are used in almost all standard H. pylori eradication regimens. Our current understanding of the mechanisms of antibiotic resistance for these two drugs now allows for rapid testing of resistance and provides clues on how to reduce the spread of resistance. Spontaneous resistance to rifampicin, tetracycline, amoxycillin, streptomycin, trovafloxacin and ciprofloxacin has also been reported. The underlying mechanisms for resistance against these drugs have been characterized in some detail and will be discussed.