Abstract
The efficacy of fluoroquinolone-based eradication therapy largely depends on the fluoroquinolone resistance of H. pylori. The aim of this study was to investigate the changes in the primary resistance rate of H. pylori to fluoroquinolone and the mechanism of resistance in Korea. A total of 153 strains and 48 strains of H. pylori were isolated at a tertiary hospital in 2005/2006 and 2017/2018, respectively. The minimum inhibitory concentrations (MICs) of fluoroquinolone were determined by the serial 2-fold agar dilution method. DNA sequences in the quinolone resistance-determining regions of gyrA/gyrB were analyzed in resistant strains. Subsequent natural transformation study was performed to determine the association between gyrase mutation and resistance. The resistance rates increased from 19.0% (29/153) to 43.8% (21/48) both for levofloxacin and moxifloxacin. The MIC values for resistant strains increased from 2–8 µg/mL to 4–16 µg/mL over time. Mutation of gyrA was detected in 93.1% (27/29) and 100% (21/21) among the resistant strains in both periods, respectively. A novel Gly-85 mutation of gyrA was found and confirmed to be associated with fluoroquinolone resistance. Fluoroquinolone resistance rate of H. pylori has markedly increased over time in Korea. The resistance is mostly due to the point mutation of gyrA. Fluoroquinolone-containing regimens should be carefully selected in Korea, considering the increasing fluoroquinolone resistance.
Highlights
Helicobacter pylori (H. pylori) infection is recognized as the most important cause of chronic gastritis, peptic ulcer and gastric cancer [1]
The aim of this study was to investigate the change in the primary resistance rate to fluoroquinolones and to examine the mechanism of resistance in H. pylori isolates from Korean patients over 14 years
This study was designed to investigate the changes in the prevalence of fluoroquinolone-resistance of H. pylori and the resistance mechanism in Korea over a 14-year period
Summary
Helicobacter pylori (H. pylori) infection is recognized as the most important cause of chronic gastritis, peptic ulcer and gastric cancer [1]. Standard triple therapy comprising a proton pump inhibitor (PPI), amoxicillin, and clarithromycin has been widely used as a popular H. pylori eradication regimen over the world, and is commonly used as a first-line therapy in Korea. Primary resistance to clarithromycin, which is the most important factor in determining the efficacy of standard triple therapy, was generally acceptable in many countries in early 2000s [2,3]. The eradication rate of standard triple therapy has been constantly decreasing in many regions [4]. This situation is mainly due to increasing resistance to main antibiotic agents used for H. pylori eradication, which is partly
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