Singleand Double Mutations in
 gyrA
 but Not in
 gyrB
 AreAssociated with Low- and High-Level Fluoroquinolone Resistance in
 Helicobacterpylori

Tankovic, Jacques; Lascols, Christine; Sculo, Quentin; Petit, Jean‐Claude; Soussy, Claude-James

doi:10.1128/aac.47.12.3942-3944.2003

Cited by 124 publications

(141 citation statements)

References 12 publications

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“…Therefore, the ideal treatment for H. pylori infection is still far from being reached and more effective and better tolerated alternative regimens are needed (16). Conversely, resistance to fluoroquinolones remains a rare occurrence, varying from 3.3% in France (17), 4.7% in the Netherlands (18), 3.9% in five Eastern European countries (19), and a high resistance rate of 20.9% in Portugal (20). And the data on the primary resistance to moxifloxicin are limited.…”

Section: Introductionmentioning

confidence: 99%

Moxifloxacin-Based Triple Therapy Versus Clarithromycin-Based Triple Therapy for First-Line Treatment of Helicobacter pylori Infection: A Meta-Analysis of Randomized Controlled Trials

Wang

Yang

et al. 2009

Intern. Med.

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Background Moxifloxacin-based (RR, 1.13; 95% CI, 1.01, 1.27; P=0.04). There were no statistically significant difference in the overall side effects (RR, 0.61; 95% CI, 0.25, 1.48; P<0.28). Conclusions Moxifloxacin-based triple therapy is more effective and does not increase the incidence of overall side effects compared to clarithromycin-based triple therapy in the treatment of H. pylori infection.

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Section: Introductionmentioning

confidence: 99%

Moxifloxacin-Based Triple Therapy Versus Clarithromycin-Based Triple Therapy for First-Line Treatment of Helicobacter pylori Infection: A Meta-Analysis of Randomized Controlled Trials

Wang

Yang

et al. 2009

Intern. Med.

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“…Although there are few reports of acquired double mutations in gyrA, Tankovic et al reported two strains with double mutations in gyrA that were highly resistant to fluoroquinolones. 15 Our study showed that STFX-containing regimens might lead to the accumulation of double mutations in gyrA with a certain degree of probability. Since both N87 and D91 are binding sites for fluoroquinolones, 8 it is reasonable that the N87 and D91 double mutation would provide stronger resistance to STFX than either mutation alone.…”

Section: Discussionmentioning

confidence: 99%

“…Regarding mutations in other genes, previous reports showed that fluoroquinolone resistance was not associated with gyrB mutations in H. pylori. 5,9,15 The genes encoding topoisomerase IV (parC/parE) mutations are representative resistant mechanisms for fluoroquinolones in several bacteria; however, the absence of genes for topoisomerase IV (parC, parE) in H. pylori has been demonstrated. 17 Further studies are needed to clarify fluoroquinolone resistance mechanisms beyond gyrA.…”

Section: Discussionmentioning

confidence: 99%

Acquisition of double mutation in gyrA caused high resistance to sitafloxacin in Helicobacter pylori after unsuccessful eradication with sitafloxacin-containing regimens

Mori

Suzuki

Matsuzaki

et al. 2017

United European Gastroenterology Journal

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Background and aim: Although sitafloxacin (STFX)-containing regimens are effective rescue treatments for Helicobacter pylori infection, prevalence of fluoroquinolone resistance in H. pylori has increased rapidly worldwide. The change in resistance levels and gyrA mutations, a major cause of fluoroquinolone resistance, after unsuccessful STFX-containing treatment has not been investigated. Methods: We conducted a retrospective, non-randomized study to compare the minimum inhibitory concentrations (MICs) of STFX and the location of gyrA mutations in H. pylori before and after unsuccessful eradication with STFX-containing regimens at Keio University Hospital between December 2011 and March 2015.Results: A total of 266 patients treated with STFX-containing regimens for third-line H. pylori eradication were evaluated. Double mutations in gyrA were acquired by 20.8% of strains that exhibited seven-fold increased STFX MICs, compared to pre-treatment MICs. The STFX MICs did not increase, however, when the location of the gyrA mutations did not change after treatment. Double mutations in gyrA developed in 60.0% of the strains in which eradication failed, which exhibited a baseline mutation at position D91, and in 11.1% of strains with baseline mutations at position N87. Conclusion: Acquisition of double mutations in gyrA evoked high-level resistance to STFX in H. pylori after unsuccessful eradication with STFX-containing regimens.

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“…Combined therapy was initially very effective, although mutations in 23S RNA [23], pbp1A [24], gyrA [25], frxA or rdxA [26], conferring resistance to each of the above mentioned antibiotic have been described, and in some populations has become so common, that the Maastricht IV consensus report urges local monitoring of H. pylori resistance [22].…”

Section: H Pylori and Antibiotic Resistancementioning

confidence: 99%

Helicobacter pylori: enemy, commensal or, sometimes, friend?

Whalen¹,

Massidda²

2015

J Infect Dev Ctries

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Helicobacter pylori is a Gram-negative ε-proteobacterium that colonizes about 50% of humans. Some pertinent characteristics are that it can survive the acid of the stomach, produces urease to neutralize it and is motile due to apical flagella. Not surprisingly given its wide distribution, it has long colonized mankind and its genome encodes many features that allows this. Consequently, it frequently has a persistent lifelong association with humans and, differently from most pathogens that are transmitted horizontally, it is preferentially transmitted vertically, often from mother to child. A variety of genes and polymorphisms, both in H pylori and in humans, mediate the complex host-bacterium relationship, and can also determine if and what pathologies will be triggered by the species. H. pylori is naturally transformable, very recombinogenic and has a high mutation rate. Microbiota studies of the stomach have shown it to be an important species with a potentially regulatory role for the gastric microbial community. Likewise, epidemiological work has suggested that, while it clearly increases the risk of peptic ulcers and gastric cancer in some populations, it is also associated with lower risk of esophageal cancer and several other important pathologies. More recently, antibacterial resistant strains have been isolated, posing a problem for public health officials who called for its eradication. Hence, study of H. pylori and how it interacts with us can help revealing mutualistic or pathogenic interactions and the immune response in the digestive niche.

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Singleand Double Mutations in gyrA but Not in gyrB AreAssociated with Low- and High-Level Fluoroquinolone Resistance in Helicobacterpylori

Cited by 124 publications

References 12 publications

Moxifloxacin-Based Triple Therapy Versus Clarithromycin-Based Triple Therapy for First-Line Treatment of Helicobacter pylori Infection: A Meta-Analysis of Randomized Controlled Trials

Moxifloxacin-Based Triple Therapy Versus Clarithromycin-Based Triple Therapy for First-Line Treatment of Helicobacter pylori Infection: A Meta-Analysis of Randomized Controlled Trials

Acquisition of double mutation in gyrA caused high resistance to sitafloxacin in Helicobacter pylori after unsuccessful eradication with sitafloxacin-containing regimens

Helicobacter pylori: enemy, commensal or, sometimes, friend?

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