scholarly journals Helicobacter pyloriResistance to Antibiotics: Prevalence, Mechanism, Detection. What’s New?

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 49B-52B ◽  
Author(s):  
Francis Mégraud

Helicobacter pyloriresistance to antibiotics is increasingly reported and may limit the efficacy of current treatment regimens. Their resistance mechanism has been found to be point mutations for all antibiotics. Macrolide resistance is the most clinically important, but can be detected efficiently by molecular methods. Metronidazole resistance has limited clinical impact but testing methods are not reliable. Seldomly found cases of resistance, such as to amoxicillin and tetracycline, have had their mechanism recently elucidated. The existance of rapid and practical methods for the detection of macrolide resistance (eg, Fluorescence Resonance Energy Transfer assay) should improve management ofH pylori-positive patients in the future, by allowing an adapted first-line therapy.

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Chao-Hung Kuo ◽  
Fu-Chen Kuo ◽  
Huang-Ming Hu ◽  
Chung-Jung Liu ◽  
Sophie S. W. Wang ◽  
...  

This paper reviews the literature about first-line therapies forH. pyloriinfection in recent years. First-line therapies are facing a challenge because of increasing treatment failure due to elevated antibiotics resistance. Several new treatment strategies that recently emerged to overcome antibiotic resistance have been surveyed. Alternative first-line therapies include bismuth-containing quadruple therapy, sequential therapy, concomitant therapy, and hybrid therapy. Levofloxacin-based therapy shows impressive efficacy but might be employed as rescue treatment due to rapidly raising resistance. Rifabutin-based therapy is also regarded as a rescue therapy. Several factors including antibiotics resistance, patient compliance, and CYP 2C19 genotypes could influence the outcome. Clinicians should use antibiotics according to local reports. It is recommended that triple therapy should not be used in areas with high clarithromycin resistance or dual clarithromycin and metronidazole resistance.


1997 ◽  
Vol 41 (12) ◽  
pp. 2724-2728 ◽  
Author(s):  
A Occhialini ◽  
M Urdaci ◽  
F Doucet-Populaire ◽  
C M Bébéar ◽  
H Lamouliatte ◽  
...  

Resistance of Helicobacter pylori to macrolides is a major cause of failure of eradication therapies. Single base substitutions in the H. pylori 23S rRNA genes have been associated with macrolide resistance in the United States. Our goal was to extend this work to European strains, to determine the consequence of this mutation on erythromycin binding to H. pylori ribosomes, and to find a quick method to detect the mutation. Seven pairs of H. pylori strains were used, the parent strain being naturally susceptible to macrolides and the second strain having acquired an in vivo resistance during a treatment regimen that included clarithromycin. The identity of the strains was confirmed by random amplified polymorphic DNA testing with two different primers, indicating that resistance was the result of the selection of variants of the infecting strain. All resistant strains were found to have point mutations at position 2143 (three cases) or 2144 (four cases) but never on the opposite DNA fragment of domain V of the 23S rRNA gene. The mutation was A-->G in all cases except one (A-->C) at position 2143. Using BsaI and BbsI restriction enzymes on the amplified products, we confirmed the mutations of A-->G at positions 2144 and 2143, respectively. Macrolide binding was tested on purified ribosomes isolated from four pairs of strains with [14C]erythromycin. Erythromycin binding increased in a dose-dependent manner for the susceptible strain but not for the resistant one. In conclusion we suggest that the limited disruption of the peptidyltransferase loop conformation, caused by a point mutation, reduces drug binding and consequently confers resistance to macrolides. Finally, the macrolide resistance could be detected without sequencing by performing restriction fragment length polymorphism with appropriate restriction enzymes.


2003 ◽  
Vol 17 (suppl b) ◽  
pp. 33B-35B ◽  
Author(s):  
Loren Laine

The most commonly used regimen forHelicobacter pyloritherapy at present is twice-daily proton pump inhibitor (PPI)-based triple therapy. Bismuth-based therapy is the next most common treatment used by gastroenterologists. When a PPI is combined with bismuth-based triple therapy (quadruple therapy), eradication rates are increased as compared with the triple therapy alone. Three separate randomized trials from three continents that compare quadruple therapy and PPIbased triple therapy revealed remarkably similar results. Eradication rates with PPI-based triple therapy and quadruple therapy were not significantly different. The eradication rates with quadruple therapy were 3% to 6% higher than PPI triple therapy, indicating that quadruple therapy should be no less effective than PPI triple therapy. Furthermore, these two therapies had similar rates of compliance and adverse events.The major potential benefit of the quadruple therapy relates to antibiotic resistance. In patients with clarithromycin resistance, PPIbased triple therapy, but not quadruple therapy, had a significantly lower eradication rate. However, due to its ability to largely overcome metronidazole resistance, quadruple therapy had little if any decrement in eradication rates compared with PPI triple therapy in patients with metronidazole-resistantH pylori. Therefore, quadruple therapy can be considered a first line therapy forH pylori.


2000 ◽  
Vol 14 (10) ◽  
pp. 879-882 ◽  
Author(s):  
Carlo A Fallone

BACKGROUND: The rate ofHelicobacter pyloriresistance to antibiotics determines the cure rate of treatment regimens containing such antibiotics. AIMS: To review the literature to determine the rates ofH pyloriresistance to metronidazole and clarithromycin in Canada, and whether these rates vary in different regions of Canada.METHODS: The literature was reviewed extensively for the prevalence of antibiotic-resistantH pyloriin Canada by searching MEDLINE from January 1980 to May 1999, as well as abstracts of the American Gastroenterology Association Digestive Disease Week, Canadian Digestive Disease Week and The EuropeanH pyloriStudy Group Meetings from January 1995 to May 1999.RESULTS: Eleven studies that estimatedH pyloriresistance to metronidazole resistance and nine that estimated resistance to clarithromycin in Canada were identified. Rates of resistance for metronidazole and clarithromycin varied from 11% to 48% and 0% to 12%, respectively. Studies that obtained their estimates using the E-test and those that did not clearly exclude patients who had undergone previous attempts atH pylorieradication had higher estimates of resistance, accounting for this variability in results.CONCLUSIONS: The prevalence of primaryH pyloriresistance in Canada appears to be 18% to 22% for metronidazole and less than 4% for clarithromycin. These rates appear to be consistent across the different regions studied in Canada, but many regions have not been studied.


1999 ◽  
Vol 43 (7) ◽  
pp. 1779-1782 ◽  
Author(s):  
Leen-Jan van Doorn ◽  
Yvette J. Debets-Ossenkopp ◽  
Armelle Marais ◽  
Ricardo Sanna ◽  
Francis Mégraud ◽  
...  

ABSTRACT A PCR-based reverse hybridization system (research prototype kit INNO-LiPA for H. pylori resistance) was developed and evaluated for simultaneous detection of 23S ribosomal DNA point mutations, associated with macrolide resistance in Helicobacter pylori. Fifty-seven H. pylori strains (51 natural, 6 laboratory-derived artificial, 52 resistant, and 5 susceptible strains) were tested by PCR-LiPA (detecting mutations A2115→G, G2141→A, A2142→G, A2142→C, A2143→G, A2143→C, and A2143→T), DNA sequencing, restriction fragment length polymorphism, and/or hybridization to oligonucleotide probes. Results were highly concordant, but PCR-LiPA appears to be more sensitive for the simultaneous detection of multiple mutants.


2015 ◽  
Vol 10 (01) ◽  
pp. 28
Author(s):  
Maja Relja ◽  
Jorge Jacinto ◽  
Joseph Jankovic ◽  
Alberto Albanese ◽  
◽  
...  

Botulinum toxin A (BoNT-A) has become the first-line therapy in cervical dystonia (CD), blepharospasm and spasticity. However, the current guidelines for the clinical use of BoNT-A are based on data published more than 20 years ago and patient satisfaction with current treatment regimens is low. There is a striking difference between the injection intervals given in everyday clinical practice and the injection intervals preferred by patients. Recent data have indicated that shorter injection intervals may improve overall patient satisfaction since re-emergence of symptoms could be prevented. Three double-blind studies have demonstrated that incobotulinumtoxin A (incoBoNT-A) is suitable for use in a flexible, patient-centric approach in blepharospasm and CD, with injection intervals starting from 6 weeks. The efficacy, tolerability and safety of this regime were excellent. There is a need to optimise and individualise the treatment using the three available formulations of BoNT- A, as well as to define parameters for switching between the formulations.


1999 ◽  
Vol 43 (11) ◽  
pp. 2657-2662 ◽  
Author(s):  
Yvette J. Debets-Ossenkopp ◽  
Raymond G. J. Pot ◽  
David J. van Westerloo ◽  
Avery Goodwin ◽  
Christina M. J. E. Vandenbroucke-Grauls ◽  
...  

ABSTRACT We found that NCTC11637, the type strain of Helicobacter pylori, the causative agent of peptic ulcer disease and an early risk factor for gastric cancer, is metronidazole resistant. DNA transformation, PCR-based restriction analysis, and DNA sequencing collectively showed that the metronidazole resistance of this strain was due to mutation in rdxA (gene HP0954 in the full genome sequence of H. pylori 26695) and that resistance did not depend on mutation in any of the other genes that had previously been suggested: catalase (katA), ferredoxin (fdx), flavodoxin (fldA), pyruvate:flavodoxin oxidoreductase (porγδαβ), RecA (recA), or superoxide dismutase (sodB). This is in accord with another recent study that attributed metronidazole resistance to point mutations inrdxA. However, the mechanism of rdxAinactivation that we found in NCTC11637 is itself also novel: insertion of mini-IS605, one of the endogenous transposable elements of H. pylori, and deletion of adjacent DNA sequences including 462 bp of the 851-bp-long rdxA gene.


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