Heteroresistance of Helicobacter pylori from the same patient prior to antibiotic treatment

Kao, Cheng Yen; Lee, Ai Yun; Huang, Angus; Song, P; Yang, Yao; Sheu, Shew Meei; Chang, Wei; Wu, Jiunn Jong

doi:10.1016/j.meegid.2014.02.009

Cited by 43 publications

(37 citation statements)

References 41 publications

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“…Such findings reinforce the need for studies to investigate the regional variations in the mutation pattern of the gyrA gene. In samples with gyrA heterogeneity (mixture of wild-type and/or mutant bands), a high resistance rate (43.2%) was found, and it is likely that this polymorphism may represent different stages in the development of mutations[35]. …”

Section: Discussionmentioning

confidence: 99%

Detection ofHelicobacter pyloriresistance to clarithromycin and fluoroquinolones in Brazil: A national survey

Sanches¹,

Martins²,

Lima³

et al. 2016

WJG

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AIMTo evaluate bacterial resistance to clarithromycin and fluoroquinolones in Brazil using molecular methods.METHODSThe primary antibiotic resistance rates of Helicobacter pylori (H. pylori) were determined from November 2012 to March 2015 in the Southern, South-Eastern, Northern, North-Eastern, and Central-Western regions of Brazil. Four hundred ninety H. pylori patients [66% female, mean age 43 years (range: 18-79)] who had never been previously treated for this infection were enrolled. All patients underwent gastroscopy with antrum and corpus biopsies and molecular testing using GenoType HelicoDR (Hain Life Science, Germany). This test was performed to detect the presence of H. pylori and to identify point mutations in the genes responsible for clarithromycin and fluoroquinolone resistance. The molecular procedure was divided into three steps: DNA extraction from the biopsies, multiplex amplification, and reverse hybridization.RESULTSClarithromycin resistance was found in 83 (16.9%) patients, and fluoroquinolone resistance was found in 66 (13.5%) patients. There was no statistical difference in resistance to either clarithromycin or fluoroquinolones (P = 0.55 and P = 0.06, respectively) among the different regions of Brazil. Dual resistance to clarithromycin and fluoroquinolones was found in 4.3% (21/490) of patients. The A2147G mutation was present in 90.4% (75/83), A2146G in 16.9% (14/83) and A2146C in 3.6% (3/83) of clarithromycin-resistant patients. In 10.8% (9/83) of clarithromycin-resistant samples, more than 01 mutation in the 23S rRNA gene was noticed. In fluoroquinolone-resistant samples, 37.9% (25/66) showed mutations not specified by the GenoType HelicoDR test. D91N mutation was observed in 34.8% (23/66), D91G in 18.1% (12/66), N87K in 16.6% (11/66) and D91Y in 13.6% (9/66) of cases. Among fluoroquinolone-resistant samples, 37.9% (25/66) showed mutations not specified by the GenoType HelicoDR test.CONCLUSIONThe H. pylori clarithromycin resistance rate in Brazil is at the borderline (15%-20%) for applying the standard triple therapy. The fluoroquinolone resistance rate (13.5%) is equally concerning.

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Section: Discussionmentioning

confidence: 99%

Detection ofHelicobacter pyloriresistance to clarithromycin and fluoroquinolones in Brazil: A national survey

Sanches¹,

Martins²,

Lima³

et al. 2016

WJG

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“…Amoxicillin-resistant and -susceptible Helicobacter pylori isolates (MICs of 2 g/ml and 0.06 g/ml, respectively) were observed in different biopsy specimens from one patient, displaying what was described as "interniche" heteroresistance (20). More recently, pairs of H. pylori isolates obtained from the same patients had different levels of resistance to levofloxacin, metronidazole, and (in only one case) clarithromycin; the antibiotic-resistant strains were mostly derived from a preexisting sensitive strain rather than from infection with different strains of H. pylori having different levels of antibiotic resistance (21). Similarly, heteroresistance in Mycobacterium tuberculosis was defined as coexistence of antituberculosis drug-susceptible and -resistant bacteria in the same patient (22,23).…”

Section: Multiple Definitions Of Heteroresistancementioning

confidence: 97%

“…Long-term infection may result in instability of bacterial genomic DNA, potentially leading to heteroresistance. For example, mutations in gene products having metronidazole nitroreductase activities, mainly oxygen-insensitive NADPH nitroreductase (RdxA) and NADPH flavin oxidoreductase (FrxA), occurred in H. pylori strains that were heteroresistant to metronidazole (21). Epigenetic variation across the bacterial population can also occur.…”

Section: Mechanisms Of Heteroresistancementioning

confidence: 99%

“…susceptibility to ciprofloxacin was linked to a natural mutation, Ser-83 to Ala (E. coli numbering), in the quinolone resistance-determining region of gyrA (96). Similarly, gyrA and gyrB mutations were associated with levofloxacin heteroresistance in H. pylori; three amino acid mutation sites (positions 87, 91, and 143) were found in GyrA of levofloxacin-resistant strains, and an A406G amino acid substitution in GyrB was found only once (21). Putrescine and, to a lesser extent, YceI contributed to heteroresistance of B. cenocepacia to norfloxacin, as mutants unable to produce either of them showed a more homogeneous response to norfloxacin (6).…”

Section: Heteroresistance To Fluoroquinolonesmentioning

confidence: 99%

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Antimicrobial Heteroresistance: an Emerging Field in Need of Clarity

2015

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SUMMARY “Heteroresistance” describes a phenomenon where subpopulations of seemingly isogenic bacteria exhibit a range of susceptibilities to a particular antibiotic. Unfortunately, a lack of standard methods to determine heteroresistance has led to inappropriate use of this term. Heteroresistance has been recognized since at least 1947 and occurs in Gram-positive and Gram-negative bacteria. Its clinical relevance may be considerable, since more resistant subpopulations may be selected during antimicrobial therapy. However, the use of nonstandard methods to define heteroresistance, which are costly and involve considerable labor and resources, precludes evaluating the clinical magnitude and severity of this phenomenon. We review the available literature on antibiotic heteroresistance and propose recommendations for definitions and determination criteria for heteroresistant bacteria. This will help in assessing the global clinical impact of heteroresistance and developing uniform guidelines for improved therapeutic outcomes.

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“…For example, treatment failure may be due to poor patient compliance, inadequate dosing, pharmacodynamic/pharmacokinetic factors and drug-drug interactions. On the other hand, the rationale for repeating culture stems from concern for newly acquired resistance or concern for ‘heteroresistance' where H. pylori strains with different antibiotic susceptibility profiles may co-exist in a single patient [9,10,11]. Antibiotic susceptibility data following the failure of culture-guided treatment for H. pylori have not previously been described.…”

Section: Introductionmentioning

confidence: 99%

Appropriateness of Repeating <b><i>Helicobacter pylori</i></b> Culture and Susceptibility Testing Following Failure of Individualized Antibiotic Therapy

et al. 2015

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Background: Current guidelines recommend direct Helicobacter pylori culture and antibiotic susceptibility testing following 2 failed eradication attempts. If this process is followed and yet subsequent treatment is unsuccessful, it is unclear whether susceptibility testing should be repeated. This is the first study to examine the appropriateness of repeated H. pylori culture and susceptibility testing following failure of individualized treatment. Methods: Between 2007 and 2014, consecutive patients who underwent at least 2 upper gastrointestinal endoscopies with H. pylori culture and susceptibility testing at our institution following several treatment failures were retrospectively identified. Antibiotic susceptibility was recorded and linked to demographic data. Results: A total of 68 cultures from 34 patients were included (12 (35.3%) men, 41.4 ± 16.6 years), and 20 (58.8%) cultures had a different antibiotic susceptibility profile on repeat testing (8 (23.5%) with new susceptibility and 13 (38.2%) with new resistance). Acquired resistance to clarithromycin, levofloxacin and metronidazole was observed in 9 (26.5%), 2 (5.9%) and 10 (29.4%) cultures, respectively. Subjects with resistance to ≤1 antibiotic at baseline were more likely to develop resistance to at least 1 antibiotic on subsequent culture, compared to subjects with resistance to ≥2 antibiotics at baseline (13 (100%) vs. 5 (23.8%), p < 0.01). Conclusion: Repeating H. pylori culture and susceptibility testing usually yields new antimicrobial susceptibility data. However, the clinical usefulness of this approach remains unclear.

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Heteroresistance of Helicobacter pylori from the same patient prior to antibiotic treatment

Cited by 43 publications

References 41 publications

Detection ofHelicobacter pyloriresistance to clarithromycin and fluoroquinolones in Brazil: A national survey

Detection ofHelicobacter pyloriresistance to clarithromycin and fluoroquinolones in Brazil: A national survey

Antimicrobial Heteroresistance: an Emerging Field in Need of Clarity

Appropriateness of Repeating <b><i>Helicobacter pylori</i></b> Culture and Susceptibility Testing Following Failure of Individualized Antibiotic Therapy

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