Resistance of Helicobacter pylori to tetracycline, amoxicillin, clarithromycin and metronidazole in Israeli children and adults

Peretz, Avi; Paritsky, Maya; Nasser, Omar; Brodsky, Diana; Glyatman, Tatyana; Segal, Sofia; On, Avi

doi:10.1038/ja.2014.38

Cited by 27 publications

(20 citation statements)

References 11 publications

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“…In addition, resistance rate to clarithromycin has increased, and is 3 times higher (similar rates in both methods) in comparison to data published earlier in Israel, in accordance with the global increasing trend [19]. A possible explanation for a lower resistance rate to fluoroquinolones in comparison to clarithromycin could be due to its later addition to treatment protocols of H. pylori infection.…”

Section: Discussionsupporting

confidence: 65%

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Binyamin

Pastukh

et al. 2017

Gut Pathog

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Background:Helicobacter pylori susceptibility to clarithromycin and fluoroquinolone can be determined through Etest or molecular assays. We examined the correlation between phenotypic susceptibility (MIC results) and genotypic susceptibility in H. pylori strains isolated from gastric biopsies. Results:Out of 85 duplicate biopsies obtained from patients from northern Israel who underwent endoscopy, 70 were positive for H. pylori using the CUTest (urease test). These biopsies were cultured for H. pylori and Etest breakpoints were determined for levofloxacin and clarithromycin. H. pylori detection, characterization of wild type (WT) or mutant alleles, and antibiotic resistance were determined molecularly using GenoType HelicoDR kit. Phenotypic and genotype results were compared. The molecular method had higher sensitivity for detection of H. pylori than culture (94.3% vs. 77.1%). Resistance to clarithromycin was higher than to levofloxacin by both methods. Levofloxacin resistance was found in 21.2 and 0% using genotypic and phenotypic methods, respectively. Clarithromycin resistance was found in 66.7 and 62.9% by genotypic and phenotypic methods, respectively. Some samples were found susceptible by Etest and resistant by GenoType HelicoDR (13/53 samples) and some vice versa (10/53 samples). Conclusion:GenoType HelicoDR kit has high sensitivity rate for H. pylori detection. It has the ability to detect many mutations and can help to determine initial antibiotic treatment at the beginning of therapy. However, there were a few cases where there was a phenotype-genotype mismatch result that could derive from possible causes. For example, a resistance mechanism that is not tested in the kit.

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Section: Discussionsupporting

confidence: 65%

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Binyamin

Pastukh

et al. 2017

Gut Pathog

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“…Peretz et al [13] found that 22.3% of H. pylori isolates from treatment naïve adults in 2011–2012 were resistant to clarithromycin. Zevit et al [16] found a rate of clarithromycin resistance of 25% among untreated children.…”

Section: Discussionmentioning

confidence: 99%

Temporal Trends in Helicobacter pylori Eradication Success in a Test-and-Treat Population

et al. 2018

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Background/Aims: Although the efficacy of first-line treatment for Helicobacter pylori infection should aim to be > 90%, it is unclear whether this target has been achieved in Israel. We aimed to determine the success rate of treatment for H. pylori and to describe temporal changes in our region. Methods: Adult patients who underwent a first-time C¹³-urea breath test (C¹³-UBT) at Clalit Health Services between January 1, 2010 and December 31, 2015 were included. In order to isolate a naïve “test-and-treat” population who were unlikely to have undergone an initial endoscopy-based H. pylori test, we excluded patients ≥45 years and those with any previous C¹³-UBT. Results: A total of 94,590 subjects (36.1% male, age 28.5 ± 6.0) who underwent at least one C¹³-UBT during the study period were included. C¹³-UBT was positive in 48,509 (51.3%) subjects. A confirmatory post-treatment C¹³-UBT was performed in 37.8, 44.1, 46.6, and 45.9% following 1st, 2nd, 3rd, and 4th-line treatment respectively. Eradication was successful in 65.4% following first-line treatment, and eradication success improved during the study period (59.2, 63.3, 65.7, 66.0, 69.0, and 73.1% in 2010, 2011, 2012, 2013, 2014, and 2015 respectively; OR 1.11; 95% CI 1.09–1.13; p < 0.0001). Eradication was successful in 44.7% following second-line treatment, although eradication success did not significantly improve during the study period (OR 1.05; 95% CI 0.99–1.10; p = 0.09). Conclusions: Despite the increasing success of first-line treatment for H. pylori infection over the study period, eradication rates remain suboptimal. Initiatives to implement the Toronto and Maastricht Consensus Reports should be advanced.

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“…A high resistance was also found among the strains isolated from children in Poland (33.3% were resistant to CH, 44.8% to MZ, whereas 1.9% of strains were resistant simultaneously to CH, MZ, and levofloxacine (LEV) . An unusually high resistance for amoxicillin (12.2%) was found in Israeli children . In a Japanese study between 2000 and 2013, among 1073 H. pylori‐ positive patients of different ages, the rate of clarithromycin resistance was extremely high (57.9%) in those under the age of 31 years .…”

Section: Diagnosismentioning

confidence: 99%

Helicobacter pylori Infection in Pediatrics

Roma

Miele

2015

Helicobacter

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This review includes the main pediatric studies published from April 2014 to March 2015. The host response of Treg cells with increases in FOXP3 and TGF‐β1 combined with a reduction in IFN‐γ by Teff cells may contribute to Helicobacter pylori susceptibility in children. Genotypic variability in H. pylori strains influences the clinical manifestation of the infection. Helicobacter pylori infection is associated with variables indicative of a crowded environment and poor living conditions, while breast‐feeding has a protective effect. Intrafamilial infection, especially from mother to children and from sibling to sibling, is the dominant transmission route. Studies showed conflicting results regarding the association between H. pylori infection and iron deficiency anemia. One study suggests that H. pylori eradication plays a role in the management of chronic immune thrombocytopenic purpura in H. pylori‐infected children and adolescents. The prevalence of H. pylori was higher in chronic urticaria patients than in controls and, following H. pylori eradication, urticarial symptoms disappeared. An inverse relationship between H. pylori infection and allergic disease was reported. Antibiotic resistance and insufficient compliance to treatment limit the efficacy of eradication therapy. Sequential therapy had no advantage over standard triple therapy. In countries where H. pylori infection is prevalent, studies focusing on virulence factors and antibiotic susceptibility may provide anticipation of the prognosis and may be helpful to reduce morbidity and mortality.

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Resistance of Helicobacter pylori to tetracycline, amoxicillin, clarithromycin and metronidazole in Israeli children and adults

Cited by 27 publications

References 11 publications

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Temporal Trends in Helicobacter pylori Eradication Success in a Test-and-Treat Population

Helicobacter pylori Infection in Pediatrics

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