Low prevalence of clarithromycin-resistant Helicobacter pylori isolates with A2143G point mutation in the 23S rRNA gene in North India

Gehlot, Valentina; Mahant, Shweta; Mukhopadhyay, Asish K.; Das, Kunal; Alam, Jawed; Ghosh, Piyali; Das, Rajashree

doi:10.1016/j.jgar.2016.02.007

Cited by 19 publications

(16 citation statements)

References 32 publications

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“…42,43 Prevalence of the particular point mutations varies across geographical areas. On the contrary, Gehlot et al (2016) and Nakamura et al (2007) reported 87.5% and 99.0% point mutation at A2143G position. 26,44 This result was consistence with the result of the studies conducted by Gehlot et al (2016) and Sun et al (2010) in which resistance to clarithromycin were 11.8% and 20.7% respectively.…”

Section: Resultsmentioning

confidence: 86%

Mutational Analysis of Clarithromycin and Levofloxacin Resistance in Helicobacter pylori from Gastric Biopsy Specimens in a Tertiary Care Hospital in Dhaka, Bangladesh

Tanni

Anwar

Ahmed

et al. 2019

Bangladesh J Med Microbiol

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Background: Clarithromycin and Levofloxacin are most frequently included in the standard triple therapies for H. pylori eradication in our country. Resistance to clarithromycin and fluoroquinolones are particularly related with treatment failure. Objectives: The objective of this study was to detect, clarithromycin and levofloxacin resistance associated with gene mutations in H. pylori directly from gastric biopsies using an allele specific primer-PCR (ASP-PCR) assay. Materials and Methods: Gastric biopsy specimens were collected from 143 adult dyspeptic patients, from Department of Gastroenterology, BSMMU and Dhaka Medical College Hospital (DMCH), during the period of March, 2018 to February, 2019. H. pylori was identified by rapid urease test, ureC gene by PCR, histological staining and culture. ASP-PCR was used to identify 23S rRNA gene and gyrA gene mutation predictive of clarithromycin and levofloxacin resistant H. pylori respectively. Results: H. pylori positive cases were 32.9% based on the case definition used in the study. Among 42 ureC positive H. pylori cases, point mutations in 23Sr RNA gene for clarithromycin resistance were detected only at A2142G position in 9 (21.4%) cases and gyrA gene mutations for levofloxacin resistance were detected in 16 (38.1%) cases. Only 1 (2.4%) case had mutation both in 23Sr RNA and gyrA gene. Conclusion: Those findings may guide toward the therapeutic choices in our country. PCR based diagnostic assays can be the alternative approach for rapid detection of antibiotic resistances of H. pylori directly from gastric biopsies, where culture and susceptibility tests are not routinely performed. Bangladesh J Med Microbiol 2019; 13 (1): 12-19

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Section: Resultsmentioning

confidence: 86%

Mutational Analysis of Clarithromycin and Levofloxacin Resistance in Helicobacter pylori from Gastric Biopsy Specimens in a Tertiary Care Hospital in Dhaka, Bangladesh

Tanni

Anwar

Ahmed

et al. 2019

Bangladesh J Med Microbiol

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“…We were unable to obtain tissue samples for the diagnosis and assessment of antibiotic sensitivity. Worldwide there is an increasing prevalence of resistant strains, although clarithromycin resistance is rare in Indian subjects 2930. Our study had an unblinded open-label design, and hence we cannot exclude a placebo effect.…”

Section: Discussionmentioning

confidence: 96%

Association ofHelicobacter pyloriwith Parkinson's Disease

et al. 2017

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Background and PurposeParkinson's disease (PD) is a major neurological disorder that requires lifelong treatment, and the combined presence of Helicobacter pylori (H. pylori) infection can increase the required anti-PD medications. We aim to investigate the effect of H. pylori infection in Indian PD patients.MethodsWe prospectively recruited 36 PD patients from December 2007 to January 2011. All patients underwent a detailed neurological evaluation and serological examination for H. pylori infection. Seropositive and seronegative patients were considered to be the cases and controls, respectively. All patients who were seropositive received triple therapy for 2 weeks. Outcome measures of the mean ‘off’ Unified Parkinson's Disease Rating Scale (UPDRS)-III score, mean ‘on’ UPDRS-III score, mean onset time, mean ‘on’ duration, and mean daily ‘on’ time were measured at baseline and at a 3-week follow-up.ResultsH. pylori-IgG positivity was present in 18 (50%) PD patients. The prevalence of men (72.2% vs. 33.3%), mean duration of disease (13.8 vs. 12.5) and mean levodopa equivalent daily dose (824 mg vs. 707 mg) were significantly higher among H. pylori positive patients than in controls (p<0.0001). Controls had a significantly longer ‘on’ duration and daily ‘on’ time, and better ‘on’ UPDRS-III scores. Seropositive patients took a significantly longer time to turn ‘on’ after a levodopa challenge. At the 3-week follow-up, H. pylori eradication significantly improved the mean ‘on’ UPDRS-III score, onset time, ‘on’ duration, and daily ‘on’ time.ConclusionsH. pylori infection was present in 50% of Indian PD patients. H. pylori seropositivity was associated with a poor response to levodopa and increased medication usage, while eradication therapy was associated with better patient outcomes.

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“…In addition, some sporadic changes were also found, including C1883T, G1949A, C2131T, C1883T, G1949A, C1953T, T2179G, A2210C and G2211T (Figure 1). For the 2182 site previously reported to be related to clarithromycin resistance (14), T to C (n=28, 90.3%) or A (n=2, 6.5%) mutation existed in resistant strains. All the 9 (100%) sensitive strains had T2182C mutation.…”

Section: Resultsmentioning

confidence: 93%

Molecular Detection of H.pylori Antibiotic-Resistant Genes and Bioinformatics Predictive Analysis

Wang

Guo

et al. 2018

Preprint

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To explore the mutation characteristics of H.pylori resistance-related 12 genes to antibiotics of clarithromycin, levofloxacin and metronidazole. 23S rRNA, 13 gyrA, gyrB, rdxA and frxA genes were amplified and sequenced, respectively. Their 14 structural alteration after mutation was predicted using bioinformatics software. In the 15 clarithromycin-resistant strains, the mutation rate in site A2143G was 74.2% (n=23). 16 The mutations in sites C1883T, C2131T and T2179G might cause structural alteration. 17In the levofloxacin-resistant strains, the mutation rates in 87 (N to K/I) and 91 (D to 18 N/Y/G) of gyrA were 28.6% (n=16) and 12.5% (n =7), respectively. Meanwhile, one 19 of the mutation strains in site 91 was accompanied by D99N variation. Additionally, a 20 D143E mutation was found in one drug-resistant strain. Some changes of tertiary 21 structure occurred after these mutations. The mutation types of RdxA protein 22 consisted of protein truncation caused by premature stop codons (n=26, 33.3%), 23 frameshift mutations (n=8, 10.3%), FMN-binding sites (n=16, 20.5%) and the others 24 (n=11, 14.1%). Predictive analysis showed that mutations in the first three groups and 25 the A118S of the last group could lead to structural alteration. Our study suggested the 26 clarithromycin-resistant sites of H.pylori were mainly located in A2143G of 23S 27 rRNA. C1883T, C2131T and T2179G might also be related to resistance. 28 Levofloxacin resistance was mainly based on the amino acid changes in 87 and 91 29 sites of gyrA. The new sites D99N and D143E might also be associated with 30 resistance. Metronidazole resistance was related to RdxA protein truncation, 31 frameshift, and FMN binding. The new site A118S might also be linked to drug 32 resistance. 33 KEYWORDS H. pylori, 23S rRNA, gyrA, rdxA, antibiotic resistance, high-risk area 34 of gastric cancer 35 It has been well known that eradicating H.pylori can prevent the progression of 36 diseases and reduce the risk of gastric cancer (1). Currently, the antibiotics used for 37 H.pylori eradication are mainly composed of proton pump inhibitors and gastric 38 mucosal protectant in combination with one or two kinds of antibiotics, including 39 clarithromycin, metronidazole, levofloxacin, and amoxicillin, etc. With the extensive 40 implementation of eradication therapy, the resistance of H.pylori to antibiotics has 41 been increasing year by year (2). 42 At present, bacterial factors are regarded as the main cause for antibiotic 43 resistance. Some changes of H. pylori genes could result in the loss of antibiotics 44 targets and thus induce bacterial resistance. For example, it has been suggested that 45 the A2143G, A2142G and A2142C mutations in 23S rRNA V region are related to 46 clarithromycin resistance (3, 4). However, the mutation sites of drug resistance-related 47 genes vary from place to place. For instance, Kim et al reported the resistant sites of 48 H.pylori to clarithromycin were located at A2143G and T2182C in South Korea (5), 49 while A2143G and A2146G exi...

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Low prevalence of clarithromycin-resistant Helicobacter pylori isolates with A2143G point mutation in the 23S rRNA gene in North India

Cited by 19 publications

References 32 publications

Mutational Analysis of Clarithromycin and Levofloxacin Resistance in Helicobacter pylori from Gastric Biopsy Specimens in a Tertiary Care Hospital in Dhaka, Bangladesh

Mutational Analysis of Clarithromycin and Levofloxacin Resistance in Helicobacter pylori from Gastric Biopsy Specimens in a Tertiary Care Hospital in Dhaka, Bangladesh

Association ofHelicobacter pyloriwith Parkinson's Disease

Molecular Detection of H.pylori Antibiotic-Resistant Genes and Bioinformatics Predictive Analysis

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