Occurrence of Mutations in the Antimicrobial Target Genes Related to Levofloxacin, Clarithromycin, and Amoxicillin Resistance inHelicobacter pyloriIsolates from Buenos Aires City

Palma, Gerardo Zerbetto De; Mendiondo, Nicolás; Wonaga, Andrés; Viola, Luis; Ibarra, Daniela; Campitelli, Esteban; Salim, Nicolas; Corti, Rodolfo; Goldman, Cinthia G.; Catalano, Mariana

doi:10.1089/mdr.2015.0361

Cited by 53 publications

(57 citation statements)

References 45 publications

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“…25 De Palma et al reported that resistance of levofloxacin was due to substitution at position 87 (K,I) and 91 (G,N,A) of gyrA QRDR in the 92.8% of the resistant isolates. 40 Miftahussurur et al reported that mutations at Asn-87 and/or Asp-91 were predominantly in levofloxacinresistant strains, and the gyrB mutation had a steady relationship with gyrA 87-91 mutations. 41 None of the substitutions found in gyrB proved conferring resistance in this study.…”

Section: Discussionmentioning

confidence: 99%

Mutations in the Antibiotic Target Genes Related to Clarithromycin, Metronidazole and Levofloxacin Resistance in Helicobacter pylori Strains from Children in China

Zhang

Wen

Xiao

et al. 2020

IDR

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Purpose: This study aimed to characterize common mutations of antibiotic-resistant gene of clarithromycin, metronidazole and levofloxacin in Helicobacter pylori (H. pylori) and determine their association with antibiotic resistance of H. pylori for providing a strategy for eradication therapy of H. pylori infection in children. Patients and Methods: The antibiotic resistance to clarithromycin, metronidazole and levofloxacin for H. pylori strains isolated from children was determined by E-test. The mutation of domain V of 23S rRNA, rdxA and frxA genes, gyrA and gyrB genes was performed by PCR-based sequencing of DNA fragments. Results: Out of the 79 H. pylori strains examined, 66 (83.5%) were resistant to at least one of the tested antibiotics and 13 (16.5%) were fully sensitive. A total of 29 (36.7%) strains were resistant to clarithromycin. Analysis of the 23S rRNA gene showed that most mutations occurred at the A2143G and T2182C sites, showing a frequency of 82.8% (24/29) and 89.7% (26/29) respectively. In the 11 sensitive strains to clarithromycin, the frequency of A2143G mutation was only 45.5%, which was significantly lower than that in resistant strains (P<0.05). There were 54 strains (68.4%) resistant to metronidazole, with most mutations occurring at G47A and T184G in the rdxA gene. T184G mutation was recognized in metronidazole-sensitive strains, but no G47A mutation was identified. Twelve strains (15.2%) were resistant to levofloxacin. Position 91 mutation of the gyrA gene occurred only in resistant strains, whereas position 87 mutations were detected in both sensitive and resistant strains to levofloxacin. Conclusion: In H. pylori resistant strains isolated from children in China, most mutations occurred at A2143G of the 23S rRNA gene for clarithromycin; G47A mutation of rdxA gene for metronidazole; and at 91 mutation of gyrA gene for levofloxacin. It is suggested that susceptibility testing together with screening the mutation of antimicrobial-resistant gene prior to treatment is important for the eradication of H. pylori in children.

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Section: Discussionmentioning

confidence: 99%

Mutations in the Antibiotic Target Genes Related to Clarithromycin, Metronidazole and Levofloxacin Resistance in Helicobacter pylori Strains from Children in China

Zhang

Wen

Xiao

et al. 2020

IDR

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“…However, their detection has been done in H. pylori bacteria recovered from human clinical specimens. 14,48,51 The final part of our survey focused on the genotyping of vacA, cagA, cagE, iceA, oipA, and babA alleles of the H. pylori bacteria. We also originated that vacA s1a, s2, m1a, and m2, and iceA1 and cagA, s1am1a, s2m1a, s1am2, s2m2, and s1a/cagA-/iceA1/oipA-/cagE-/babA-, m1a/cagA-/ iceA1/oipA-/cagE-/babA-, s2/cagA-/iceA1/oipA-/cagE-/ babA-, s1a/cagA+/iceA1/oipA+/cagE-/babA-, m1a/cagA +/iceA1/oipA+/cagE+/babA-, m1a/cagA+/iceA1/oipA +/cagE-/babA-, m2/cagA-/iceA1/oipA-/cagE-/babA-, s1a/ cagA+/iceA1/oipA+/cagE+/babA-, s1a/cagA-/iceA1/oipA-/ cagE+/babA-, s1a/cagA-/iceA1/oipA+/cagE-/babA-, s1b/ cagA-/iceA1/oipA-/cagE-/babA-, m1a/cagA-/iceA1/oipA-/ cagE+/babA-, m1a/cagA-/iceA1/oipA+/cagE-/babA-, m1b/ cagA-/iceA1/oipA-/cagE-/babA-, s1a/cagA+/iceA1/oipA-/ cagE+/babA-, s2/cagA+/iceA1/oipA+/cagE-/babA-, s2/ cagA-/iceA1/oipA-/cagE+/babA-, s2/cagA-/iceA1/oipA+/ca gE-/babA-, m1a/cagA+/iceA1/oipA-/cagE-/babA+, and m1a/cagA+/iceA1/oipA-/cagE+/babA-were the most generally perceived genotypes amongst the H. pylori bacteria.…”

Section: Combined Genotyping Patterns Distribution* (%)mentioning

confidence: 99%

“…11,13 The presence of certain antibiotic resistance genes, particularly rdxA, pbp1A, gyrA, and cla which encode resistance toward metronidazole, amoxicillin, fluoroquinolone, and clarithromycin antibiotic agents, respectively, is one of the most important reasons for occurrence of antibiotic resistance. 14,15 Therefore, it is significant to know the exact phenotypic and genotypic patterns of antibiotic resistance of H. pylori bacteria recovered from foods with animal origins.…”

Section: Introductionmentioning

confidence: 99%

Phenotypic and Genotypic Assessment of Antibiotic Resistance and Genotyping of vacA, cagA, iceA, oipA, cagE, and babA2 Alleles of Helicobacter pylori Bacteria Isolated from Raw Meat

Mashak¹,

Jafariaskari²,

Alavi³

et al. 2020

IDR

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Background: Foodstuffs with animal origins, particularly meat, are likely reservoirs of Helicobacter pylori. Purpose: An existing survey was accompanied to assess phenotypic and genotypic profiles of antibiotic resistance and genotyping of vacA, cagA, cagE, iceA, oipA, and babA2 alleles amongst the H. pylori bacteria recovered from raw meat. Methods: Six-hundred raw meat samples were collected and cultured. H. pylori isolates were tested using disk diffusion and PCR identification of antibiotic resistance genes and genotyping. Results: Fifty-two out of 600 (8.66%) raw meat samples were contaminated with H. pylori. Raw ovine meat (13.07%) had the uppermost contamination. H. pylori bacteria displayed the uppermost incidence of resistance toward tetracycline (82.69%), erythromycin (80.76%), trimethoprim (65.38%), levofloxacin (63.46%), and amoxicillin (63.46%). All H. pylori bacteria had at least resistance toward one antibiotic, even though incidence of resistance toward more than eight antibiotics was 28.84%. Total distribution of rdxA, pbp1A, gyrA, and cla antibiotic resistance genes were 59.61%, 51.92%, 69.23%, and 65.38%, respectively. VacA s1a (84.61%), s2 (76.92%), m1a (50%), m2 (39.13%), iceA1 (38.46%), and cagA (55.76%) were the most generally perceived alleles. S1am1a (63.46%), s2m1a (53.84%), s1am2 (51.92%), and s2m2 (42.30%) were the most generally perceived genotyping patterns. Frequency of cagA-, oipA-, and babA2-genotypes were 44.23%, 73.07%, and 80.76%, respectively. A total of 196 combined genotyping patterns were also perceived. Conclusion: The role of raw meat, particularly ovine meat, in transmission of virulent and resistant H. pylori bacteria was determined. VacA and cagA genotypes had the higher incidence. CagE-, babA2-, and oipA-H. pylori bacteria had the higher distribution. Supplementary surveys are compulsory to originate momentous relations between distribution of genotypes, antibiotic resistance, and antibiotic resistance genes.

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“…Among the 6 common mutations in gyrA that invoke fluoroquinolone resistance, N87 and D91 are reported to be the most commonly encountered (14,19,40), and these mutations were the most frequent gyrA mutations in our cohort (Table 4). However, we did not observe a significant correlation between gyrA mutations and treatment success.…”

Section: Discussionmentioning

confidence: 82%

“…Tetracycline resistance is due to mutation in the binding site of tetracycline in 16S rRNA (14). Fluoroquinolone resistance is due to point mutations in the quinolone resistance determining region (QRDR) of gyrA at positions encoding amino acids 86, 87, 88, 91, or 97 (14,19). We used 3 pairs of primers to amplify the three gene regions: gyrA, (forward) 5=-AAGGTTAGGCAGACGGCT-3= and (reverse) 5=-TTAACCACCCCCATGGCGA-3=; 23S rRNA gene, (forward) 5=-GGTGGTATCTCAAGGATGGC-3= and (reverse) 5=-GATCTAACCGCGGCAAGACG-3= (20); and 16S rRNA gene, (forward) 5=-TGGAGCATGTGG TTTAATTCGA-3= and (reverse) 5=-TGCGGGACTTAACCCAACA-3= (21).…”

Section: Methodsmentioning

confidence: 99%

Helicobacter pylori Mutations Detected by Next-Generation Sequencing in Formalin-Fixed, Paraffin-Embedded Gastric Biopsy Specimens Are Associated with Treatment Failure

et al. 2019

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Helicobacter pylori antibiotic resistance is widespread and increasing worldwide. Routine detection of H. pylori mutations that invoke antimicrobial resistance may be a useful approach to guide antimicrobial therapy and possibly avert treatment failure. In this study, formalin-fixed, paraffin-embedded (FFPE) gastric biopsy specimens from a cohort of individuals from northern Ohio in the United States were examined using a next-generation sequencing (NGS) assay to detect H. pylori mutations that are known to confer resistance to clarithromycin, levofloxacin, and tetracycline. From January 2016 to January 2017, 133 H. pylori-infected gastric biopsy specimens were identified histologically and subsequently analyzed by NGS to detect mutations in gyrA, 23S rRNA, and 16S rRNA genes. The method successfully detected H. pylori in 126 of 133 cases (95% sensitivity). Mutations conferring resistance were present in 92 cases (73%), including 63 cases with one mutation (50%) and 29 cases with mutations in multiple genes (23%). Treatment outcomes were available in 58 cases. Sixteen of the 58 cases failed therapy (28%). Therapy failure correlated with the number of mutated genes: no failure in cases with no mutations (0/15), 19% (5/27) failure in cases with one gene mutation, and 69% (11/16) failure in cases with more than one mutated gene. Common 23S rRNA mutations (A2142G or A2413G) were present in 88% (14/16) of failed cases as opposed to in only 10% (4/42) of eradicated cases (P Ͻ 0.001). This NGS assay can be used on remnant specimens collected during standard-of-care testing to detect mutations that correlate with increased risk of treatment failure. A prospective study is needed to determine if the risk of treatment failure can be decreased by using this assay to guide antibiotic therapy.

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Occurrence of Mutations in the Antimicrobial Target Genes Related to Levofloxacin, Clarithromycin, and Amoxicillin Resistance inHelicobacter pyloriIsolates from Buenos Aires City

Cited by 53 publications

References 45 publications

<p>Mutations in the Antibiotic Target Genes Related to Clarithromycin, Metronidazole and Levofloxacin Resistance in <em>Helicobacter pylori</em> Strains from Children in China</p>

<p>Mutations in the Antibiotic Target Genes Related to Clarithromycin, Metronidazole and Levofloxacin Resistance in <em>Helicobacter pylori</em> Strains from Children in China</p>

<p>Phenotypic and Genotypic Assessment of Antibiotic Resistance and Genotyping of <em>vacA</em>, <em>cagA</em>, <em>iceA</em>, <em>oipA</em>, <em>cagE</em>, and <em>babA2</em> Alleles of <em>Helicobacter pylori</em> Bacteria Isolated from Raw Meat</p>

Helicobacter pylori Mutations Detected by Next-Generation Sequencing in Formalin-Fixed, Paraffin-Embedded Gastric Biopsy Specimens Are Associated with Treatment Failure

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