ArticleRevista do Instituto de Medicina Tropical de Sao Paulo2018
The interplay between mutations in cagA, 23S rRNA, gyrA and drug resistance in Helicobacter pylori.
Article in Revista do Instituto de Medicina Tropical de Sao Paulo, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 10 citations in OpenAlex.
- Overcoming antibiotic-resistantWorld journal of gastroenterology · 2025Review
- First insight into the whole genome sequence variations in clarithromycin resistant Helicobacter pylori clinical isolates in Russia.Scientific reports · 2024Article
- Mutations Related to Antibiotics Resistance inAntibiotics (Basel, Switzerland) · 2023Article
- Clarithromycin-resistant H. pylori primary strains and virulence genotypes in the Northeastern region of Brazil.Revista do Instituto de Medicina Tropical de Sao Paulo · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In this study, we evaluated the mutations of Helicobacter pylori associated with resistance to clarithromycin and levofloxacin. Furthermore, based on the proposed interaction between antimicrobial resistance and pathogenicity, we correlated the mutation profiles of the strains with the presence of the pathogenicity gene cagA. We analyzed 80 gastric biopsy specimens from H. pylori-infected patients for point mutations in the 23S rRNA gene region and in the gyrA gene, which are related to clarithromycin and levofloxacin resistance, respectively, and investigated the presence of the cagA gene in these strains. We observed that in the assayed biopsies, 8.7% (7/80) had mutations in the 23S rRNA gene region at positions 2143 and 2142, while 22.5% (18/80) had mutations in gyrA at codons 87 and 91. Moreover, absence of the CagA-EPIYA pathogenicity factor was observed in 68% (17/25) of resistant samples. The knowledge of the local profile of antimicrobial resistance and the complex interplay involving resistance and pathogenicity can contribute to an appropriate clinical approach.
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