Detection of and the Genotypes of Resistance to Clarithromycin, Fluoroquinolones, and Metronidazole in Gastric Biopsies: An In Silico Analysis to Help Understand Antibiotic Resistance.

Antibiotic resistance in is increasing rapidly and emerging as a major factor in treatment failure. We aimed to identify genetic mutations associated with resistance to clarithromycin (23S rRNA peptidyl transferase), fluoroquinolones (), and metronidazole (), and to explore their mechanisms of action through molecular modeling. detection and the molecular characterization of genes were conducted directly on gastric biopsies by real-time PCR followed by nucleotide sequencing. A 3D model was used to evaluate molecular interactions between the antibiotics and respective target proteins. was identified in 66.7% of 33 patients. An analysis of revealed novel mutations that, by in silico analysis, do not appear to contribute to clarithromycin resistance. In , mutations in amino acid residues 87 and 91 had an incidence of 27%, and the in silico analysis revealed that these positions are relevant in the binding and resistance to fluoroquinolones. It is also reported for other mutations, some of which are never described. All mutations were missense, with R16H, M56V, H97T, G98S, A118T, V123T, and R131K predicted by in silico analysis to impact metronidazole resistance. Monitoring gene mutations is crucial for tailoring effective antibiotic therapies. Our study advances personalized medicine by introducing novel methods to detect resistance-related mutations and uncovering the molecular mechanisms driving this resistance.