Unraveling the molecular basis of antibiotic resistance in S. aureus focusing on plasmid-mediated mechanisms

  • 1Department of Biosciences, Faculty of Life Sciences, Shaheed Zulfikar Ali Bhutto Institute of Science and Technology (SZABIST) University, Karachi, Pakistan.
  • 2Molecular Biology & Structural Biochemistry Research Laboratory, Department of Biochemistry, University of Karachi, Karachi, Pakistan.
  • 3Department of Chemistry, University of Karachi, Pakistan.

Abstract

This study investigates antibiotic resistance mechanisms in Staphylococcus aureus, focusing on plasmid-mediated resistance, and evaluates triazole compounds as potential inhibitors against resistant strains. The study was conducted at SZABIST, Karachi, using ten Staphylococcus isolates. Identification was performed via biochemical assays and 16S rRNA PCR. Antibiotic resistance was assessed and the RepA gene, responsible for plasmid-mediated resistance, was detected. In-silico molecular docking studies were conducted with triazole compounds (C1, C2, C3, C4). Statistical analysis was performed using SPSS and ANOVA was used to assess significant differences. S. aureus exhibited resistance to methicillin and vancomycin. 75% of isolates did not produce biofilm. PCR revealed the presence of the RepA gene. Among the compounds tested, C3 showed the strongest antimicrobial activity and stable binding interactions with RepA. The study concluded that resistance in clinical S. aureus strains is not encoded by mecA and vanA genes, but rather by the plasmid-mediated RepA gene. Compound C3 emerged as a potent inhibitor, offering a promising direction for future research in combating multi drug resistant S. aureus strains.

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