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Isolation and Identification of Waterborne Antibiotic-Resistant Bacteria and Molecular Characterization of their Antibiotic Resistance Genes
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Gentamicin resistance in Pseudomonas aeruginosa: R-factor-mediated resistance

L E Bryan, M S Shahrabadi, H M van den Elzen

    Antimicrobial Agents and Chemotherapy
    |August 1, 1974
    PubMed

    Insights

    Gentamicin resistance in Pseudomonas aeruginosa was observed, with some strains transferring this resistance via R-factors. Detection of transferable resistance was more effective in P. aeruginosa recipients, highlighting challenges in identifying resistance due to phenotypic lag.

    Area of Science:

    • Microbiology
    • Antimicrobial Resistance
    • Molecular Biology

    Background:

    • Pseudomonas aeruginosa is an opportunistic pathogen frequently associated with hospital-acquired infections.
    • Gentamicin is a critical antibiotic used to treat P. aeruginosa infections.
    • Antimicrobial resistance in P. aeruginosa poses a significant public health threat.

    Purpose of the Study:

    • To investigate the prevalence of gentamicin resistance in Pseudomonas aeruginosa.
    • To identify mechanisms of gentamicin resistance, including R-factors and inactivating enzymes.
    • To evaluate the transferability of gentamicin resistance and its associated mechanisms.

    Main Methods:

    • Disk diffusion antimicrobial susceptibility testing was performed on clinical isolates of P. aeruginosa.
    • Gentamicin-resistant strains were screened for R-factors and antibiotic-inactivating enzymes.
    • Conjugation experiments were conducted using P. aeruginosa and Escherichia coli as recipients to assess the transfer of gentamicin resistance.
    • Phenotypic lag in resistance expression was investigated by varying gentamicin concentrations in selection media.

    Main Results:

    • 11% of P. aeruginosa strains were resistant and 31% were moderately resistant to gentamicin.
    • No R-factors or inactivating enzymes were found in gentamicin-resistant strains from the University of Alberta Hospital.
    • Eight of 13 strains from American sources possessed gentamicin-acetylating or -adenylating activity and transferred resistance via conjugation.
    • P. aeruginosa recipients were more effective than E. coli for detecting transferable gentamicin resistance.
    • R-factors belonged to P-2 and P-3 incompatibility groups.
    • Phenotypic lag in gentamicin resistance expression was observed, particularly in P. aeruginosa strain 280, potentially leading to underestimation of resistance transfer.

    Conclusions:

    • Transferable gentamicin resistance mediated by antibiotic-inactivating enzymes exists in P. aeruginosa.
    • The choice of recipient strain and selection antibiotic concentration is crucial for detecting R-factor-mediated resistance.
    • Understanding the mechanisms and transfer of gentamicin resistance is vital for effective treatment strategies against P. aeruginosa infections.

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