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Is plasmid-mediated quinolone resistance a clinically significant problem?

L Poirel, V Cattoir, P Nordmann

    Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases
    |January 15, 2008
    PubMed

    Insights

    Plasmid-mediated quinolone resistance (PMQR) mechanisms like Qnr, AAC(6')-Ib-cr, and QepA are emerging in Enterobacteriaceae. These low-level resistance factors may promote the development of higher-level chromosomal resistance.

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Genetics

    Background:

    • Enterobacteriaceae commonly exhibit chromosomal quinolone resistance.
    • Plasmid-mediated quinolone resistance (PMQR) is an emerging concern.
    • Known PMQR mechanisms include Qnr proteins, AAC(6 ext{ extprime}) -Ib-cr, and QepA efflux pumps.

    Discussion:

    • Qnr proteins inhibit quinolone action by protecting DNA gyrase and topoisomerase IV.
    • AAC(6 ')-Ib-cr acetylates fluoroquinolones like norfloxacin and ciprofloxacin.
    • QepA facilitates the extrusion of hydrophilic fluoroquinolones via an efflux pump mechanism.

    Key Insights:

    • PMQR determinants confer low-level resistance to quinolones and fluoroquinolones.
    • These low-level resistance mechanisms can act as a predisposing factor.
    • Facilitates the selection and emergence of additional chromosomally-encoded resistance mechanisms.

    Outlook:

    • Understanding PMQR is crucial for developing effective antimicrobial strategies.
    • Monitoring the spread of PMQR is essential to combat rising antibiotic resistance.
    • Further research into novel therapeutic targets to overcome PMQR is warranted.

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