Rifampicin curing of plasmids in Escherichia coli K12-rifampicin resistant host

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E E Obaseiki-Ebor

    The Journal of Pharmacy and Pharmacology
    |July 1, 1984
    PubMed

    Insights

    Rifampicin effectively removes certain R-plasmids from Escherichia coli. Plasmid type, not host strain resistance, determines successful rifampicin curing of these plasmids.

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Genetics

    Background:

    • R-plasmids and F'-plasmids are extrachromosomal DNA elements in bacteria that can confer antibiotic resistance.
    • Rifampicin is an antibiotic used to treat bacterial infections, and its ability to eliminate plasmids (curing) is of interest.
    • Understanding plasmid curing mechanisms is crucial for controlling antibiotic resistance spread.

    Purpose of the Study:

    • To investigate the in vitro efficacy of rifampicin in curing specific R-plasmids and an F'-plasmid from Escherichia coli.
    • To determine if host cell resistance to rifampicin affects the plasmid curing process.
    • To identify factors that influence the success of rifampicin-mediated plasmid elimination.

    Main Methods:

    • In vitro experiments were conducted using Escherichia coli K12 strains.
    • Rifampicin was used at various concentrations to assess its plasmid curing ability.
    • The frequency of plasmid curing was compared between rifampicin-resistant and rifampicin-sensitive host cells.
    • Specific R-plasmids (JR225, BN102, BN106, R222, RP4) and an F'-plasmid (F'lac+/R386) were tested.

    Main Results:

    • Rifampicin successfully cured R-plasmids JR225, BN102, BN106, and F'-plasmid F'lac+/R386 from Escherichia coli J62-2.
    • The minimum rifampicin curing concentration and curing frequency were similar in both rifampicin-resistant (J62-2) and isogenic rifampicin-sensitive (J62-1) host cells.
    • Rifampicin failed to cure R-plasmids R222 and RP4 from both resistant and sensitive host cells.

    Conclusions:

    • The susceptibility of R-plasmids to rifampicin-mediated curing is determined by the plasmid's genetic makeup, not the host bacterium's resistance profile.
    • Rifampicin curing is plasmid-specific, with some R-plasmids being resistant to elimination by this antibiotic.
    • These findings highlight the importance of plasmid characteristics in predicting the outcome of antibiotic-induced curing strategies.

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