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Related Experiment Videos

High-level resistance to gentamicin in Enterococcus faecium.

N Woodford1, E McNamara, E Smyth

  • 1Antibiotic Reference Laboratory, Central Public Health Laboratory, London, UK.

The Journal of Antimicrobial Chemotherapy
|April 1, 1992
PubMed
Summary
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High-level gentamicin resistance in Enterococcus faecium strains was identified in an Irish hospital. This resistance is linked to a transferable plasmid encoding a specific aminoglycoside-modifying enzyme.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Enterococcus faecium is an opportunistic pathogen.
  • High-level gentamicin resistance (HLGR) is a growing concern in Gram-positive bacteria.
  • Previous reports of HLGR in Enterococcus faecium were primarily from the USA.

Purpose of the Study:

  • To investigate the prevalence and mechanism of high-level gentamicin resistance in Enterococcus faecium strains isolated from a hospital in Ireland.
  • To characterize the genetic basis of gentamicin resistance in these strains.

Main Methods:

  • Six strains of Enterococcus faecium were isolated from patients over a six-month period.
  • Minimum Inhibitory Concentrations (MICs) for gentamicin were determined.
  • Plasmid DNA was analyzed, and conjugation experiments were performed.

Related Experiment Videos

  • Plasmid DNA was hybridized with a DNA probe specific for the AAC(6 extprime)-APH(2 extprime extprime) enzyme.

    • Main Results:

    • Four patients were infected and two were colonized with Enterococcus faecium strains exhibiting high-level gentamicin resistance (MICs > 1000 mg/L).
    • All six strains possessed a 50 MDa plasmid.
    • Gentamicin resistance was transferable via conjugation, associated with the 50 MDa plasmid.
    • The plasmid hybridized with a probe for the bifunctional AAC(6 extprime)-APH(2 extprime extprime) aminoglycoside-modifying enzyme.

    Conclusions:

    • The mechanism of high-level gentamicin resistance in these Irish Enterococcus faecium strains is mediated by the bifunctional AAC(6 extprime)-APH(2 extprime extprime) enzyme.
    • This mechanism is identical to that observed in Enterococcus faecalis and previously reported in Enterococcus faecium strains in the USA.
    • The findings highlight the spread of gentamicin resistance in Enterococcus faecium.