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Related Experiment Videos

Inducible, transferable resistance to vancomycin in Enterococcus faecium, D399.

D M Shlaes1, S Al-Obeid, J H Shlaes

  • 1Université de Paris VI, Laboratoire de Microbiologie Médicale, France.

The Journal of Antimicrobial Chemotherapy
|April 1, 1989
PubMed
Summary

A novel strain of Enterococcus faecium (D399) exhibits inducible vancomycin resistance, transferable to other bacteria. This glycopeptide resistance mechanism suggests wider dissemination in clinical settings.

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Enterococcus faecium is a significant cause of healthcare-associated infections.
  • Vancomycin resistance in enterococci is a growing public health concern.
  • Previous studies identified inducible glycopeptide resistance mechanisms in Enterococcus faecalis.

Purpose of the Study:

  • To characterize the vancomycin resistance of Enterococcus faecium D399.
  • To investigate the mechanism and transferability of this resistance.
  • To compare the resistance phenotype with previously described enterococcal strains.

Main Methods:

  • Isolation and identification of Enterococcus faecium D399 from clinical samples.
  • Determination of vancomycin Minimum Inhibitory Concentration (MIC).

Related Experiment Videos

  • Assessment of resistance inducibility and transferability via conjugation experiments.
  • Analysis of protein synthesis induction associated with resistance.

    • Main Results:

    • Enterococcus faecium D399 demonstrated high-level vancomycin resistance (MIC = 1000 mg/l).
    • The resistance was inducible and transferable to a susceptible strain (JH2-2).
    • Resistance correlated with the induction of a 39 kDa protein synthesis, similar to E. faecalis A256.
    • The resistance phenotype of D399 showed some unique characteristics compared to other inducible resistance strains.

    Conclusions:

    • Enterococcus faecium D399 possesses an inducible and transferable vancomycin resistance mechanism.
    • This finding suggests the dissemination of this glycopeptide resistance mechanism among enterococci.
    • The unique resistance phenotype warrants further investigation into the molecular basis of resistance in D399.