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VanD-type vancomycin-resistant Enterococcus faecium 10/96A.

Florence Depardieu1, Peter E Reynolds, Patrice Courvalin

  • 1Unité des Agents Antibactériens, Institut Pasteur, 75724 Paris, Cedex 15, France.

Antimicrobial Agents and Chemotherapy
|December 25, 2002
PubMed
Summary
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VanD type Enterococcus faecium exhibits vancomycin resistance due to D-alanyl-D-lactate synthesis. Mutations in D-alanine:D-alanine ligase and vanY(D) contribute to resistance, alongside an ISEfa4 insertion in the vanS(D) gene.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • VanD type Enterococcus faecium 10/96A displays constitutive resistance to vancomycin and low-level resistance to teicoplanin.
  • This resistance is primarily mediated by the synthesis of peptidoglycan precursors terminating in D-alanyl-D-lactate.
  • Previous studies identified a G184S mutation in D-alanine:D-alanine ligase (Ddl) affecting peptidoglycan precursor synthesis.

Purpose of the Study:

  • To elucidate the genetic basis and molecular mechanisms underlying vancomycin resistance in VanD type Enterococcus faecium 10/96A.
  • To characterize the vanD gene cluster organization and identify key mutations contributing to resistance.

Main Methods:

  • Sequencing of the vanD gene cluster to identify open reading frames and mutations.

Related Experiment Videos

  • Analysis of D-alanine:D-alanine ligase (Ddl) activity and peptidoglycan precursor synthesis.
  • Investigation of the vanY(D) gene for frameshift mutations and their impact on D,D-carboxypeptidase activity.
  • Identification and characterization of insertion sequences within the vanD operon, specifically ISEfa4.

    • Main Results:

    • The vanD gene cluster comprises eight open reading frames, organized similarly to other VanD type strains.
    • A G184S mutation in Ddl impairs its function, leading to reduced D-alanyl-D-alanine precursor synthesis.
    • A frameshift mutation in vanY(D) abolishes D,D-carboxypeptidase activity and results in a fusion protein with homology to penicillin-binding proteins.
    • Insertion of ISEfa4 within the vanS(D) gene causes constitutive expression of vancomycin resistance.

    Conclusions:

    • The vanD gene cluster, including vanH(D), vanD, vanX(D), vanY(D), vanR(D), and vanS(D), is crucial for vancomycin resistance.
    • Mutations in Ddl and vanY(D), along with the insertion of ISEfa4, collectively contribute to the constitutive vancomycin resistance phenotype.
    • The identified insertion sequence ISEfa4, belonging to the IS605 family, plays a significant role in regulating vancomycin resistance expression.