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Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
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Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

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Penicillin tolerance and modification of lipoteichoic acid associated with expression of vancomycin resistance in

L Gutmann1, S Al-Obeid, D Billot-Klein

  • 1Laboratoire de Recherche Moléculaire sur les Antibiotiques, Université Paris VI, France.

Antimicrobial Agents and Chemotherapy
|January 1, 1996
PubMed

Insights

Vancomycin resistance in Enterococcus faecium, specifically VanB-type, was linked to penicillin tolerance. This was not due to autolysin changes but to increased D-alanine attached to lipoteichoic acid.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Enterococcus faecium is a significant cause of hospital-acquired infections.
  • Vancomycin resistance in enterococci is a growing public health concern.
  • Penicillin tolerance can complicate treatment strategies for enterococcal infections.

Purpose of the Study:

  • To investigate the relationship between vancomycin resistance and penicillin tolerance in Enterococcus faecium.
  • To elucidate the molecular mechanisms underlying this association.
  • To identify potential targets for therapeutic intervention.

Main Methods:

  • Induction of vancomycin resistance in Enterococcus faecium D366 (VanB-type).
  • Analysis of penicillin tolerance by measuring cell lysis and killing.
  • Assessment of autolysin expression and activity.
  • Quantification of D-alanine attachment to lipoteichoic acid.

Main Results:

  • Vancomycin resistance induction and constitutive expression correlated with decreased cell lysis and killing upon penicillin exposure.
  • No significant changes were observed in autolysin expression or lytic activity.
  • A notable increase, approximately double the normal amount, in D-alanine attachment to lipoteichoic acid was detected.

Conclusions:

  • Penicillin tolerance in vancomycin-resistant Enterococcus faecium is associated with alterations in cell wall composition, specifically increased D-alanine on lipoteichoic acid.
  • This modification, rather than changes in autolysins, appears to mediate tolerance.
  • Understanding this mechanism could inform new approaches to treating resistant enterococcal infections.

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