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Updated: Aug 14, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
Published on: October 25, 2013
Vancomycin resistance in gram-positive cocci
1Unite des Agents Antibacteriens, Institut Pasteur, Paris, France. pcourval@pasteur.fr
Abstract:
The first vancomycin-resistant clinical isolates of Enterococcus species were reported in Europe in 1988. Similar strains were later detected in hospitals on the East Coast of the United States. Since then, vancomycin-resistant enterococci have spread with unexpected rapidity and are now encountered in hospitals in most countries. This article reviews the mode of action and the mechanism of bacterial resistance to glycopeptides, as exemplified by the VanA type, which is mediated by transposon Tn1546 and is widely spread in enterococci. The diversity, regulation, evolution, and recent dissemination of methicillin-resistant Staphylococcus aureus are then discussed.
Insights
Vancomycin-resistant enterococci (VRE) emerged in 1988 and have rapidly spread globally. This review covers VRE resistance mechanisms, focusing on the VanA type, and discusses methicillin-resistant Staphylococcus aureus.
Area of Science:
- Microbiology and Infectious Diseases
- Molecular Biology
- Antimicrobial Resistance
Background:
- Vancomycin-resistant enterococci (VRE) first identified in 1988, rapidly disseminated worldwide.
- VRE are a significant nosocomial pathogen, prevalent in healthcare settings globally.
- Methicillin-resistant Staphylococcus aureus (MRSA) is another critical multidrug-resistant bacterium.
Purpose of the Study:
- To review the mechanism of bacterial resistance to glycopeptides, exemplified by VanA type.
- To discuss the genetic basis (transposon Tn1546) and spread of VanA-mediated resistance in enterococci.
- To explore the diversity, regulation, evolution, and dissemination of MRSA.
Main Methods:
- Literature review of scientific articles on vancomycin resistance in enterococci and MRSA.
- Analysis of molecular mechanisms of glycopeptide resistance, including the VanA system.
- Examination of epidemiological data on the spread of VRE and MRSA.
Main Results:
- Vancomycin resistance in enterococci is primarily mediated by the VanA phenotype, encoded by transposon Tn1546.
- The VanA system alters bacterial cell wall precursors, preventing vancomycin binding and action.
- MRSA exhibits significant diversity and has evolved complex regulatory mechanisms for its resistance traits.
Conclusions:
- The rapid global spread of VRE highlights the urgent need to understand resistance mechanisms.
- The VanA type represents a well-characterized model for glycopeptide resistance in enterococci.
- Understanding MRSA evolution and dissemination is crucial for controlling its spread in healthcare environments.
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