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Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
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Updated: Jun 30, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
11:56

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

Published on: October 25, 2013

Acquired vancomycin resistance in clinically relevant pathogens.

Guido Werner1, Birgit Strommenger, Wolfgang Witte

  • 1FG 13 Nosocomial Infections, Robert Koch Institute, Wernigerode Branch, Wernigerode, Germany. wernerg@rki.de

Future Microbiology
|September 25, 2008
PubMed
Summary

Acquired vancomycin resistance in bacteria, particularly Enterococcus, is a growing concern. New van gene clusters enable resistance, posing challenges, especially when acquired by MRSA.

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Last Updated: Jun 30, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
11:56

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

Published on: October 25, 2013

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Acquired vancomycin resistance is a significant and increasing problem in pathogenic bacteria.
  • This resistance is most prevalent and studied in Enterococcus species, with various van genotypes (vanA-G) described.
  • Van gene clusters, comprising up to nine genes, encode proteins that alter cell wall precursors, reducing susceptibility to glycopeptides.

Purpose of the Study:

  • To review the mechanisms and prevalence of vancomycin resistance in bacteria.
  • To highlight the role of Enterococcus faecium as a reservoir for van resistance genes.
  • To discuss the implications of vancomycin resistance acquisition by other pathogens, such as MRSA.

Main Methods:

  • Literature review of studies on vancomycin resistance mechanisms and epidemiology.
  • Analysis of van gene cluster structures and functions.
  • Examination of clinical reports and outbreaks related to vancomycin-resistant bacteria.

Main Results:

  • VanA and VanB types are globally distributed, with VanA predominating, primarily in Enterococcus faecium.
  • Hospital-adapted subpopulations of Enterococcus have acquired van gene clusters, leading to worldwide outbreaks of vancomycin-resistant enterococci.
  • Acquisition of vanA by methicillin-resistant Staphylococcus aureus (MRSA) has been reported in seven cases.
  • Glycopeptide nonsusceptibility can also arise independently of van genes, presenting a growing therapeutic challenge, particularly in MRSA.

Conclusions:

  • Vancomycin resistance, driven by van gene clusters, is a major threat, especially from Enterococcus reservoirs.
  • The emergence of vancomycin resistance in MRSA is a critical clinical concern.
  • Alternative mechanisms of glycopeptide resistance necessitate ongoing surveillance and development of new therapeutic strategies.