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Updated: Aug 24, 2026

Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
Glycopeptide resistance in Staphylococcus aureus: is it a real threat?
1Department of Bacteriology, Glasgow Royal Infirmary, Division of Immunology, Infection and Inflammation, University of Glasgow Medical School, 86 Castle Street, Glasgow, G4 0SF, UK. c.g.gemmell@clinmed.gla.ac.uk
Abstract:
Following the discovery in 1992 that resistance to vancomycin could be transferred in vitro from a strain of Staphylococcus haemolyticus to Staphylococcus aureus, the threat that a similar event could happen in vivo has existed. In 1996, the threat became a reality in Japan followed by reports of low-level heteroresistant S. aureus from elsewhere in the world. However, the threat has not gone away; indeed it has become more intimidating within the past 2 years with the isolation of higher-level resistance to vancomycin transferred on a plasmid from Enterococcus faecalis. The mechanisms of resistance are different in each of the types of S. aureus with reduced susceptibility to the glycopeptides: in one hetero-vancomycin intermediate-susceptible S. aureus (hVISA) and vancomycin intermediate-susceptible S. aureus (VISA), cell wall biosynthesis is altered, hindering glycopeptide reaching its target, and in the other vancomycin-resistant S. aureus (VRSA) the target is altered. This review attempts to place into context the threat posed to patients by the appearance of strains of S. aureus more resistant to one of the key therapeutic agents used in our hospitals. It will do so by raising a number of important questions followed by the presentation of experimental evidence that may or may not provide answers that heighten or lower the threat.
Insights
The emergence of vancomycin-resistant Staphylococcus aureus strains poses a significant threat. Understanding the different resistance mechanisms is crucial for combating these infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Antimicrobial Resistance
Background:
- Vancomycin resistance in Staphylococcus aureus (S. aureus) has evolved significantly since 1992.
- Initial concerns of in vitro vancomycin resistance transfer have materialized into in vivo threats.
- Recent isolations show higher-level vancomycin resistance transferred via plasmids, increasing the threat.
Purpose of the Study:
- To review the evolving threat of vancomycin-resistant S. aureus.
- To contextualize the clinical implications of S. aureus strains with reduced vancomycin susceptibility.
- To explore the mechanisms and impact of emerging resistance.
Main Methods:
- Literature review of S. aureus vancomycin resistance.
- Analysis of resistance transfer events (in vitro and in vivo).
- Examination of distinct resistance mechanisms in different S. aureus phenotypes.
Main Results:
- Two primary mechanisms of reduced glycopeptide susceptibility identified: altered cell wall biosynthesis (hVISA/VISA) and altered target (VRSA).
- Evidence suggests increasing prevalence and severity of vancomycin resistance in S. aureus.
- Plasmid-mediated transfer from Enterococcus faecalis contributes to higher resistance levels.
Conclusions:
- Vancomycin resistance in S. aureus represents a growing challenge in healthcare settings.
- Understanding the diverse mechanisms of resistance is vital for effective treatment strategies.
- Continued vigilance and research are necessary to mitigate the threat of resistant S. aureus infections.
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