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Updated: Jul 19, 2026

Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
The escalating challenge of vancomycin resistance in Staphylococcus aureus
1BD Diagnostic Systems, 7 Loveton Circle, Mail Stop 628, Sparks, MD, 21152, USA. rpfeltz@bd.com
Abstract:
The glycopeptide antibiotic vancomycin is considered indispensable for the treatment of multidrug-resistant Staphylococcus aureus infections, and so the acquisition by these organisms of transmissible glycopeptide resistance elements from enterococci had been anticipated with apprehension. It was therefore a considerable surprise when vancomycin-intermediate S. aureus (VISA) clinical isolates were reported in 1997, with a novel, borderline-resistance phenotype acquired without genetic exchange. Clinical vancomycin-resistant S. aureus (VRSA) were not reported until 2002, expressing high level, transmissible resistance by virtue of vanA resistance determinants within enterococcal transposable elements residing on staphylococcal plasmids. This review will provide an update on the frustratingly variable characteristics of the VISA phenotype, focus on the progress made in understanding the molecular basis of the VISA resistance mechanism from the viewpoint of genetic regulation and cell wall stress response, and summarize the information currently available on VRSA. Finally, alternatives to vancomycin that are already available or nearing approval will be briefly reviewed, with attention to their limitations and potential for resistance development.
Insights
Vancomycin resistance in Staphylococcus aureus emerged unexpectedly, with intermediate resistance (VISA) appearing first without genetic exchange. High-level resistance (VRSA) later developed via enterococcal elements, necessitating new treatment strategies.
Area of Science:
- Microbiology and Infectious Diseases
- Molecular Biology
- Pharmacology
Background:
- Vancomycin is crucial for treating multidrug-resistant Staphylococcus aureus (MRSA).
- The emergence of vancomycin resistance in S. aureus was a significant clinical concern.
- Initial vancomycin-intermediate S. aureus (VISA) isolates appeared without evidence of genetic exchange.
Purpose of the Study:
- To review the evolving characteristics of the VISA phenotype.
- To elucidate the molecular mechanisms underlying VISA resistance, focusing on genetic regulation and cell wall stress.
- To summarize current knowledge on vancomycin-resistant S. aureus (VRSA) and discuss alternative therapies.
Main Methods:
- Literature review of clinical isolates and molecular studies.
- Analysis of genetic regulation and cell wall stress response pathways.
- Summary of available and emerging alternative antibiotics.
Main Results:
- VISA exhibits variable resistance characteristics and arises through novel mechanisms.
- VRSA emerged later, acquiring high-level resistance via enterococcal vanA elements on plasmids.
- Understanding resistance mechanisms is key to developing effective treatments.
Conclusions:
- The development of vancomycin resistance in S. aureus is complex and multifaceted.
- Further research into VISA/VRSA mechanisms is essential for clinical management.
- Alternative antibiotics are needed, but their limitations and resistance potential require careful consideration.
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