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Updated: Aug 24, 2026
Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
Vancomycin resistance in Staphylococcus aureus
Peter C Appelbaum1, Bülent Bozdogan
1Department of Pathology, Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA. pappelbaum@psu.edu
Abstract:
Vancomycin resistance in enterococci, predominantly Enterococcus faecium, developed in the latter half of the 1980s, and the long anticipated development of vancomycin resistance in Staphylococcus aureus has now occurred. A number of vancomycin-intermediate strains have been described, and these strains have abnormal, thickened cell walls in the presence of vancomycin. Two mechanisms of resistance have been described in the strains: affinity trapping of vancomycin molecules by cell wall monomers and clogging of the outer layers of peptidoglycan by bound vancomycin molecules, and change in the structure or metabolism of teichoic acids. Of more serious concern has been the description in 2002 of two patients with vancomycin-resistant S aureus infections. In one instance, the patient had skin lesions coinfected with vancomycin resistant, vanA genotype, E faecalis, and the vanA resistance genes could have been transferred to the S aureus strain. Expression of resistance was high in one S aureus strain and low in the other, making detection more challenging in the latter instance. These developments are of great concern, and every effort should be made to prevent further development and spread of vancomycin resistance in staphylococci.
Insights
Vancomycin resistance, a growing concern in enterococci, has now emerged in Staphylococcus aureus. This development, marked by altered cell walls and resistance mechanisms, poses a significant threat to public health.
Area of Science:
- Microbiology
- Infectious Diseases
- Antimicrobial Resistance
Background:
- Vancomycin resistance in enterococci emerged in the late 1980s.
- Vancomycin resistance in Staphylococcus aureus is a significant and concerning development.
- Vancomycin-intermediate strains exhibit thickened cell walls when exposed to vancomycin.
Purpose of the Study:
- To review the mechanisms and implications of vancomycin resistance in Staphylococcus aureus.
- To highlight the emergence of vancomycin-resistant Staphylococcus aureus (VRSA) infections.
- To emphasize the need for strategies to prevent the further spread of vancomycin resistance.
Main Methods:
- Review of existing literature on vancomycin resistance mechanisms.
- Analysis of reported cases of vancomycin-resistant Staphylococcus aureus infections.
- Examination of genetic mechanisms, including potential gene transfer events.
Main Results:
- Two primary resistance mechanisms identified: altered cell wall synthesis and changes in teichoic acid.
- Reported cases of vancomycin-resistant Staphylococcus aureus infections in 2002.
- Potential vanA gene transfer from Enterococcus faecalis to Staphylococcus aureus observed.
- Variable expression levels of resistance in Staphylococcus aureus strains complicate detection.
Conclusions:
- The emergence of vancomycin resistance in Staphylococcus aureus is a serious clinical concern.
- Understanding resistance mechanisms and spread is crucial for effective treatment and prevention.
- Urgent measures are needed to prevent the further development and dissemination of vancomycin resistance in staphylococci.
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