Vancomycin-resistant Staphylococcus aureus (VRSA) is a strain of Staphylococcus aureus that has become resistant to the glycopeptide antibiotic vancomycin. With the increase of staphylococcal resistance to methicillin, vancomycin (or teicoplanin) is often a treatment of choice in infections with methicillin-resistant Staphylococcus aureus (MRSA).

Vancomycin resistance is still a rare occurrence. Unfortunately, VRSA may also be resistant to meropenem and imipenem, two other antibiotics that can be used in sensitive staphylococcus strains.

VISA (vancomycin-intermediate Staphylococcus aureus) was first identified in Japan in 1997 and has since been found in hospitals in England, France, the US, Asia and Brazil. It is also termed GISA (glycopeptide-intermediate Staphylococcus aureus) indicating resistance to all glycopeptide antibiotics. These bacterial strains present a thickening of the cell wall which is believed to deplete the vancomycin available to kill the bacterium. This mechanism of resistance to vancomycin is different to that which happens in enterococcus where there is a change in the target site of the antibiotic, leading to a lower affinity for vancomycin, which gives vancomycin-resistant enterococci high levels of resistance.

Many enterococcus strains display resistance against vancomycin, and it has been suggested that vancomycin resistance has been transmitted[1] between enterococci and staphylococci on a plasmid on at least two occasions in the United States. This worries many physicians and microbiologists because it leads to high level resistance to vancomycin in Staphylococcus aureus. This has the potential of spreading rapidly throughout large populations of Staphylococcus aureus in hospitals, as opposed to the traditional VISA mode of intermediate resistance to vancomycin, which has to be acquired by the bacterium during treatment with this drug.