[5] This mechanism differs from strains of vancomycin-intermediate Staphylococcus aureus (VISA), which appear to develop elevated MICs to vancomycin through sequential mutations resulting in a thicker cell wall and the synthesis of excess amounts of D-ala-D-ala residues.

For people with methicillin-resistant Staphylococcus aureus (MRSA) bacteremia in the setting of vancomycin failure the Infectious Diseases Society of America recommends high-dose daptomycin, if the isolate is susceptible, in combination with another agent (e.g., gentamicin, rifampin, linezolid, trimethoprim/sulfamethoxazole, or a beta-lactam antibiotic).

[10] Vancomycin-intermediate S. aureus (VISA) (/ˈviːsə/ or /viːaɪɛseɪ/) was first identified in Japan in 1996[11] and has since been found in hospitals elsewhere in Asia, as well as in the United Kingdom, France, the U.S., and Brazil.

The DNA sequence of the VRSA vanA gene was identical to that of a vancomycin-resistant strain of Enterococcus faecalis recovered from the same catheter tip.

The vanA gene was later found to be encoded within a transposon located on a plasmid carried by the VRSA isolate.

[16] As of 2019, 52 VRSA strains have been identified in the United States, India, Iran, Pakistan, Brazil, and Portugal.

[17] The definition of hVISA according to Hiramatsu et al. is a strain of Staphylococcus aureus that gives resistance to vancomycin at a frequency of 10−6 colonies or even higher.