Vancomycin-intermediate S. aureus (VISA) and Vancomycin-resistant S. aureus (VRSA)

How to Subscribe
MLS & MLT Comprehensive CE Package
Includes 176 CE courses, most popular
$109Add to cart
Pick Your Courses
Up to 8 CE hours
$55Add to cart
Individual course$25Add to cart
Need multiple seats for your university or lab? Get a quote
The page below is a sample from the LabCE course Drug-Resistant Superbugs, Multi-drug Resistant Organisms: MRSA, VRE, Clostridioides difficile, and CRE. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

Learn more about Drug-Resistant Superbugs, Multi-drug Resistant Organisms: MRSA, VRE, Clostridioides difficile, and CRE (online CE course)
Vancomycin-intermediate S. aureus (VISA) and Vancomycin-resistant S. aureus (VRSA)

Like methicillin, vancomycin exerts its antimicrobial effect by inhibiting cell wall synthesis, binding irreversibly to cell wall precursors – D-alanyl-D-alanine; and attacking sites responsible for cell wall synthesis.
Resistance in VISA strains is thought to be due to:
  • Accelerated peptidoglycan synthesis with increased quantities of D-alanyl-D-alanine residues, which bind & sequester vancomycin molecules
  • Thicker cell walls with reduced peptidoglycan cross-linking (impedes progress of drug molecules)
  • Increased glutamine mucopeptides
All strains with MIC ≥4 µg/mL should be considered candidate VISA or VRSA strains, and should be sent to a reference laboratory for confirmation.
Cell wall thickening and transfer of genetic material underlie the development of vancomycin resistance. There is evidence to support the transfer of genetic material among vancomycin-resistant bacterial isolates; the Michigan (2002) VRSA isolate acquired the vanA gene via interspecies transfer from a co-isolated vancomycin-resistant Enterococcus faecalis.