|0.225 gmg/L <ref name="[1]" /> in water

Two distinct forms of vancomycin resistance exist. The milder form of vancomycin resistance, exhibited for example by VISA (vancomycin intermediate staphylococcus aureus) strains, develops in patients undergoing prolonged vancomycin therapy. The prolonged exposure to vancomycin puts selective pressure on the pathogens. The treatment turns a heterogenous colony of bacteria with only a small subpopulation having a vancomycin MIC (minimum inhibitory concentration) greater than 2 µgmg/mLL, into a homogenous colony with a MIC of 8 µgmg/mLL. The resulting colony becomes very difficult to eradicate with vancomycin therapy <ref name="[12]">Gardete, S. & Tomasz, A. (2014). Mechanisms of vancomycin resistance in Staphylococcus aureus. ''The Journal of Clinical investigation, 124''(7), 2836-2840. [https://doi.org/10.1172/JCI68834 doi:10.1172/JCI68834]</ref>.

The second, more serious form of vancomycin resistance, demonstrated by bacterial strains such as VRSA (vancomycin resistant staphylococcus aureus), is not due to spontaneous mutations of pathogens upon continued exposure to the drug <ref name="[10]" />. Instead, pathogenic microorganisms appear have directly copied the defense mechanisms of the antibiotic producing actinomycetes. This defense mechanism is used by the actinomycetes to avoid suicide during antibiotic production <ref name="[10]" /><ref name="[7]" /><ref name="[14]">Binda, E., Marinelli, F., Marcone, G.L. (2014). Old and New Glycopeptide Antibiotics: Action and Resistance. ''Antibiotics, 3''(4), 572-594. [https://doi.org/10.3390/antibiotics3040572 doi:10.3390/antibiotics3040572]</ref>. Pathogens resistant to GPAs obtain resistance through plasmid-borne copies of transposons coding for genes named ''van'', which reprogram the biosynthesis of cell walls, replacing the D-Ala-D-Ala peptide terminus with a D-alanyl-D-lactate (D-Ala-D-Lac) terminus <ref name="[14]" /><ref name="[10]" /><ref name="[13]">Miller, W.R., Munita, J.M., Arias, C.A. (2014). Mechanisms of antibiotic resistance in enterococci. ''Expert Review of Anti-Infective Therapy, 12''(10), 1221-1236. [https://doi.org/10.1586/14787210.2014.956092 doi:10.1586/14787210.2014.956092]</ref>. This small change reduces the binding affinity of vancomycin to the target around a 1000-fold, resulting in a vancomycin MIC ≥ 100 µgmg/mL L making treatment with vancomycin impossible and effectively rendering the organism resistant <ref name="[10]" /><ref name="[7]" /><ref name="[13]" />.

For patients with severe, deep-seated infections (including but not limited to meningitis, pneumonia osteomyelitis, endocarditis, bacteremia and prosthetic joint infection) a serum trough concentration of 15 to 20 µgmg/mL L is recommended <ref name="[17]">Consgrove, S.E., Avdic, E., Dzintars, K. & Smith, J. (2015). Antibiotic Guide. ''Johns Hopkins Medicine, The Johns Hopkins Hospital Antimicrobial Stewardship Program.''</ref><ref name="[18]">Drew, R.H. & Sakoulas, G. (2017). Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults. Accessed on 26 September 2017, at ''https://www.uptodate.com/contents/vancomycin-parenteral-dosing-monitoring-and-adverse-effects-in-adults.''</ref>. To achieve this concentration more rapidly an initial loading dose of 20-25 mg/kg is often given, followed by intermittent maintenance dosing of typically around 15-20 mg/kg every 8 to 12 hours <ref name="[17]" />. Patients with less severe infections (soft tissue infections) do not require a loading dose, and are started immediately on intermittent dosing with the aim of achieving a minimum serum trough concentration of 10-15 µgmg/mL L <ref name="[18]" />. Trough concentrations are measured as these constitute the most practical and accurate indicator for treatment effectiveness and toxicity. Peak levels are rarely measured and are not clinically relevant <ref name="[17]" />.

|20 – 25 mg / kg|15 – 20 µgmg/mLL

|10 – 15 µgmg/mLL

|3 - 100 μgmg/mLL

|4 - 80 μgmg/mLL

|2 - 50 μgmg/mLL