What to do with a vancomycin MIC?

In response to a spate of papers suggesting that elevated vancomycin MICs within the susceptible range are associated with poor clinical outcome, many clinicians now reflexively change to alternative therapy (daptomycin or linezolid) for treatment of any MRSA isolate with a vancomycin MIC of 2 mcg/mL. The most recent such paper can be found here.

As a result of this evolving standard of practice, one particular section of the new IDSA MRSA treatment guideline is generating discussion on our clinical microbiology listserv:

How should results of vancomycin susceptibility testing be used to guide therapy?

For isolates with a vancomycin minimum inhibitory concentration (MIC) ≤2 μg/mL (eg, susceptible according to Clinical and Laboratory Standards Institute [CLSI] breakpoints), the patient's clinical response should determine the continued use of vancomycin, independent of the MIC (A-III).

--If the patient has had a clinical and microbiologic response to vancomycin, then it may be continued with close follow-up

--If the patient has not had a clinical or microbiologic response to vancomycin despite adequate debridement and removal of other foci of infection, an alternative to vancomycin is recommended regardless of MIC.

For isolates with a vancomycin MIC >2 μg/mL (eg, vancomycin-intermediate S. aureus [VISA] or vancomycin-resistant S. aureus [VRSA]), an alternative to vancomycin should be used (A-III).

The bottom line? S is S, I is I, R is R. Treat the patient, not the MIC. If the patient is responding, good. If not, then you ought to be seeking alternatives, regardless of the exact MIC.

I agree with this approach for several reasons, not the least of which is that exact vancomycin MICs are method and laboratory dependent. In addition, +/- 1 dilution step in MIC is within the usual variability of our clinical laboratory MIC testing (MIC quality control ranges usually encompass 3 or 4 dilution steps). Even if every clinical microbiology laboratory did population analysis profiling of each MRSA strain, other treatment and host factors would likely have overriding impact on the clinical outcome.

Despite the fact that vancomycin is a bad (and mysterious) drug, we still lack alternatives that have been convincingly shown to be better for most MRSA infections….

Comments

  1. The potential inferiority of the generic forms of vancomycin is terrifying (Vesga, 2010). Is someone following that up with more studies?

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  2. I agree, Jason--very disturbing. I have not heard much about follow-on studies, but have discussed some ideas with Eli and others. In addition to in vitro and animal model work, we need some quick retrospective analyses where the vancomycin provenance is/was known. Not an easy task, but there should be datasets out there where this could be accomplished. Perhaps other readers can chime in if they are aware of other work being done in this area......

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