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At the University of Pittsburgh Medical Center, laboratory-based surveillance of coagulase-negative staphylococci found that 4% were linezolid-resistant. MIC's to linezolid were generally > 256 µg/mL; the isolates were all susceptible to vancomycin and daptomycin.

Abstract & Commentary: An early warning of staph resistance to linezolid?

Abstract & Commentary

An early warning of staph resistance to linezolid?

Resistance in coag-neg strain raises questions

Synopsis: In one university medical center, 4% of all coagulase-negative staphylococci were linezolid-resistant. A case control study found that admission to a particular unit and prior receipt of linezolid were significant, independent risk factors for isolation of a linezolid-resistant isolate. Pulsed-field gel electrophoresis (PFGE) analysis found that 84% of linezolid-resistant isolates were genetically related.

Source: Potoski BA, et al. Epidemiological profile of linezolid-resistant coagulase-negative staphylococci. Clin Infect Dis 2006; 43:165-171.

At the University of Pittsburgh Medical Center, laboratory-based surveillance of coagulase-negative staphylococci found that 4% were linezolid-resistant. MIC's to linezolid were generally > 256 µg/mL; the isolates were all susceptible to vancomycin and daptomycin. In a case control study, prior receipt of linezolid (OR, 20.6; 95% CI, 5.8-73) and location on a particular hospital unit (OR, 12.4; 95% CI, 3.4-45) were independently associated with isolation of a linezolid-resistant strain. The identified unit served as a the receiving unit for an intensive care unit that had an unusually high level of linezolid use, approximately eight times higher than that of the facility as a whole. PFGE analysis showed that 21 of 25 (84%) resistant strains were genetically related. Strains of susceptible coagulase-negative staphylococci were genetically diverse.

Commentary by Robert Muder, MD, hospital epidemiologist at Pittsburgh VA Medical Center. (Editor's note: Dr. Muder does research for Aventis and Pharmacia.)

Resistance to linezolid among staphylococci has been rare in prior studies; less than 0.1% of isolates of coagulase-negative staphylococci have been resistant in prior studies. The study by Potoski and colleagues demonstrates a markedly higher rate of linezolid resistance among coagulase-negative staphylococci in their facility. Although prior receipt of linezolid was a significant independent risk factor, it is of note that most resistant strains were genetically related, and that admission to a particular ward also was a significant risk factor. This demonstrates that both antimicrobial exposure and patient-to-patient transmission are likely to be important in the epidemiology of linezolid resistance of coagulase-negative staphylococci.

More importantly, coagulase-negative staphylococci and S. aureus can exchange resistance genes. The study by Potoski et al did not examine the mechanism of linezolid resistance in coagulase-negative staphylococci, and it is not known whether linezolid resistance is transferable among staphylococcal species. However, this report suggests that possibility that linezolid resistance could become widely disseminated among S. aureus isolates. Should this happen, the arsenal of antimicrobial agents effective against MRSA would be further restricted.