Linezolid-Resistant Coagulase-Negative Staphylococci
Abstract & Commentary
By Robert Muder, MD, Hospital Epidemiologist, Pittsburgh VA Medical Center. Dr. Muder does research for Aventis and Pharmacia.
This article originally appeared in the September 2006 issue of Infectious Disease Alert. It was edited by Stan Deresinski, MD, FACP, and peer reviewed by Connie Price, MD. Dr. Deresinski is Clinical Professor of Medicine, Stanford University; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, and Dr. Price is Assistant Professor, University of Colorado School of Medicine. Dr. Deresinski serves on the speaker's bureau for Merck, Pharmacia, GlaxoSmithKline, Pfizer, Bayer, and Wyeth, and does research for Merck. Dr. Price reports no financial relationship relevant to this field of study.
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. 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. MICs to linezolid were generally > 256 ug/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 the receiving unit for an intensive care unit that had an unusually high level of linezolid use, approximately 8 times higher than that of the facility as a whole. PFGE analysis showed that 21/25 (84%) resistant strains were genetically related. Strains of susceptible coagulase-negative staphylococci were genetically diverse.
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 was also 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 or not 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.