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Fellow, Division of Infectious Diseases, Montefiore Medical Center, 111 East 210th Street, Bronx, New York 10463, fax 718/266-9507, kmc2007{at}columbia.edu
Assistant Clinical Professor, Department of Medicine, Montefiore Medical Center
Infectious Diseases Fellow, Montefiore Medical Center
Associate Professor of Clinical Medicine, Albert Einstein College of Medicine/Jacobi Medical Center, Bronx, New York
Published Online, March 6, 2007. www.theannals.com, DOI 10.1345/aph.1H568
Case Reports. A 49-year-old man was admitted to the intensive care unit with sepsis 1 month after completing a 6 week course of linezolid via a central venous catheter. Blood culture on day 1 grew Staphylococcus auricularis that was sensitive to linezolid; intravenous therapy with linezolid 600 mg twice daily was started on hospital day 1. Eight days later, while the patient was still on linezolid, blood culture grew linezolid-resistant Staphylococcus epidermidis (isolate 1). On day 12, another blood culture grew linezolid-resistant S. auricularis (isolate 2). Linezolid therapy was changed to vancomycin, but the patient died shortly thereafter.
An 82-year-old woman developed vancomycin-resistant Enterococcus catheter-related sepsis, which was treated with intravenous linezolid 600 mg twice daily for 2 weeks. One month later, she was readmitted with fever, and linezolid-resistant S. epidermidis (isolate 3) was recovered from her blood culture.
Discussion. Antimicrobial susceptibilities were performed by MicroScan on all 3 isolates. The automated system reported intermediate susceptibility to linezolid for isolates 1, 2, and 3. All isolates were resistant to linezolid, with a minimum inhibitory concentration (MIC) greater than 256 µg/mL by Etest. The isolates were sent to Pfizer Global Research and Development for MIC confirmation by broth microdilution and molecular testing. To detect the mutated alleles, a real-time polymerase chain reaction (PCR) assay with TaqMan probes was used. This PCR method allows for rapid detection of single-nucleotide mutations by using 2 labeled probes: one detects susceptible alleles and the other detects mutated alleles.5 All isolates were resistant to linezolid, with an MIC greater than 64 µg/mL. Isolates 1 and 2 had the G2576T mutation, which appears to be the most common point mutation causing linezolid resistance.1 Molecular testing was not performed on isolate 3.
Multiple risk factors for emerging resistance have been described, including recent receipt of linezolid, prolonged course of linezolid therapy, insertion of a central venous catheter, and complicated clinical courses, including intensive care unit admission, immunosuppression, and renal failure.1,3 Both of our patients had more than one risk factor. In Case 1, we suspect that linezolid therapy played a role in the emergence of resistance. Although molecular typing was unavailable, an identical susceptibility profile (Table 1) suggested that the linezolid-resistant S. auricularis developed from a previously susceptible strain during treatment. To prevent further emergence of resistance, linezolid should be used cautiously in patients on prolonged therapy, and susceptibility testing of CoNS in individuals with prior linezolid exposure should be considered, especially if therapy is failing.
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Footnotes
Presented, in part, as an abstract at the 44th Annual Meeting of the Infectious Diseases Society of America, Toronto, Ontario, Canada, October 12-15, 2006.
References
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