Journal Article

Epidemiological Profile of Linezolid-Resistant Coagulase-Negative Staphylococci

Brian A. Potoski, Jennifer Adams, Lloyd Clarke, Kathleen Shutt, Peter K. Linden, Carla Baxter, A. William Pasculle, Blair Capitano, Anton Y. Peleg, David L. Paterson and Dora Szabo

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 43, issue 2, pages 165-171
Published in print July 2006 | ISSN: 1058-4838
Published online July 2006 | e-ISSN: 1537-6591 | DOI:
Epidemiological Profile of Linezolid-Resistant Coagulase-Negative Staphylococci

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Background. Surveillance studies have shown that <0.1% of coagulase-negative staphylococci are linezolid resistant; however, at our institution, 4% of such organisms were found to be resistant. We investigated the risk factors for and the epidemiological profile of linezolid-resistant coagulase-negative staphylococci.

Methods. Susceptibility testing and pulsed-field gel electrophoresis were performed to analyze the genetic relatedness of both linezolid-resistant and linezolid-susceptible isolates. Clinical data were retrieved from medical records, and a case-case-control study was performed to identify unique risk factors for linezolid resistance.

Results. Isolates recovered from 25 patients with linezolid-resistant coagulase-negative staphylococci were examined; all but 1 of the isolates were identified as Staphylococcus epidermidis, and all but 1 had a minimum inhibitory concentration of linezolid of >256 µg/mL. Pulsed-field gel electrophoresis showed that 21 (84%) of 25 linezolid-resistant isolates exhibited genetic relatedness, whereas linezolid-susceptible isolates were of diverse clones. Unique, independent predictors of linezolid resistance included receipt of linezolid in the 3 months preceding isolation of the coagulase-negative staphylococci (odds ratio, 20.6; 95% confidence interval, 5.8–73.0).

Conclusion. Linezolid-resistant coagulase-negative staphylococci have emerged at our institution and are predominately of a single clone. We believe that the most likely scenario to explain this emergence is that person-to-person spread of linezolid-resistant coagulase-negative staphylococci led to establishment of skin colonization with the strain. Subsequent use of linezolid was followed by selection of the linezolid-resistant strain, which then became the dominant skin flora. The potential for a parallel scenario involving clonal dissemination followed by selection of linezolid-resistant methicillin-resistant Staphylococcus aureus is a real possibility.

Journal Article.  3563 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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