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 microg/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.
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 microg/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.
Authors: Ronald N Jones; Matthew G Stilwell; Patricia A Hogan; Daniel J Sheehan Journal: Antimicrob Agents Chemother Date: 2007-01-08 Impact factor: 5.191
Authors: M Treviño; L Martínez-Lamas; P A Romero-Jung; J M Giráldez; J Alvarez-Escudero; B J Regueiro Journal: Eur J Clin Microbiol Infect Dis Date: 2008-11-05 Impact factor: 3.267
Authors: Agnes Wong; Shilpa P Reddy; Davida S Smyth; Maria E Aguero-Rosenfeld; George Sakoulas; D Ashley Robinson Journal: Antimicrob Agents Chemother Date: 2009-11-23 Impact factor: 5.191
Authors: A Sorlozano; J Gutierrez; T Martinez; M E Yuste; J A Perez-Lopez; A Vindel; J Guillen; T Boquete Journal: Eur J Clin Microbiol Infect Dis Date: 2009-10-30 Impact factor: 3.267
Authors: Elias Abrutyn; Christopher H Cabell; Vance G Fowler; Bruno Hoen; José M Miro; Carlos A Mestres; Daniel J Sexton; G Ralph Corey Journal: Curr Infect Dis Rep Date: 2007-07 Impact factor: 3.725
Authors: Robin L Macintosh; Jane L Brittan; Ritwika Bhattacharya; Howard F Jenkinson; Jeremy Derrick; Mathew Upton; Pauline S Handley Journal: J Bacteriol Date: 2009-09-11 Impact factor: 3.490