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Intensive care unit dissemination of multiple clones of linezolid-resistant Enterococcus faecalis and Enterococcus
Eleni Ntokou1, Constantinos Stathopoulos, Ioulia Kristo
1Department of Microbiology, Medical School, University of Thessaly, Larissa, Greece.
Objectives:
Outbreaks caused by linezolid-resistant (LR) enterococci remain rare. We report the epidemiological and molecular characteristics of the multiclonal dissemination of LR enterococci in the intensive care unit (ICU) of a Greek hospital.
Methods:
All LR enterococcal isolates recovered from patients hospitalized in the ICU of the University Hospital of Larissa, Greece, between January 2007 and October 2008 were included. Isolates were tested by PFGE and PCR followed by sequence analysis of the entire 23S rRNA gene. Patient records were retrieved to access patterns of acquisition and outcome.
Results:
Sixteen separate patients were infected and/or colonized by 22 LR enterococcal isolates (17 Enterococcus faecium and 5 Enterococcus faecalis). Linezolid MICs varied from 8 to 16 mg/L; 12 isolates showed cross-resistance to vancomycin. Genotyping revealed as many as seven and three PFGE types among E. faecium and E. faecalis isolates, respectively, indicating multiclonal spread of LR enterococci. Nine patients had received linezolid prior to the recovery of LR enterococci, while the remaining seven patients were not exposed to the drug. All isolates carried the mutation G2576T; the mutated position was heterogeneous in 12 isolates and homogeneous in 10.
Conclusions:
The multiclonal composition of LR enterococci indicates that linezolid resistance possibly occurred on several independent occasions. Its acquisition was often not related to linezolid administration; patients might have acquired their LR isolate from another patient that had received linezolid or, alternatively, resistance may have arisen by mutation that occurred independently.
Insights
Linezolid-resistant enterococci spread across multiple clones in a Greek ICU, suggesting independent resistance development. Acquisition often occurred without prior linezolid exposure, highlighting diverse transmission routes.
Area of Science:
- Infectious Diseases
- Microbiology
- Clinical Medicine
Background:
- Linezolid is a critical antibiotic for treating infections caused by resistant Gram-positive bacteria.
- Enterococci are common causes of hospital-acquired infections, and resistance to antibiotics like linezolid is a growing concern.
- Understanding the epidemiology and molecular basis of linezolid resistance is crucial for infection control.
Purpose of the Study:
- To investigate the epidemiological and molecular characteristics of linezolid-resistant (LR) enterococci.
- To determine the patterns of acquisition and outcomes in patients with LR enterococcal infections or colonization.
- To identify the genetic mechanisms underlying linezolid resistance in enterococci.
Main Methods:
- Retrospective analysis of LR enterococcal isolates from a Greek hospital's ICU (January 2007-October 2008).
- Phenotypic testing including antimicrobial susceptibility (linezolid, vancomycin).
- Molecular characterization using Pulse Field Gel Electrophoresis (PFGE) for genotyping and sequencing of the 23S rRNA gene for resistance mutations.
Main Results:
- Twenty-two LR enterococcal isolates (17 Enterococcus faecium, 5 Enterococcus faecalis) from 16 patients were identified.
- Linezolid minimum inhibitory concentrations (MICs) ranged from 8 to 16 mg/L; 12 isolates were also vancomycin-resistant.
- PFGE revealed multiclonal spread with up to seven PFGE types in E. faecium and three in E. faecalis.
- The G2576T mutation in the 23S rRNA gene was present in all isolates, with heterogeneous or homogeneous patterns.
- Nine patients had prior linezolid exposure, while seven did not, suggesting non-linezolid-associated acquisition.
Conclusions:
- The multiclonal nature of LR enterococci suggests independent emergence of resistance.
- Linezolid resistance acquisition was not always linked to prior linezolid use.
- Patients may acquire LR enterococci from other patients or develop resistance through independent mutations.
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