Abstract
Background
We describe an outbreak with an extended-spectrum β-lactamase-producing Klebsiella pneumoniae strain in an intensive care unit in a secondary care hospital in Norway. The outbreak source was a fibreoptic intubation endoscope in which the outbreak strain survived despite chemothermal disinfection in a decontaminator designated for such use. The genetic marker clpK, which increases microbial heat resistance, has previously been described in K. pneumoniae outbreak strains.
Aim
To investigate the role of clpK in biofilm formation and heat-shock stability in the outbreak strain.
Methods
The outbreak investigation was done by review of clinical records, screening of patients and culture from intubation endoscopes and bronchoscopes. Amplified fragment length polymorphism was used to identify the outbreak strain. clpK detection was performed by polymerase chain reaction, followed by mutant construction and heat-shock assays.
Findings
Five patients and one intubation endoscope contained K. pneumoniae with the same amplified fragment length polymorphism pattern. The outbreak strain contained the clpK genetic marker, which rendered the strain its increased heat resistance. The survival rate of the strain grown as biofilm following heat treatment was also strongly dependent on clpK.
Conclusion
Although clpK has been associated with clinical isolates of K. pneumoniae in earlier outbreaks, this is the first time that a ClpK-producing strain has been isolated from an environmental outbreak source. Heat resistance of certain K. pneumoniae strains may facilitate survival in biofilms on medical equipment and hence increase the potential of those strains to persist and disperse in the hospital environment.
We describe an outbreak with an extended-spectrum β-lactamase-producing Klebsiella pneumoniae strain in an intensive care unit in a secondary care hospital in Norway. The outbreak source was a fibreoptic intubation endoscope in which the outbreak strain survived despite chemothermal disinfection in a decontaminator designated for such use. The genetic marker clpK, which increases microbial heat resistance, has previously been described in K. pneumoniae outbreak strains.
Aim
To investigate the role of clpK in biofilm formation and heat-shock stability in the outbreak strain.
Methods
The outbreak investigation was done by review of clinical records, screening of patients and culture from intubation endoscopes and bronchoscopes. Amplified fragment length polymorphism was used to identify the outbreak strain. clpK detection was performed by polymerase chain reaction, followed by mutant construction and heat-shock assays.
Findings
Five patients and one intubation endoscope contained K. pneumoniae with the same amplified fragment length polymorphism pattern. The outbreak strain contained the clpK genetic marker, which rendered the strain its increased heat resistance. The survival rate of the strain grown as biofilm following heat treatment was also strongly dependent on clpK.
Conclusion
Although clpK has been associated with clinical isolates of K. pneumoniae in earlier outbreaks, this is the first time that a ClpK-producing strain has been isolated from an environmental outbreak source. Heat resistance of certain K. pneumoniae strains may facilitate survival in biofilms on medical equipment and hence increase the potential of those strains to persist and disperse in the hospital environment.
Originalsprog | Engelsk |
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Tidsskrift | Journal of Hospital Infection |
Vol/bind | 93 |
Udgave nummer | 1 |
Sider (fra-til) | 57-62 |
ISSN | 0195-6701 |
DOI | |
Status | Udgivet - 1 maj 2016 |
Emneord
- Det Sundhedsvidenskabelige Fakultet