Heat Resistance Mediated by a New Plasmid Encoded Clp ATPase, ClpK, as a Possible Novel Mechanism for Nosocomial Persistence of Klebsiella pneumoniae

被引:65
作者
Bojer, Martin Saxtorph [1 ]
Struve, Carsten [1 ]
Ingmer, Hanne [2 ]
Hansen, Dennis Schroder [3 ,4 ]
Krogfelt, Karen Angeliki [1 ]
机构
[1] Statens Serum Inst, Dept Microbiol Surveillance & Res, DK-2300 Copenhagen, Denmark
[2] Univ Copenhagen, Fac Life Sci, Dept Vet Pathobiol, Frederiksberg, Denmark
[3] Univ Copenhagen, Hvidovre Hosp, Dept Clin Microbiol, DK-2650 Hvidovre, Denmark
[4] Hillerod Hosp, Dept Clin Microbiol, Hillerod, Denmark
关键词
SPECTRUM-BETA-LACTAMASE; ESCHERICHIA-COLI; SHOCK-PROTEIN; LACTOCOCCUS-LACTIS; STRESS TOLERANCE; BACTEREMIA; INFECTIONS; EPIDEMIOLOGY; PROTEOLYSIS; GENES;
D O I
10.1371/journal.pone.0015467
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Klebsiella pneumoniae is an important opportunistic pathogen and a frequent cause of nosocomial infections. We have characterized a K. pneumoniae strain responsible for a series of critical infections in an intensive care unit over a two-year period. The strain was found to be remarkably thermotolerant providing a conceivable explanation of its persistence in the hospital environment. This marked phenotype is mediated by a novel type of Clp ATPase, designated ClpK. The clpK gene is encoded by a conjugative plasmid and we find that the clpK gene alone renders an otherwise sensitive E. coli strain resistant to lethal heat shock. Furthermore, one third of a collection of nosocomial K. pneumoniae isolates carry clpK and exhibit a heat resistant phenotype. The discovery of ClpK as a plasmid encoded factor and its profound impact on thermal stress survival sheds new light on the biological relevance of Clp ATPases in acquired environmental fitness and highlights the challenges of mobile genetic elements in fighting nosocomial infections.
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页数:9
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