由MgrB调节因子失活引起的黏菌素耐药性与序列型258产KPC碳青霉烯酶肺炎克雷伯菌的毒力降低无关。
Colistin Resistance Caused by Inactivation of the MgrB Regulator Is Not Associated with Decreased Virulence of Sequence Type 258 KPC Carbapenemase-Producing Klebsiella pneumoniae.
作者信息
Arena Fabio, Henrici De Angelis Lucia, Cannatelli Antonio, Di Pilato Vincenzo, Amorese Marina, D'Andrea Marco Maria, Giani Tommaso, Rossolini Gian Maria
机构信息
Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Department of Surgery and Translational Medicine, University of Florence, Florence, Italy.
出版信息
Antimicrob Agents Chemother. 2016 Mar 25;60(4):2509-12. doi: 10.1128/AAC.02981-15. Print 2016 Apr.
Abstract
Using aGalleria mellonellaanimal model, we compared the virulence of two sequence type 258 (ST258) KPC-producingKlebsiella pneumoniaestrains, which were representative of the two clades of this clonal lineage, with that of isogenic colistin-resistantmgrBmutants. With both strains, themgrBmutants did not exhibit modification in virulence. In theG. mellonellamodel, the clade 1 strain (capsular typecps-1[wzi29, producing KPC-2]) was significantly more virulent than the clade 2 strain (capsular typecps-2[wzi154, producing KPC-3]).
摘要
利用家蚕模型，我们比较了两个序列型258（ST258）产KPC的肺炎克雷伯菌菌株（它们代表了该克隆谱系的两个分支）与同基因耐黏菌素mgrB突变体的毒力。对于这两个菌株，mgrB突变体的毒力均未表现出改变。在家蚕模型中，分支1菌株（荚膜型cps-1[wzi29，产KPC-2]）的毒力显著高于分支2菌株（荚膜型cps-2[wzi154，产KPC-3]）。
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