首页> 美国卫生研究院文献>Antimicrobial Agents and Chemotherapy >Doripenem MICs and ompK36 Porin Genotypes of Sequence Type 258 KPC-Producing Klebsiella pneumoniae May Predict Responses to Carbapenem-Colistin Combination Therapy among Patients with Bacteremia
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Doripenem MICs and ompK36 Porin Genotypes of Sequence Type 258 KPC-Producing Klebsiella pneumoniae May Predict Responses to Carbapenem-Colistin Combination Therapy among Patients with Bacteremia

机译:258型序列的Doripenem MIC和ompK36孔蛋白基因型可产生KPC的肺炎克雷伯菌可预测细菌血症患者对碳青霉烯-科力汀联合疗法的反应

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摘要

Treatment failures of a carbapenem-colistin regimen among patients with bacteremia due to sequence type 258 (ST258), KPC-2-producing Klebsiella pneumoniae were significantly more likely if both agents were inactive in vitro, as defined by a colistin MIC of >2 μg/ml and the presence of either a major ompK36 porin mutation (guanine and alanine insertions at amino acids 134 and 135 [ins aa 134–135 GD], IS5 promoter insertion [P = 0.007]) or a doripenem MIC of >8 μg/ml (P = 0.01). Major ompK36 mutations among KPC-K. pneumoniae strains are important determinants of carbapenem-colistin responses in vitro and in vivo.
机译:如果细菌和细菌的MIC≥2μg,则两种细菌在体外均无活性,那么由于序列类型258(ST258),产生KPC-2的肺炎克雷伯菌而导致的细菌血症患者中碳青霉烯-colistin方案的治疗失败可能性更高/ ml或存在主要的ompK36孔蛋白突变(在134和135位氨基酸的鸟嘌呤和丙氨酸插入[在134–135 GD氨基酸中],IS5启动子插入[P = 0.007])或多立尼姆MIC> 8μg/ ml(P = 0.01)。 KPC-K中的主要ompK36突变。肺炎菌株是体外和体内碳青霉烯-colistin反应的重要决定因素。

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