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乌拉圭产KPC肺炎克雷伯菌的出现:感染控制与分子特征分析

Emergence of KPC-producing Klebsiella pneumoniae in Uruguay: infection control and molecular characterization.

作者信息

Marquez C, Ingold A, Echeverría N, Acevedo A, Vignoli R, García-Fulgueiras V, Viroga J, Gonzalez O, Odizzio V, Etulain K, Nuñez E, Albornoz H, Borthagaray G, Galiana A

机构信息

Cátedra de Microbiología, Instituto de Química Biológica, Facultad de Ciencias y de Química-UdelaR, Universidad de la República Montevideo, Uruguay.

Facultad de Química-UdelaR, Cátedra de Microbiología, UdelaR Montevideo, Uruguay.

出版信息

New Microbes New Infect. 2014 May;2(3):58-63. doi: 10.1002/nmi2.40. Epub 2014 Apr 4.

DOI:10.1002/nmi2.40
PMID:25356345
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4184659/
Abstract

We describe the first outbreak of Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-KP), the infection control measures adopted and the shift in resistance patterns of isolates during antibiotic treatment. The ST258 KPC-KP strain exhibited a multiresistant antibiotic phenotype including co-resistance to gentamycin, colistin and tigecycline intermediate susceptibility. Isolates before and after treatment had different behaviour concerning their antibiotic susceptibility and the population analysis profile study. A progressive increase in the aminoglycosides (acquiring amicacin resistance) and β-lactam MICs, and a decreased susceptibility to fosfomycin was observed throughout the administration of combined antimicrobial regimens including meropenem. A high meropenem resistance KPC-KP homogeneous population (MIC 256 Jg/mL), could arise from the meropenem heterogeneous low-level resistance KPC-KP population (MIC 8 Jg/mL), by the selective pressure of the prolonged meropenem therapy. The kpc gene was inserted in a Tn4401 isoform a, and no transconjugants were detected. The core measures adopted were successful to prevent evolution towards resistance dissemination.

摘要

我们描述了首例产肺炎克雷伯菌碳青霉烯酶的肺炎克雷伯菌(KPC-KP)疫情、所采取的感染控制措施以及抗生素治疗期间分离株耐药模式的变化。ST258 KPC-KP菌株表现出多重耐药的抗生素表型,包括对庆大霉素、黏菌素和替加环素中介敏感性的共同耐药。治疗前后的分离株在抗生素敏感性和群体分析谱研究方面表现出不同的行为。在包括美罗培南在内的联合抗菌方案给药过程中,观察到氨基糖苷类(获得阿米卡星耐药性)和β-内酰胺类最低抑菌浓度(MIC)逐渐增加,对磷霉素的敏感性降低。通过延长美罗培南治疗的选择压力,高美罗培南耐药的KPC-KP同源群体(MIC为256μg/mL)可能源自美罗培南异质低水平耐药的KPC-KP群体(MIC为8μg/mL)。kpc基因插入Tn4401亚型a中,未检测到接合子。所采取的核心措施成功地防止了耐药性传播的演变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a30/4184659/577b72667684/nmi20002-0058-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a30/4184659/577b72667684/nmi20002-0058-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a30/4184659/577b72667684/nmi20002-0058-f1.jpg

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