在一株奇异变形杆菌临床分离株中 blaNDM-1 碳青霉烯酶基因整合到变形杆菌基因组岛 1（PGI1-PmPEL）中。
Integration of the blaNDM-1 carbapenemase gene into Proteus genomic island 1 (PGI1-PmPEL) in a Proteus mirabilis clinical isolate.
机构信息
INSERM U914 'Emerging Resistance to Antibiotics', Faculté de Médecine et Université Paris Sud, K.-Bicêtre, France.
INSERM U914 'Emerging Resistance to Antibiotics', Faculté de Médecine et Université Paris Sud, K.-Bicêtre, France Medical and Molecular Microbiology Unit, Department of Medicine, Faculty of Science, University of Fribourg, Fribourg, Switzerland.
出版信息
J Antimicrob Chemother. 2015 Jan;70(1):98-102. doi: 10.1093/jac/dku371. Epub 2014 Sep 18.
OBJECTIVES
To decipher the mechanisms and their associated genetic determinants responsible for β-lactam resistance in a Proteus mirabilis clinical isolate.
METHODS
The entire genetic structure surrounding the β-lactam resistance genes was characterized by PCR, gene walking and DNA sequencing.
RESULTS
Genes encoding the carbapenemase NDM-1 and the ESBL VEB-6 were located in a 38.5 kb MDR structure, which itself was inserted into a new variant of the Proteus genomic island 1 (PGI1). This new PGI1-PmPEL variant of 64.4 kb was chromosomally located, as an external circular form in the P. mirabilis isolate, suggesting potential mobility.
CONCLUSIONS
This is the first known description of the bla(NDM-1) gene in a genomic island structure, which might further enhance the spread of the bla(NDM-1) carbapenemase gene among enteric pathogens.
目的
解析导致奇异变形杆菌临床分离株产生β-内酰胺类耐药的机制及其相关遗传决定因素。
方法
通过 PCR、基因步移和 DNA 测序对β-内酰胺类耐药基因周围的整个遗传结构进行了特征描述。
结果
编码碳青霉烯酶 NDM-1 和 ESBL VEB-6 的基因位于一个 38.5 kb 的多药耐药结构中，该结构本身插入到一个新的奇异变形杆菌基因组岛 1（PGI1）变体中。这个 64.4 kb 的新型 PGI1-PmPEL 变体位于染色体上，以 P. mirabilis 分离株的外环形式存在，表明其具有潜在的可移动性。
结论
这是首次在基因组岛结构中描述 bla(NDM-1) 基因，这可能进一步促进 bla(NDM-1)碳青霉烯酶基因在肠道病原体中的传播。
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