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ISPpu22,一种来自伊朗德黑兰一名烧伤患者的耐碳青霉烯类铜绿假单胞菌分离株的oprD孔蛋白基因中的新型插入序列。

ISPpu22, a novel insertion sequence in the oprD porin gene of a carbapenem-resistant Pseudomonas aeruginosa isolate from a burn patient in Tehran, Iran.

作者信息

Kalantar-Neyestanaki Davood, Emaneini Mohammad, Jabalameli Fereshteh, Taherikalani Morovat, Mirsalehian Akbar

机构信息

Department of Microbiology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

Department of Microbiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Iran J Microbiol. 2015 Oct;7(5):247-50.

Abstract

BACKGROUND AND OBJECTIVES

The oprD mutation and AmpC overproduction are the main mechanisms of intrinsic resistance to carbapenems such as imipenem and meropenem in Pseudomonas aeruginosa.

MATERIALS AND METHODS

In this study, we investigated intrinsic resistance to carbapenems including mutation of oprD and AmpC overproduction in a carbapenem-resistant P. aeruginosa isolated from a burn patient by phenotypic and molecular methods.

RESULTS

In our study, the carbapenem-resistant P. aeruginosa isolate was resistant to imipenem, meropenem, cefepime, gentamicin, ceftriaxone, carbenicillin, aztreonam and ciprofloxacin but was susceptible to ceftazidime and polymyxin B. The minimum inhibitory concentrations (MICs) against imipenem, meropenem and ceftazidime were 64 μg/ml, 16 μg/ml and 2μg/ml, respectively. The isolate was ESBLs and AmpC overproducer. No carbapenemase activity was detected by Modified Hodge test (MHT). This isolate was carrying only bla OXA-10 . PCR amplification and sequencing of oprD performed on isolate resulted in PCR product of 2647bp. Sequence analysis of the 2647bp product revealed insertion of a sequence of 1232 bp at position 8 in coding region of oprD.

CONCLUSION

According to the results of this study, oprD mutation and AmpC overproduction can cause the main mechanism of resistance of P. aeruginosa to carbapenems.

摘要

背景与目的

oprD基因突变和AmpC过度表达是铜绿假单胞菌对亚胺培南和美罗培南等碳青霉烯类抗生素固有耐药的主要机制。

材料与方法

在本研究中,我们通过表型和分子方法,对从一名烧伤患者分离出的耐碳青霉烯类铜绿假单胞菌的碳青霉烯类抗生素固有耐药性进行了研究,包括oprD基因突变和AmpC过度表达情况。

结果

在我们的研究中,耐碳青霉烯类铜绿假单胞菌分离株对亚胺培南、美罗培南、头孢吡肟、庆大霉素、头孢曲松、羧苄青霉素、氨曲南和环丙沙星耐药,但对头孢他啶和多粘菌素B敏感。对亚胺培南、美罗培南和头孢他啶的最低抑菌浓度(MIC)分别为64μg/ml、16μg/ml和2μg/ml。该分离株为超广谱β-内酰胺酶(ESBLs)和AmpC过度表达菌株。改良Hodge试验(MHT)未检测到碳青霉烯酶活性。该分离株仅携带blaOXA-10。对分离株进行oprD的PCR扩增和测序,得到2647bp的PCR产物。对2647bp产物的序列分析显示,在oprD编码区第8位插入了一段1232bp的序列。

结论

根据本研究结果,oprD基因突变和AmpC过度表达可导致铜绿假单胞菌对碳青霉烯类抗生素耐药的主要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c79/4695505/33749e893b2f/IJM-7-247-g001.jpg

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