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作 者:张艳芳[1] 冯广满 ZHANG Yan-fang;FENG Guang-man(Department of Clinical Laboratory, Huangpu District People' s Hospital, Zhongshan 528429, Chin)
机构地区:[1]中山市黄圃人民医院检验科,广东中山528429
出 处:《南昌大学学报(医学版)》2018年第2期19-22,26,共5页Journal of Nanchang University:Medical Sciences
基 金:中山市医学科研基金(2016A020227)
摘 要:目的分析铜绿假单胞菌(PA)引起院内感染的分布特点及其耐药性,探讨耐亚胺培南类PA的耐药机制。方法采用全自动细菌鉴定系统分析297例院内感染患者的PA分布及耐药性;应用结晶紫和实时定量聚合酶链反应方法分别检测亚胺培南耐药型和敏感型PA的生物膜形成能力及oprD基因的mRNA表达水平。结果分离出327株PA,检出率约为8.0%(327/4103),其中PA在痰液中分布最广,占51.1%(167/327),内二科的标本检出率最高,约占25.4%(83/327);对阿米卡星的耐药率最低,为8.6%,对头孢曲松的耐药率最高,占87.8%,对阿米卡星敏感率最高,约90.2%,对头孢噻肟敏感率最低,仅7.5%;亚胺培南耐药型PA的生物膜形成能力较敏感型PA更强,且oprD基因的mRNA表达水平较敏感型PA更低(均P<0.05)。结论 PA院内感染以内二科多见,多存在于痰液中,易对头孢曲松产生耐药,对阿米卡星更敏感;亚胺培南耐药型PA易于形成生物膜,其发生机制可能与oprD基因mRNA表达水平下降有关。Objective To analyze the distribution characteristics and drug resistance of nosocomial Pseudomonas aeruginosa(PA),and to investigate the mechanism of imipenem resistance.Methods The distribution and resistance of PA were analyze using the automatic bacterial identification system in 297 patients with nosocomial infection.In addition,imipenem resistance and biofilm formation of sensitive PA were detected crystal violet staining,and mRNA expression of oprD gene was measured by quantitative real-time PCR.Results A total of 327 strains of PA were isolated.The detection rate was 8.0%(327/4103).The PA was distributed most widely in phlegm(51.1%,167/327),and was detected mostly in the Second Department of Internal Medicine(25.4%,83/327).The highest and lowest resistance rates were found for ceftriaxone(87.8%)and amikacin(8.6%),respectively.The highest and lowest sensitive rates were found for amikacin(90.2%)and cefotaxime(7.5%),respectively.Compared with sensitive PA,biofilm forming ability but oprD mRNA expression decreased in resistant PA(P〈0.05).Conclusion Nosocomial PA is detected mostly in the Second Department of Internal Medicine and found mostly in phlegm.The PA is often resistant to ceftriaxone and sensitive to amikacin.Biofilm formation easily occurred in imipenem-resistant PA,and the mechanism may be involved in the down-regulation of oprD expression.
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