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作 者:罗润齐[1] 叶晓光[1] 王若伦[2] 何少璋[3]
机构地区:[1]广州医学院第二附属医院感染病科,510260 [2]广州医学院第二附属医院药学部,510260 [3]广州医学院第二附属医院预防保健科,510260
出 处:《中华生物医学工程杂志》2010年第5期430-433,共4页Chinese Journal of Biomedical Engineering
基 金:广州市医药卫生科技一般引导项目(2008-YB-165)
摘 要:目的 对比临床耐药株与经头孢他啶诱导形成的耐药株(诱导耐药株)CTX-M型超广谱β-内酰胺酶(ESBL)基因在阴沟肠杆菌中的表达情况.方法 取临床分离的对头孢他啶敏感的10株阴沟肠杆菌,应用不同浓度梯度头孢他啶[1/2×最小抑菌浓度(MIC)、1× MIC、2×MIC、4×MIC并呈倍数到128 mg/L]逐级诱导并使其成为耐药株.分别培养诱导耐药株及临床敏感株、临床耐药株各10株,并提取其DNA.采用PCR检测诱导耐药株及临床敏感株、临床耐药株CTX-M型ESBL基因的表达情况.结果 成功诱导出对头孢他啶耐药的阴沟肠杆菌形成诱导耐药株.PCR结果显示在10株诱导耐药株中,有5株表达CTX-M型ESBL基因,可见约900 bp的条带形成 在10株临床耐药株中,则有4株可见约900 bp的条带形成 在10株临床敏感株中则未见此条带形成.结论 头孢他啶可以诱导CTX-M型ESBL基因的表达,临床头孢他啶的不合理使用可能是诱导其产生的重要原因之一.Objective To compare the different expressions of CTX-M type extended spectrum β-lactamases (ESBLs) gene in ceftazidime-induced vs clinically isolated strains of drug-resistant Enterobacter cloacae. Methods Ten ceftazidime-sensitivestrains of Enterobacter cloacae isolated from clinical patients were induced into drug-resistant strains by different concentrations of ceftazidime [half time of the minimal inhibitory concentration (MIC) , one time of the MIC, two times of the MIC, four times of the MIC and multiplied to 128 mg/L]. Each 10 of induced drug-resistant strains, clinical sensitive strains and clinical drug-resistant strains were cultured and extracted for their DNAs. Different expressions of CTX-M type ESBLs gene of induced drug- resistant strains, clinical sensitive strains and clinical drug- resistant strains were amplified by PCR. Results Induced drug- resistant strains of Enterobacter cloacae previously sensitive to ceftazidime were obtained. Of the induced drug-resistant strains, five expressed CTX-M type ESBLs with a PCR product fragment about 900 bp in size. Of the clinical drug-resistant strains, four expressed CTX-M type ESBLs with a PCR product fragment about 900 bp in size. No such PCR product fragment was found in clinical sensitive strains. Conclusion CTX- M type ESBLs can be expressed in sensitive Enterobacter cloacae stains after induction with ceftazidime, suggesting that irrational use of ceftazidime in clinical practice may be one of the major causes for ESBLs production.
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