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作 者:史利宁[1] 张慧[1] 邵海枫[1] 王卫萍[1] 张小卫[1] 范明[1] 王洁[1]
机构地区:[1]南京军区南京总医院临床中心实验科,南京210002
出 处:《临床检验杂志》2008年第5期327-330,共4页Chinese Journal of Clinical Laboratory Science
基 金:江苏省医学重点学科基金资助项目(批准号:苏卫科教[2001]34)
摘 要:目的了解泛耐型鲍曼不动杆菌(pan-drug resistantAcinetobacter baumannii,PDRAB)的耐药性和产耐药酶的情况,以及介导碳青霉烯酶的基因型及外膜蛋白的改变。方法收集临床分离的PDRAB 68株,用三维试验测定菌株产耐药酶的情况;用琼脂稀释法测定最低抑菌浓度(M IC);用PCR法检测OXA-23基因和IMP-1基因;用SDS-PAGE检测外膜蛋白。结果以头孢三嗪(CRO)为底物,68株PDRAB中单产AmpC酶4株,同时产AmpC酶和ESBL酶1株,产可水解头孢三嗪但不能被克拉维酸(CA)和氯唑西林(CLO)抑制的酶的17株,不分解CRO的46株;以亚胺培南(IMP)为底物,所有PDRAB均产可水解亚胺培南的酶,但不能被EDTA、CA和CLO抑制。M IC结果示PDRAB株对包括IMP在内的常用抗菌药物均高度耐药。68株PDRAB均扩增出OXA-23基因,而IMP-1基因均为阴性。与鲍曼不动杆菌敏感株(S株)相比,PDRAB株和仅亚胺培南敏感株(M株)缺失了分子量约27 000处的蛋白质条带,但在31 000处出现一条新的蛋白质条带;与M株相比,有12株PDRAB在约33 000处出现蛋白质条带的缺失。结论我院分离的68株PDRAB携带OXA-23型碳青霉烯酶基因,大多数存在外膜蛋白的缺失或改变,这些改变可能共同介导了细菌在多重耐药前题下继发的对碳青霉烯类药物的耐药。Objective To investigate the mechanisms of pan-drug resistance Acinetobacter baumannii (PDRAB). Methods Sixty-eight pan-drug resistant Acinetobacter baumannii isolates were collected in our hospital from February 2005 to January 2006. Three-dimensional test, antibiotic susceptibility test, PCR and SDS-PAGE were used to analyze the mechanisms of PDRAB isolates. Results With the substrate of ceftriaxone, 4 PDRAB strains produced AmpC enzyme, 1 strain produced AmpC and ESBL enzyme, 17 strains produced the enzyme which could hydrolyze ceftriaxone but not be inhibited by clavulamic acid (CA) and cloxacillin (CLO). Forty-six strains did not produce enzymes which could hydrolyze ceftriaxone. With the substrate of imipenem, all the PDRAB strains produced the enzyme which could hydrolyze imipenem but not be inhibited by EDTA, CA and CLO. blaOXA-23 gene was confirmed in pan-drug resistance Acinetobacter baumannii. Compared with the susceptible strains, the 27KD protein was lost and a new 31KD protein was found in the resistant strains. Twelve strains of PDRAB lost the protein of 33 KD. Conclusions All PDRABs in Our hospital carded blaOXA-23 gene, and most of them showed loss or modification of outer membrane protein. These changes may be jointly responsible for the carbapenem resistance based on the multiple drug resistance.
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