甲型副伤寒沙门菌超广谱β-内酰胺酶和喹诺酮类耐药基因检测  

Detection of Extended-spectrum β-Lactamases and Quinolone Resistant Gene in Salmonella paratyphi A

作　　者：陈希莲[1] 朱德全[2] 季海生[2] 

机构地区：[1]临沂市人民医院门诊部,山东临沂276003 [2]临沂市人民医院临床检验中心,山东临沂276003

出　　处：《中华医院感染学杂志》2010年第18期2749-2751,共3页Chinese Journal of Nosocomiology

摘　　要：目的探讨甲型副伤寒沙门菌(SAA)对喹诺酮类药物的耐药性变异产超广谱β-内酰胺酶(ESBLs)的机制。方法对2007-2008年67株萘啶酸耐药菌株进行喹诺酮类药物耐药分析和耐药基因检测,药敏检测采用VITEK32、Etest和纸片扩散法进行;耐药基因采用聚合酶链反应(PCR)技术扩增含有喹诺酮类耐药基因决定区(QRDR)gyrA、gyrB、parC、parE基因片段;ESBL包括SHV、TEM、CTX-M和AmpC型β-内酰胺酶。结果 67株萘啶酸耐药菌株58株发生gyrA基因在Ser83位或Asp87位发生突变,gyrB、parC和parE未发现突变,突变株SHV、TEM、CTX-M阳性率分别为7.5%、4.8%、1.5%,未检出AmpC耐药基因;萘啶酸耐药率由0上升至100.0%。结论 SAA对喹诺酮类耐药严重,主要机制是QRDR gyrA基因的第Ser83位或Asp87位表现出高频突变,其耐药表型和基因突变有较高的一致性。OBJECTIVE To evaluate the variation in drug resistance of Salmonella paratyphi A（SAA） to quinolones and extended-spectrum β-lactamases（ESBLs） and their mechanism.METHODS A total of 67 strains of clinical SAA were collected between 2003 and 2008,the drug resistance was analyzed to nalidixic acid（collected between 2007 and 2008）.Antimicrobial susceptibility test was conducted by VITEK-32 system or disk agar diffusion method and Etest;genotypes（gyrA,gyrB,parC and parE、） of quinolone resistance-determining region（QRDR） and ESBLs of SHV,TEM,CTX-M and AmpC determination were analyzed by PCR method and DNA sequencingg.RESULTS The resistance rate to nalidixic acid increased from 0.0% to 100%.The laboratory examination of genotypes of 58 quinolone-resistant SAA strains had identical mutation of gyrA gene,that had Ser at the site of Ser 83 and Asp87.The mutations of gyrB,parC and parE genes were not found.The positive rates of SHV,TEM and CTX-M were 7.5%,4.8%and 1.5%,respectively.AmpC β-lactamase was not found.CONCLUSION The drug resistance of SAA to quinolones is severe,the main mechanism is point mutation Ser 83 and Asp87 of QRDA gyrA gene,and the drug-resistance phenotype and the gene mutation have a high identity.

关 键 词：沙门菌属 甲型副伤寒 喹诺酮类药 耐药 

分 类 号：R378.24[医药卫生—病原生物学]