产超广谱β-内酰胺酶大肠埃希菌耐药性及基因型分析

目的 了解本院超广谱β-内酰胺酶(ESBLs)基因在大肠埃希菌中的分布类型及对常用抗菌药物耐药情况,为临床合理用药提供依据.方法 用确证法对54株产超广谱β-内酰胺酶大肠埃希菌进行确证,用PCR的方法扩增ESBLs基因片段,用K-B纸片扩散法检测对抗菌药物的敏感性.结果 125株大肠埃希菌中,ESBLs阳性率为43.2%.对青霉素类和第一、二代头孢菌素的耐药率为100%,对头孢噻肟、头孢哌酮和头孢曲松的耐药率在95%以上,对头孢他啶的耐药率为31.5%;对环丙沙星和复方新诺明的耐药率分别为79.6%和83.3%;对β-内酰胺类/酶抑制剂复合制剂仍保持较高的敏感性;未发现耐亚胺培南菌株.含耐药基因型CTX-M 型49株、TEM型33株、SHV型1株,同时含有两种基因型达29株.结论 产ESBLs大肠埃希菌对18种抗菌药物的耐药情况明显高于非产ESBLs大肠埃希菌.基因型主要为CTX-M,其次为TEM,同时含有两种基因型达29株.明确产ESBLs病原菌的基因型及耐药性对临床抗感染治疗及感染控制有较大意义.

Drug resistance and genotype analysis of Escherichia coil producing ESBLs

Objective To investigate the genotype and antimicrobial resistance of ESBL-producing Escherichia coil(E.coli) in this hospital to provide basis of reasonable drug usage.Methods Strains with a zone diameter for cefpodoxime less or equal with 23 mm were detected by phenotypic confirmatory test for ESBLs production and all screening test-positive strains were examined with PCR to detect the following ESBL genes:CTX-M,SHV and TEM.ESBLs-positive strains were detected for antimicrobial resistance by using disc diffusion test.Results The positive rate of ESBLs-producing was 43.2% in 125 strains of E.coil.Of these 54 strains,antimicrobial resistance rates to penicillin and cephalosporin I,II were 100%,to cephalosporins,cefoperazone and ceftriaxone were all above 95%,to ceftazidime was 31.5%,to ciprofloxacin and cotrimoxazole were 79.6% and 83.3%,respectively.ESBLs-producing E.coli was sensitive to most β-Lactamase inhibitors,and resistant to imipenem.The distribution of isolates with the ESBLs positive were as follows:CTX-M(n=21),TEM(n=4),SHV and TEM(n=1),TEM and CTX-M(n=28).Conclusion Antimicrobial resistances of ESBLs-producing E.coli might be more sensitive in 18 types of antibiotics than non ESBL-producing E.coli.The majority of the ESBLs positive clinical isolates of E.coli could carry CTX-M gene followed by both TEM and CTX-M.ESBL production in E.coli should be promptly detected and reported as it could help in treating individual cases and also in controlling the spread of these resistant phenotypes to other individuals.