阴沟肠杆菌高产AmpC酶和ESBLs的检测及其耐药性研究

目的:了解本地区阴沟肠杆菌高产AmpC酶和超广谱β-内酰胺酶(ESBLs)的流行状况及其耐药性。方法:收集154株临床分离无重复阴沟肠杆菌,通过改良三维实验检测阴沟肠杆菌高产AmpC酶和超广谱β-内酰胺酶(ESBLs),运用K-B琼脂扩散法进行药物敏感性试验。结果:在154株菌中,18.83%的菌株单产ESBLs,22.73%的菌株单产AmpC酶,5.19%的菌株同时产AmpC酶和ESBLs,53.25%的菌株AmpC酶和ESBLs均不产生。产不同类型β-内酰胺酶其耐药性有所不同。结论:本地区阴沟肠杆菌产AmpC酶和ESBLs的流行处于一个相对较高的水平。高产AmpC酶菌株对一、二、三代头孢菌素、头孢西丁、酶抑制剂复合制剂等高度耐药,对头孢吡肟敏感,而产ESBLs菌株对三代头孢菌素、头孢吡肟均不同程度耐药,而对各种酶抑制剂复合制剂保持较高的敏感性,因此,产Ampc酶及ES-BLs酶的细菌的耐药性不完全相同,产酶类型不同需选用不同类型的抗生素。

Study on the Detection of AmpC Enzyme Hyperproduction and Extended-spectrum β-lactamases and its Antimicribial Resistance in Clinical Isolates of Enterobacter Cloacae

Objective To detect the stably derepressed expression of AmpC β-lactamases(AmpC)and extended spectrum β-lactamases(ESBLs)of Enterobacter cloacae,and its antimicrobial activities.Methods 154 clinical strains of Enterobacter cloacae were collected from five hospitals in Xi'an area from January 2004 to June 2005;Modified three-dimensional of cefoxitin/cefiriaxone test were used to detect AmpC and ESBLs respectively;Lirby-Bauer(K-B)method were performed to detect the susceptibility of 16 antimicrobial agents against Enterobacter cloacae.Results The incidence rate of single producing AmpC was 22.73%;the incidence rate of single producing ESBLs was 18.83%;the incidence rate of producing both enzymes was 5.19%;the incidence rate of producing neither AmpC nor ESBLs was 53.25%.Conclusion The study demonstrated that the prevalence of strains producing AmpC and/or ESBLs isolated from patients in Xi'an area was at a higher level compared with other cities in our country;the strains producing AmpC and/or producing ESBLs were multiple-antibiotics-resistant to β-lactamases cephalosporins;the best antibiotics for treatment of infections caused by AmpC-producing strains in Enterobacier cloacae is Imipenem,followed by Cefpirome;the best antibiotics for treatment of infections caused by ESBLs-producing strains is Imipenem,followed by Piperacillin/Tazobactam and Cefoperazone/Sulbatam;hyperproduction of the AmpC β-lactamase and/or ESBLs had been documented as a prevalent mechanism of β-lactam resistance in Enterobacter cloacae.