引发泌尿系感染的表皮葡萄球菌致病性研究

Pathogenicity of Staphylococcus epidermidis Causing Urinary Tract Infection

目的 了解引发泌尿系感染的表皮葡萄球菌的致病性。方法 收集2003～2004年临床出现泌尿系感染患者尿液分离的表皮葡萄球菌35株，检测其对红霉素、氨苄西林、头孢西丁、头孢曲松、替考拉宁、环丙沙星、四环素、复方新诺明、万古霉素的最小抑菌浓度（MIC）；对ermA、ermB、ermC、msrA、mecA、icaA基因进行PCR扩增；定量检测生物被膜的产生并用脉冲场凝胶电泳分析其同源性。结果 所分离的菌株中MRSE占71．4％（25株），MSSE占28．6％（10株），对红霉素、氨苄西林、头孢曲松、环丙沙星、四环素和复方新诺明的敏感性较低，分别为22．8％、6．34％、34．9％、26．9％、44．4％和62．2％；对替考拉宁和万古霉素的敏感性较高，分别为99．2％和100．0％；所有对头孢西丁耐药的菌株均检测出mecA基因；在27株红霉素耐药的菌株中以ermC为主，占81．5％；有14株检测出icaA基因，其中生物被膜定量检测中有10株产生物被膜，4株定量试验阴性；PFGE分为18型，显示细菌基因多态性。结论 引发泌尿系感染的表皮葡萄球菌的耐药性较高，且呈多重耐药，临床分离的表皮葡萄球菌检出ica对判断其致病性有提示作用。

OBJECTIVE To understand the pathogenicity of Staphylococcus epidermidis causing urinary tract infection. METHODS Thirty five isolates were collected in the patients with urinary tract infection during 2003- 2004 to test the minimal inhibitory concentration （MIC） to erythromycin, ampicillin, cefoxitin, ceftriaxone, teicoplanin, ciprofloxacin, tetracycline, trimethoprim-sulfamethoxazole and vancomycin. The genes of ermA, ermB, ermC, msrA, mecA, and icaA were amplified by PCR. The biofilm producing of the isolates was determined by the quantitative method. The pulsed-field gel electrophoresis （PFGE） was used to discriminate the homology among the isolates. RESULTS Among the isolates, MRSE accounted for 71.4%. The antibiotic susceptibility to erythromycin, ampicillin, ceftriaxone, ciprofloxacin, tetracycline and trimethoprim-sulfamethoxazole were 22. 8 %, 6.34 %, 34.9 %, 26.9 %, 44.4 % and 62.2 %, respectively, whereas to teicoplanin and vancomycin were 99.2% and 100%. All the isolates resistant to cefoxitin carried mecA. ermC Was the predominant determinant among the erythromycin resistant isolates. Among the 14 icaA positive isolates, 10 isolates were biofilm producing. All the isolates were classified into 18 types by PFGE. CONCLUSIONS The high and multiple antibiotic resistance of S. epidermidis isolates causing urinary tract infection were shown. The detection of icaA gene in clinical S. epidermidis isolates was a signal of their pathogenicity.