In order to compare and evaluate three animal models for studying the pathogenicity of Staphylococcus epidermidis strains, three experimental animal models, namely, murine intra2venous LD50, mouse foreign body infection and rat central venous catheter (CVC) infection models were used to assess the relative virulence of two S. epidermidis strains, ATCC 12228 and 972337. The results from three animal models were comparable, indicating S. epidermidis 972337 was more viru-lent than strain ATCC 12228. The rat CVC infection model best mimicked the conditions of clinical patients with intra2venous catheters, and more information could be obtained from this model. We conclude that different in vivo models serve for dif-ferent purposes, and the rat CVC infection model is most suitable for studying specific characteristics of catheter related in-fections caused by S. epidermidis strains.

目的 检测福氏志贺菌喹诺酮类耐药临床分离株DNA旋转酶gyrA和拓扑异构酶ⅣparC基因的突变情况，探讨GyrA和ParC氨基酸改变与喹诺酮类耐药的相关性。方法 根据药敏实验结果选取47株福氏志贺菌临床分离菌，对其gyrA、parC喹诺酮耐药决定区（QRDR）进行聚合酶链反应（PCR）扩增和测序分析，并采用SAS（V8.2）软件分析GyrA和ParC改变和喹诺酮类耐药性的关联程度。结果 44株喹诺酮类耐药菌在gyrA、parC基因QRDR均发生有义突变，gyrA83位密码子突变（TCG→TTG）最为常见，存在于43株耐药菌。混合模型分析结果显示GyrA83位、ParC80位氨基酸改变与萘啶酸的耐药性密切相关（P<0.01，R2=0.999），GyrA83、87位氨基酸改变与环丙沙星的耐药性密切相关（P<0.05，R2=0.872）。结论 GyrASer83→Leu突变是导致福氏志贺菌临床株对喹诺酮类耐药的关键突变，此单位点突变即可介导福氏志贺菌对萘啶酸的耐药，但对环丙沙星耐药需同时存在GyrA和/或ParC多个位点突变或其他耐药机制。