Azoulay-Dupuis E, Bédos J P, Mohler J, Moine P, Cherbuliez C, Peytavin G, Fantin B, Köhler T
INSERM EMI-U 9933, Faculté Xavier Bichat, 16, rue Henri Huchard, 75870 Paris Cedex 18, France.
Antimicrob Agents Chemother. 2005 Mar;49(3):1046-54. doi: 10.1128/AAC.49.3.1046-1054.2005.
Gemifloxacin is a novel fluoronaphthyridone quinolone with enhanced in vitro activity against Streptococcus pneumoniae. We investigated the activities of gemifloxacin and trovafloxacin, their abilities to select for resistance in vitro and in vivo, and their efficacies in a mouse model of acute pneumonia. Immunocompetent Swiss mice were infected with 10(5) CFU of a virulent, encapsulated S. pneumoniae strain, P-4241, or its isogenic parC, gyrA, parC gyrA, and efflux mutant derivatives (serotype 3); and leukopenic mice were infected with 10(7) CFU of two poorly virulent clinical strains (serotype 11A) carrying either a parE mutation or a parC, gyrA, and parE triple mutation. The drugs were administered six times every 12 h, starting at either 3 or 18 h postinfection. In vitro, gemifloxacin was the most potent agent against strains with and without acquired resistance to fluoroquinolones. While control mice died within 6 days, gemifloxacin at doses of 25 and 50 mg/kg of body weight was highly effective (survival rates, 90 to 100%) against the wild-type strain and against mutants harboring a single mutation, corresponding to area under the time-versus-serum concentration curve at 24 h (AUC(24))/MIC ratios of 56.5 to 113, and provided a 40% survival rate against a mutant with a double mutation (parC and gyrA). A total AUC(24)/MIC ratio of 28.5 was associated with poor efficacy and the emergence of resistant mutants. Trovafloxacin was as effective as gemifloxacin against mutants with single mutations but did not provide any protection against the mutant with double mutations, despite treatment with a high dose of 200 mg/kg. Gemifloxacin preferentially selected for parC mutants both in vitro and in vivo.
吉米沙星是一种新型氟萘啶酮喹诺酮类药物,对肺炎链球菌具有增强的体外活性。我们研究了吉米沙星和曲伐沙星的活性、它们在体外和体内诱导耐药的能力以及它们在急性肺炎小鼠模型中的疗效。免疫功能正常的瑞士小鼠感染10⁵CFU的强毒、有荚膜肺炎链球菌菌株P-4241或其同基因的parC、gyrA、parC gyrA和外排突变衍生物(血清型3);白细胞减少的小鼠感染10⁷CFU的两种携带parE突变或parC、gyrA和parE三重突变的低毒临床菌株(血清型11A)。药物在感染后3或18小时开始,每12小时给药6次。在体外,吉米沙星是对氟喹诺酮类有或无获得性耐药的菌株最有效的药物。对照小鼠在6天内死亡,而体重25和50mg/kg的吉米沙星对野生型菌株和携带单个突变的突变体高度有效(存活率90%至100%),对应的24小时时间-血清浓度曲线下面积(AUC₂₄)/MIC比值为56.5至113,对双突变(parC和gyrA)突变体的存活率为40%。总AUC₂₄/MIC比值为28.5与疗效不佳和耐药突变体的出现有关。曲伐沙星对单突变突变体的效果与吉米沙星相同,但尽管给予200mg/kg的高剂量治疗,对双突变突变体却没有提供任何保护。吉米沙星在体外和体内都优先选择parC突变体。