Entenza J M, Que Y A, Vouillamoz J, Glauser M P, Moreillon P
Division of Infectious Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland.
Antimicrob Agents Chemother. 2001 Nov;45(11):3076-83. doi: 10.1128/AAC.45.11.3076-3083.2001.
The new 8-methoxyquinolone moxifloxacin was tested against two ciprofloxacin-susceptible Staphylococcus aureus strains (strains P8 and COL) and two ciprofloxacin-resistant derivatives of strain P8 carrying a single grlA mutation (strain P8-4) and double grlA and gyrA mutations (strain P8-128). All strains were resistant to methicillin. The MICs of ciprofloxacin and moxifloxacin were 0.5 and 0.125 mg/liter, respectively, for P8; 0.25 and 0.125 mg/liter, respectively, for COL; 8 and 0.25 mg/liter, respectively, for P8-4; and >or=128 and 2 mg/liter, respectively, for P8-128. In vitro, the rate of spontaneous resistance of P8 and COL was 10(-7) on agar plates containing ciprofloxacin at two times the MIC, whereas it was <or=10(-10) on agar plates containing moxifloxacin at two times the MIC. Rats with experimental aortic endocarditis were treated with doses of drugs that simulate the kinetics in humans: moxifloxacin, 400 mg orally once a day; ciprofloxacin, 750 mg orally twice a day; or vancomycin, 1 g intravenously twice a day. Treatment was started either 12 or 24 h after infection and lasted for 3 days. Moxifloxacin treatment resulted in culture-negative vegetations in a total of 20 of 21 (95%) rats infected with P8, 10 of 11 (91%) rats infected with COL, and 19 of 24 (79%) rats infected with P8-4 (P < 0.05 compared to the results for the controls). In contrast, ciprofloxacin treatment sterilized zero of nine (0%) vegetations infected with first-level resistant mutant P8-4. Vancomycin sterilized only 8 of 15 (53%), 6 of 11 (54%), and 12 of 23 (52%) of the vegetations, respectively. No moxifloxacin-resistant derivative emerged among these organisms. However, moxifloxacin treatment of highly ciprofloxacin-resistant mutant P8-128 failed and selected for variants for which the MIC increased two times in 2 of 10 animals. Thus, while oral moxifloxacin might deserve consideration as treatment for staphylococcal infections in humans, caution related to its use against strains for which MICs are borderline is warranted.
新型8-甲氧基喹诺酮莫西沙星针对两株对环丙沙星敏感的金黄色葡萄球菌菌株(P8和COL菌株)以及P8菌株的两株对环丙沙星耐药的衍生物进行了测试,这两株衍生物分别携带单个grlA突变(P8-4菌株)和grlA与gyrA双突变(P8-128菌株)。所有菌株均对甲氧西林耐药。环丙沙星和莫西沙星对P8菌株的最低抑菌浓度(MIC)分别为0.5和0.125mg/L;对COL菌株分别为0.25和0.125mg/L;对P8-4菌株分别为8和0.25mg/L;对P8-128菌株分别为≥128和2mg/L。在体外,P8和COL菌株在含两倍MIC环丙沙星的琼脂平板上的自发耐药率为10^(-7),而在含两倍MIC莫西沙星的琼脂平板上则≤10^(-10)。对患有实验性主动脉心内膜炎的大鼠给予模拟人体动力学的药物剂量进行治疗:莫西沙星,每日口服400mg一次;环丙沙星,每日口服750mg两次;或万古霉素,每日静脉注射1g两次。在感染后12或24小时开始治疗,持续3天。莫西沙星治疗使感染P8的21只大鼠中有20只(95%)、感染COL的11只大鼠中有10只(91%)以及感染P8-4的24只大鼠中有19只(79%)的赘生物培养转为阴性(与对照组结果相比,P<0.05)。相比之下,环丙沙星治疗使感染一级耐药突变体P8-4的9个赘生物中无菌生长(0%)。万古霉素分别仅使15个赘生物中的8个(53%)、11个赘生物中的6个(54%)以及23个赘生物中的12个(52%)无菌生长。在这些生物体中未出现对莫西沙星耐药的衍生物。然而,莫西沙星治疗对环丙沙星高度耐药的突变体P8-128失败,并在10只动物中的2只中筛选出MIC增加两倍的变体。因此,虽然口服莫西沙星可能值得考虑用于治疗人类葡萄球菌感染,但对于其用于MIC处于临界值的菌株时应谨慎使用。