Azoulay-Dupuis E, Mohler J, Bédos J P
INSERM, EMI-9933, Faculté de Médecine Xavier Bichat, Paris, France.
Antimicrob Agents Chemother. 2004 Jan;48(1):80-5. doi: 10.1128/AAC.48.1.80-85.2004.
The efficacy of BB-83698, a novel potent peptide deformylase inhibitor, was evaluated in a mouse model of acute pneumonia. The Streptococcus pneumoniae isolates tested included four virulent strains (one penicillin-susceptible wild-type strain, one macrolide-resistant strain, and two quinolone-resistant mutants [a mutant carrying mutations in ParC and GyrA and an efflux mutant] isogenic to the wild type) and two poorly virulent penicillin-resistant strains. Pneumonia was induced by intratracheal inoculation of 10(5) CFU (virulent strains) into immunocompetent mice or 10(7) CFU (less virulent strains) into leukopenic mice. Animals received three or six subcutaneous injections of antibiotics at 12- or 24-h intervals, with antibiotic treatment initiated at 3, 6, 12, or 18 h postinfection (p.i.). BB-83698 showed potent in vitro activity against all strains (MICs, 0.06 to 0.25 micro g/ml). In the in vivo model, all control animals died within 2 to 5 days of infection. BB-83698 (80 mg/kg of body weight twice daily or 160 mg/kg once daily) protected 70 to 100% of the animals, as measured 10 days p.i., regardless of the preexisting resistance mechanisms. In contrast, the survival rates for animals treated with the comparator antibiotics were 30% for animals treated with erythromycin (100 mg/kg) and infected with the macrolide-resistant strain, 34% for animals treated with amoxicillin (200 mg/kg every 8 h) and infected with the penicillin-resistant strain, and 0 and 78% for animals treated with ciprofloxacin (250 mg/kg) and infected with the ParC and GyrA mutant and the efflux mutant, respectively. At 80 mg/kg, BB-83698 generated a peak concentration in lung tissue of 61.9 micro g/ml within 1 h and areas under the concentration-times curves of 57.4 and 229.4 micro g. h/ml for plasma and lung tissue, respectively. The emergence of S. pneumoniae isolates with reduced susceptibilities to BB-83698 was not observed following treatment with a suboptimal dosing regimen. In conclusion, the potent in vitro activity of BB-83698 against S. pneumoniae, including resistant strains, translates into good in vivo efficacy in a mouse pneumonia model.
在急性肺炎小鼠模型中评估了新型强效肽脱甲酰基酶抑制剂BB - 83698的疗效。所检测的肺炎链球菌分离株包括4株强毒株(1株对青霉素敏感的野生型菌株、1株对大环内酯类耐药的菌株以及2株与野生型同基因的喹诺酮类耐药突变株[1株携带ParC和GyrA突变的突变株以及1株外排突变株])和2株低毒力的耐青霉素菌株。通过向免疫活性小鼠气管内接种10⁵CFU(强毒株)或向白细胞减少的小鼠气管内接种10⁷CFU(低毒力菌株)来诱导肺炎。动物在感染后3、6、12或18小时接受抗生素皮下注射,每12或24小时注射一次,共注射3次或6次。BB - 83698对所有菌株均显示出强大的体外活性(MIC为0.06至0.25μg/ml)。在体内模型中,所有对照动物在感染后2至5天内死亡。无论先前存在何种耐药机制,BB - 83698(每日两次,80mg/kg体重或每日一次,160mg/kg)在感染后10天测量时可保护70%至100%的动物。相比之下,用对照抗生素治疗的动物的存活率如下:用红霉素(100mg/kg)治疗并感染大环内酯类耐药菌株的动物为30%,用阿莫西林(每8小时200mg/kg)治疗并感染耐青霉素菌株的动物为34%,用环丙沙星(250mg/kg)治疗并感染ParC和GyrA突变株及外排突变株的动物分别为0和78%。在80mg/kg剂量下,BB - 83698在1小时内可使肺组织中的峰值浓度达到61.9μg/ml,血浆和肺组织的浓度 - 时间曲线下面积分别为57.4和229.4μg·h/ml。在采用次优给药方案治疗后,未观察到对BB - 83698敏感性降低的肺炎链球菌分离株的出现。总之,BB - 83698对包括耐药菌株在内的肺炎链球菌具有强大的体外活性,在小鼠肺炎模型中转化为良好的体内疗效。