Gerber A U, Vastola A P, Brandel J, Craig W A
J Infect Dis. 1982 Nov;146(5):691-7. doi: 10.1093/infdis/146.5.691.
The therapeutic failure of aminoglycosides in leukopenic mice was studied. Pseudomonas aeruginosa isolated from experimentally infected leukopenic mice was analyzed for susceptibility to gentamicin. Bacterial population analyses were performed before, during, and after therapy with high doses of gentamicin. Inocula from numerous strains, including P. aeruginosa strain ATCC 27853, harbored slowly growing aminoglycoside-resistant subpopulations. In leukopenic mice (in contrast to normal mice) receiving gentamicin, the breakthrough growth of these subpopulations occurred 6 hr after treatment. Resistance to gentamicin reversed in vivo when gentamicin treatment was stopped. The emergence of gentamicin-resistant subpopulations was successfully suppressed by a combined treatment regimen of gentamicin and ticarcillin. Gentamicin-ticarcillin synergy in these infections is due, in part, to antimicrobial suppression of slowly growing aminoglycoside-resistant subpopulations of bacteria.
对氨基糖苷类药物在白细胞减少小鼠中的治疗失败情况进行了研究。对从实验感染的白细胞减少小鼠中分离出的铜绿假单胞菌进行了庆大霉素敏感性分析。在用高剂量庆大霉素治疗前、治疗期间及治疗后进行了细菌群体分析。来自包括铜绿假单胞菌ATCC 27853菌株在内的众多菌株的接种物中,含有生长缓慢的耐氨基糖苷类亚群。在接受庆大霉素治疗的白细胞减少小鼠(与正常小鼠相比)中,这些亚群在治疗后6小时出现突破性生长。当停止庆大霉素治疗时,体内对庆大霉素的耐药性逆转。庆大霉素和替卡西林联合治疗方案成功抑制了耐庆大霉素亚群的出现。在这些感染中,庆大霉素 - 替卡西林协同作用部分归因于对生长缓慢的耐氨基糖苷类细菌亚群的抗菌抑制作用。