Rifampicin enhances activity of daptomycin and vancomycin against both a polysaccharide intercellular adhesin (PIA)-dependent and -independent Staphylococcus epidermidis biofilm.
Rifampicin enhances activity of daptomycin and vancomycin against both a polysaccharide intercellular adhesin (PIA)-dependent and -independent Staphylococcus epidermidis biofilm.
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Rifampicin 增强达托霉素和万古霉素对抗多糖细胞间粘附素 (PIA) 依赖性和非依赖性表皮葡萄球菌生物膜的活性。
DOI：
10.1093/jac/dkq314
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Fey,PaulD
中科院分区：
文献类型：
--
作者：
Olson,MichaelE;Slater,ShawnR;Rupp,MarkE;Fey,PaulD
Objectives and methodsThis study addressed the efficacy of daptomycin, vancomycin, rifampicin, daptomycin/rifampicin and vancomycin/rifampicin against a polysaccharide intercellular adhesin (PIA)-dependent and -independentStaphylococcus epidermidisbiofilm using flow cell and guinea pig tissue cage models.ResultsThe flow cell model of both PIA-dependent and -independent biofilms demonstrated that the viable cell count after treatment with daptomycin/rifampicin was significantly lower (P< 0.05) than after treatment with vancomycin, vancomycin/rifampicin, daptomycin or rifampicin alone. To validate these observations, a guinea pig tissue cage model was used. The results demonstrated that the addition of rifampicin to daptomycin or vancomycin sterilized 5/6 tissues cages colonized withS. epidermidis1457 (PIA producing). Similar results were noted withS. epidermidis1457 icaADBC::dhfr (non-PIA producing), where daptomycin/rifampicin and vancomycin/rifampicin sterilized 5/6 and 6/6 tissue cages, respectively. There was no statistical difference in comparison with the no-treatment control when both 1457 and 1457 icaADBC::dhfr were treated with vancomycin and daptomycin alone. Furthermore, treatment with rifampicin alone sterilized 5/6 and 3/6 1457 and 1457 icaADBC::dhfr tissue cages, respectively.ConclusionsInterpretation of these data suggests that rifampicin is highly active againstS. epidermidisbiofilms and both vancomycin and daptomycin are effective at reducing the subpopulation of bacteria that develop rifampicin resistance.
