Di Bonaventura Giovanni, Spedicato Ilaria, D'Antonio Domenico, Robuffo Iole, Piccolomini Raffaele
Dipartimento di Scienze Biomediche, Laboratorio di Microbiologia Clinica, Università G. D'Annunzio Istituto per i Trapianti d'organo e Immunocitologia, Consiglio Nazionale delle Ricerche, Sezione di Chieti, Chieti, Italy.
Antimicrob Agents Chemother. 2004 Jan;48(1):151-60. doi: 10.1128/AAC.48.1.151-160.2004.
We investigated the in vitro effects of seven fluoroquinolones (ciprofloxacin, grepafloxacin, levofloxacin, moxifloxacin, norfloxacin, ofloxacin, and rufloxacin), compared to those of trimethoprim-sulfamethoxazole (SXT) and ceftazidime on total biomass and cell viability of Stenotrophomonas maltophilia biofilm. S. maltophilia attached rapidly to polystyrene, within 2 h of incubation, and then biofilm formation increased over time, reaching maximum growth at 24 h. In the presence of fluoroquinolones at one-half and one-fourth the MIC, biofilm biomass was significantly (P < 0.01) reduced to 55 to 70% and 66 to 76% of original mass, respectively. Ceftazidime and SXT did not exert any activity. Biofilm bacterial viability was significantly reduced by all antibiotics tested at one-half the MIC. At one-fourth the MIC all antibiotics, except levofloxacin, significantly reduced viability. Treatment of preformed biofilms with bactericidal concentrations (500, 100, and 50 micro g/ml) of all fluoroquinolones caused, except for norfloxacin, significant reduction of biofilm biomass to 29.5 to 78.8, 64.1 to 83.6, and 70.5 to 82.8% of original mass, respectively. SXT exerted significant activity at 500 micro g/ml only. Ceftazidime was completely inactive. Rufloxacin exhibited the highest activity on preformed biofilm viability, significantly decreasing viable counts by 0.6, 5.4, and 17.1% at 500, 100, and 50 micro g/ml, respectively. Our results show that (i) subinhibitory (one-half and one-fourth the MIC) concentrations of fluoroquinolones inhibit adherence of S. maltophilia to polystyrene and (ii) clinically achievable concentrations (50 and 100 micro g/ml) of rufloxacin are able to eradicate preformed S. maltophilia biofilm.
我们研究了七种氟喹诺酮类药物（环丙沙星、格帕沙星、左氧氟沙星、莫西沙星、诺氟沙星、氧氟沙星和芦氟沙星）与甲氧苄啶-磺胺甲恶唑（SXT）及头孢他啶相比，对嗜麦芽窄食单胞菌生物膜总生物量和细胞活力的体外影响。嗜麦芽窄食单胞菌在孵育2小时内迅速附着于聚苯乙烯，随后生物膜形成随时间增加，在24小时达到最大生长。在氟喹诺酮类药物浓度为最低抑菌浓度（MIC）的二分之一和四分之一时，生物膜生物量分别显著（P<0.01）降至原始质量的55%至70%和66%至76%。头孢他啶和SXT没有任何活性。所有测试抗生素在MIC的二分之一浓度时显著降低生物膜细菌活力。在MIC的四分之一浓度时，除左氧氟沙星外的所有抗生素均显著降低活力。用所有氟喹诺酮类药物的杀菌浓度（500、100和50μg/ml）处理预先形成的生物膜，除诺氟沙星外，生物膜生物量分别显著降至原始质量的29.5%至78.8%、64.1%至83.6%和70.5%至82.8%。SXT仅在500μg/ml时具有显著活性。头孢他啶完全无活性。芦氟沙星对预先形成的生物膜活力表现出最高活性，在500、100和50μg/ml时分别使活菌数显著减少0.6%、5.4%和17.1%。我们的结果表明：（i）氟喹诺酮类药物的亚抑菌浓度（MIC的二分之一和四分之一）抑制嗜麦芽窄食单胞菌对聚苯乙烯的附着；（ii）芦氟沙星临床可达到的浓度（50和100μg/ml）能够根除预先形成的嗜麦芽窄食单胞菌生物膜。
