Catheter lock solutions influence staphylococcal biofilm formation on abiotic surfaces.
Catheter lock solutions influence staphylococcal biofilm formation on abiotic surfaces.
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DOI：
10.1093/ndt/gfl170
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发表时间：
2006-08
期刊：
影响因子：
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通讯作者：
R. Shanks;J. Sargent;R. M. Martínez;Martha L. Graber;G. O’Toole
中科院分区：
文献类型：
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作者：
R. Shanks;J. Sargent;R. M. Martínez;Martha L. Graber;G. O’Toole
微生物生物膜在中心静脉导管上形成，并且可能与全身感染以及由于导管血栓形成导致的透析效率降低有关。在美国使用最广泛的抗凝剂导管封管液是肝素钠。我们以前已经表明，临床相关浓度的肝素钠可增强金黄色葡萄球菌生物膜的形成。在本研究中，我们通过实验室和临床分离的S.金黄色葡萄球菌和凝固酶阴性葡萄球菌（CNS）。方法采用聚苯乙烯、聚氨酯和硅橡胶作为生物被膜材料，观察来匹卢定、低分子量肝素、组织型纤溶酶原激活剂、枸橼酸钠、枸橼酸钠+庆大霉素和乙二胺四乙酸钠（EDTA）对生物被膜形成的影响。结果0.5%以上浓度的柠檬酸钠能有效抑制S.金黄色葡萄球菌和表皮葡萄球菌。亚抑菌浓度的柠檬酸钠显著刺激大多数试验的S.金黄色葡萄球菌菌株，但不是在中枢神经系统菌株。EDTA钠在预防生物膜形成方面是有效的，柠檬酸钠和庆大霉素的组合也是如此。低分子量肝素刺激S.金黄色葡萄球菌，而来匹卢定和组织型纤溶酶原激活剂对S.金黄色葡萄球菌生物膜形成。结论：本体外研究表明肝素替代品柠檬酸钠和EDTA钠可以防止S。金黄色葡萄球菌生物膜，这表明它们可以降低留置导管中生物膜相关并发症的风险。这一发现表明，在肝素和柠檬酸三钠作为导管封管液的近期临床比较中观察到的导管相关结局改善的生物学机制。本研究的一个新的和潜在的临床相关发现是观察到低水平的柠檬酸盐强烈刺激S.金黄色。
BACKGROUND Microbial biofilms form on central venous catheters and may be associated with systemic infections as well as decreased dialysis efficiency due to catheter thrombosis. The most widely used anticoagulant catheter lock solution in the US is sodium heparin. We have previously shown that sodium heparin in clinically relevant concentrations enhances Staphylococcus aureus biofilm formation. In the present study, we examine the effect of several alternative catheter lock solutions on in vitro biofilm formation by laboratory and clinical isolates of S. aureus and coagulase-negative staphylococci (CNS). METHODS Lepirudin, low molecular weight heparin, tissue plasminogen activator, sodium citrate, sodium citrate with gentamicin and sodium ethylene diamine tetra-acetic acid (EDTA) were assessed for their effect on biofilm formation on polystyrene, polyurethane and silicon elastomer. RESULTS Sodium citrate at concentrations above 0.5% efficiently inhibits biofilm formation and cell growth of S. aureus and Staphylococcus epidermidis. Subinhibitory concentrations of sodium citrate significantly stimulate biofilm formation in most tested S. aureus strains, but not in CNS strains. Sodium EDTA was effective in prevention of biofilm formation as was a combination of sodium citrate and gentamicin. Low molecular weight heparin stimulated biofilm formation of S. aureus, while lepirudin and tissue plasminogen activator had little effect on S. aureus biofilm formation. CONCLUSIONS This in vitro study demonstrates that heparin alternatives, sodium citrate and sodium EDTA, can prevent the formation of S. aureus biofilms, suggesting that they may reduce the risk of biofilm-associated complications in indwelling catheters. This finding suggests a biological mechanism for the observed improvement in catheter-related outcomes in recent clinical comparisons of heparin and trisodium citrate as catheter locking solutions. A novel and potential clinically relevant finding of the present study is the observation that citrate at low levels strongly stimulates biofilm formation by S. aureus.