Frei Elisabeth, Hodgkiss-Harlow Kelley, Rossi Peter J, Edmiston Charles E, Bandyk Dennis F
Division of Vascular & Endovascular Surgery, University of South Florida College of Medicine, Tampa, FL 33606, USA.
Vasc Endovascular Surg. 2011 Nov;45(8):688-96. doi: 10.1177/1538574411419528. Epub 2011 Sep 15.
Vascular surgical site infection (SSI) is caused by pathogenic bacterial strains whose preferred mode of growth is within a surface biofilm. Bacterial biofilm formation can develop within hours to days in a wound and produces a recalcitrant infectious process especially in the presence of a prosthetic graft. The initial steps of biofilm formation are bacterial adhesion to biologic or inert surgical site structures followed by organism production of exopolysaccaride matrix which encases developing bacteria colonies to produce a protective microenvironment. As the biofilm matures, a dynamic process of organism cell-to-cell signaling occurs with varying growth modes of sessile bacteria within the biofilm and the release of planktonic bacteria with the potential to spread and expand the biofilm-mediated infection. The prevalence of staphyloccocal strains causing vascular SSI is best understood when viewed as a biofilm-mediated infection with virulence factors related to specific cell surface adhesion proteins and bacteria-derived matrix production. Nonhealing surgical sites following lower limb revascularization, the late appearance of prosthetic graft infection caused by Staphylococcus epidermidis, and the development of groin site tracts after aortofemoral bypass grafting are clinical examples of a biofilm-mediated SSI. A mature biofilm within a wound or coating a prosthetic device exhibits resistance to host defenses and selected antibiotics, impairs wound healing, and is a perpetual irritant to that host by inciting a chronic inflammatory process. By understanding the microbial pathogenesis of biofilm formation, strategies to treat and prevent biofilm-mediated infection can be developed and utilized to reduce vascular SSIs.
血管手术部位感染(SSI)是由致病性细菌菌株引起的,这些菌株的首选生长方式是在表面生物膜内。细菌生物膜的形成可在伤口内数小时至数天内发展,并产生顽固的感染过程,特别是在存在人工血管移植物的情况下。生物膜形成的初始步骤是细菌粘附于生物或惰性手术部位结构,随后生物体产生胞外多糖基质,该基质包裹正在形成的细菌菌落以产生保护性微环境。随着生物膜成熟,生物膜内固着细菌的生长模式各异,会发生生物体细胞间信号传导的动态过程,同时释放浮游细菌,这些浮游细菌有可能传播并扩大生物膜介导的感染。当将引起血管SSI的葡萄球菌菌株的流行情况视为一种与特定细胞表面粘附蛋白和细菌衍生基质产生相关的毒力因子的生物膜介导感染时,就能得到最好的理解。下肢血管重建术后手术部位不愈合、表皮葡萄球菌引起的人工血管移植物感染的晚期出现以及主动脉股动脉旁路移植术后腹股沟部位窦道的形成,都是生物膜介导的SSI的临床实例。伤口内或覆盖人工装置的成熟生物膜对宿主防御和某些抗生素具有抗性,会损害伤口愈合,并通过引发慢性炎症过程对宿主造成持续刺激。通过了解生物膜形成的微生物发病机制,可以制定和利用治疗及预防生物膜介导感染的策略,以减少血管SSI。