Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA.
Department of Microbial Pathogenesis, School of Dentistry, University of Maryland-Baltimore, Baltimore, Maryland, USA.
Appl Environ Microbiol. 2020 Sep 17;86(19). doi: 10.1128/AEM.01234-20.
Periprosthetic joint infection (PJI) occurring after artificial joint replacement is a major clinical issue requiring multiple surgeries and antibiotic interventions. is the bacterium most commonly responsible for PJI. Recent research has shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid (SF). We hypothesize that these aggregates provide early protection to bacteria entering the wound site, allowing them time to attach to the implant surface, leading to biofilm formation. Thus, understanding the attachment kinetics of these aggregates is critical in understanding their adhesion to various biomaterial surfaces. In this study, the number, size, and surface area coverage of aggregates as well as of single cells of were quantified under various conditions on different orthopedic materials relevant to orthopedic surgery: stainless steel (316L), titanium (Ti), hydroxyapatite (HA), and polyethylene (PE). It was observed that, regardless of the material type, SF-induced aggregation resulted in reduced aggregate surface attachment and greater aggregate size than the single-cell populations under various shear stresses. Additionally, the surface area coverage of bacterial aggregates on PE was relatively high compared to that on other materials, which could potentially be due to the rougher surface of PE. Furthermore, increasing shear stress to 78 mPa decreased aggregate attachment to Ti and HA while increasing the aggregates' average size. Therefore, this study demonstrates that SF induced inhibition of aggregate attachment to all materials, suggesting that biofilm formation is initiated by lodging of aggregates on the surface features of implants and host tissues. Periprosthetic joint infection occurring after artificial joint replacement is a major clinical issue that require repeated surgeries and antibiotic interventions. Unfortunately, 26% of patients die within 5 years of developing these infections. is the bacterium most commonly responsible for this problem and can form biofilms to provide protection from antibiotics as well as the immune system. Although biofilms are evident on the infected implants, it is unclear how these are attached to the surface in the first place. Recent investigations have shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid and provide protection to bacteria, thus allowing them time to attach to the implant surface, leading to biofilm formation. In this study, we investigated the attachment kinetics of aggregates on different orthopedic materials. The information presented in this article will be useful in surgical management and implant design.
人工关节置换术后发生的假体周围关节感染(PJI)是一个主要的临床问题,需要多次手术和抗生素干预。 是最常导致 PJI 的细菌。最近的研究表明,葡萄球菌菌株在滑液(SF)存在下迅速形成聚集体。我们假设这些聚集体为进入伤口部位的细菌提供早期保护,使它们有时间附着在植入物表面,从而导致生物膜形成。因此,了解这些聚集体的附着动力学对于理解它们对各种生物材料表面的附着至关重要。在这项研究中,我们在不同的骨科材料上研究了不同条件下 的聚集体的数量、大小和表面积覆盖率,以及单细菌细胞。结果观察到,无论材料类型如何,SF 诱导的聚集都会导致聚集体的表面附着减少,并且在各种剪切应力下,聚集体的大小大于单细胞群体。此外,与其他材料相比,PE 上细菌聚集体的表面积覆盖率相对较高,这可能是由于 PE 的表面较粗糙。此外,将剪切应力增加到 78 mPa 会减少 Ti 和 HA 上的聚集体附着,但会增加聚集体的平均大小。因此,这项研究表明,SF 抑制了聚集体在所有材料上的附着,这表明生物膜的形成是由聚集体在植入物和宿主组织的表面特征上的定植引起的。人工关节置换术后发生的假体周围关节感染是一个主要的临床问题,需要反复手术和抗生素干预。不幸的是,26%的患者在感染后 5 年内死亡。 是最常导致这个问题的细菌,它可以形成生物膜,以提供对抗生素和免疫系统的保护。尽管在感染的植入物上可以看到生物膜,但尚不清楚这些生物膜最初是如何附着在表面上的。最近的研究表明,葡萄球菌菌株在滑液存在下迅速形成聚集体,并为细菌提供保护,从而使它们有时间附着在植入物表面,导致生物膜形成。在这项研究中,我们研究了不同骨科材料上 的聚集体的附着动力学。本文提供的信息将有助于手术管理和植入物设计。