Investigation of synovial fluid induced Staphylococcus aureus aggregate development and its impact on surface attachment and biofilm formation.

摘要: Periprosthetic joint infections (PJIs) are a devastating complication that occurs in 2% of patients following replacement. These costly and difficult to treat, often requiring multiple corrective surgeries prolonged antimicrobial treatments. The Gram-positive bacterium Staphylococcus aureus is one the most common causes PJIs, it resistant number commonly used antimicrobials. This tolerance can be partially attributed ability S. form biofilms. Biofilms associated with surface indwelling medical devices have been observed on components removed during chronic infection, however, development localization biofilms PJIs remains unclear. Prior studies demonstrated synovial fluid, cavity, promotes bacterial aggregates many biofilm-like properties, including antibiotic resistance. We anticipate these an important role biofilm formation PJIs. Therefore, we sought determine specifically how fluid aggregate impact this process attachment. Using flow cytometry microscopy, quantified aggregation various clinical strains exposure purified components. determined fibrinogen fibronectin promoted aggregation, while cell free DNA, serum albumin, hyaluronic acid had minimal effect. To mediated affects attachment, utilized microscopy measure Surprisingly, found significantly impeded attachment variety materials. conclude from study crucial promoting inhibiting adhesion PJI. Collectively, propose may conflicting protective roles for host by preventing surfaces, but also contributing tolerance.