On day 0, samples (blood and synovial fluid) were collected, epidural medication was administered, and S. Baseline radiographs and ultrasound images were taken 3-5 days before the start of the study (day 0). Baseline diagnostic imaging and epidural catheter placement was performed 24-48 hours prior to the start of the study. aureus antimicrobial biofilm cartilage infectious arthritis platelets synovial fluid synovium.Ĭopyright © 2022 Gilbertie, Schaer, Engiles, Seiler, Deddens, Schubert, Jacob, Stefanovski, Ruthel, Hickok, Stowe, Frink and Schnabel.ĭiagram of the experimental design and timing of major events such as sample collection and ultrasound. Our results demonstrate the in vivo efficacy of AMK+BIO-PLY and represents a new approach to restore and potentiate antimicrobial activity against synovial fluid biofilms. Most importantly, AMK+BIO-PLY treatment reduced the loss of infection-associated cartilage proteoglycan content in articular cartilage and decreased synovial tissue fibrosis and inflammation. aureus and subsequently treated with BIO-PLY combined with the antibiotic amikacin (AMK) had decreased bacterial concentrations within both synovial fluid and synovial tissue and exhibited lower systemic and local inflammatory scores compared to horses treated with AMK alone. We found that horses experimentally infected with S. The goal of this study was to test BIO-PLY for in vivo efficacy using an equine model of infectious arthritis. Additional in vitro studies using equine synoviocytes and chondrocytes showed that BIO-PLY protected these cells of the joint from inflammation. aureus synovial fluid free-floating biofilm aggregates. To address this problem, we developed a platelet-rich plasma (PRP)-derived biologic, termed BIO-PLY (for the BIOactive fraction of Platelet-rich plasma LYsate) which has potent in vitro bactericidal activity against S. Consequently, there is a lack of antibiofilm agents in the antibiotic development pipeline. Biofilms are highly tolerant to conventional antibiotics which were developed against planktonic cells. The leading cause of treatment failure in Staphylococcus aureus infections is the development of biofilms.
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