PhD Student, Clinical Instructor VA-MD College of Veterinary Medicine Christiansburg, Virginia
Biofilms cause antimicrobial resistance and treatment failure in equine orthopedic infections. Equine bone marrow-derived stromal cells (MSC) kill planktonic bacteria by secreting antimicrobial peptides, but their ability to disrupt mature biofilms is unknown. Our objective was to evaluate the ability of MSC to reduce mature S. aureus or E. coli biofilms in vitro. We hypothesized that MSC would reduce biofilm matrix and associated live bacteria and that MSC with amikacin sulfate would reduce these components more than MSC alone. Biofilms formed from 2 x 105S. aureus or E. coli for 24 hours were co-cultured in transwell plates with 1 x 106 passage 3 MSC (n = 5 horses) with or without 30 µg/mL amikacin.After 24 or 48 hours, biofilms were photographed and crystal violet-stained biomass and live bacterial colony-forming units (CFU) were quantified. Groups were compared using mixed model ANOVA (p < 0.05). MSC reduced biomass of S. aureus biofilms compared to untreated controls but did not reduce CFU in biofilms of either bacterium. MSC with amikacin reduced biomass of S. aureus biofilms and CFU in S. aureus and E. coli biofilms compared to untreated controls. MSC with amikacin reduced CFU more than amikacin in E. coli biofilms at 48 hours. MSC-treated biofilms were less organized with smaller central pellicles than untreated or amikacin-treated biofilms. Our findings suggest that MSC disrupt biofilm matrix and differentially affect S. aureus versus E. coli biofilms. Early anti-biofilm effects remain unknown. MSC show promise for adjunct therapy against biofilms with optimization.
