Enterococcus faecalis can cause healthcare-associated biofilm infections, including those of orthopedic devices. Treatment of enterococcal prosthetic joint infection is difficult, in part, due to biofilm-associated antimicrobial resistance. We previously showed that the E. faecalis OG1RF genes ahrC and eep are in vitro biofilm determinants and virulence factors in animal models of endocarditis and catheter-associated urinary tract infection. In this study, we evaluated the role of these genes in a rat acute foreign body osteomyelitis model and in in vitro biofilm-associated antimicrobial resistance. Osteomyelitis was established for one week following the implantation of stainless steel orthopedic wires inoculated with E. faecalis strains OG1RF, δahrC, and Δeep into the proximal tibiae of rats. The median bacterial loads recovered from bones and wires did not differ significantly between the strains at multiple inoculum concentrations. We hypothesize that factors present at the infection site that affect biofilm formation, such as the presence or absence of shear force, may account for the differences in attenuation in the various animal models we have used to study the ΩahrC and Δeep strains. No differences among the three strains were observed in the planktonic and biofilm antimicrobial susceptibilities to ampicillin, vancomycin, daptomycin, linezolid, and tetracycline. These findings suggest that neither ahrC nor eep directly contribute to E. faecalis biofilm-associated antimicrobial resistance. Notably, the experimental evidence that the biofilm attachment mutant ΩahrC displays biofilm-associated antimicrobial resistance suggests that surface colonization alone is sufficient for E. faecalis cells to acquire the biofilm antimicrobial resistance phenotype.
Bibliographical noteFunding Information:
The authors thank Dawn Manias, Suzannah Schmidt-Malan, and Jennifer Nilson for technical and logistical assistance. This work was supported by the National Institutes of Health [R01 AI058134]. AMTB received additional support from the University of Minnesota Medical Scientist Training Program [T32 GM008244]. CLB received support for this work from the National Institute of Arthritis and Musculoskeletal and Skin Diseases for the Musculoskeletal Research Training Program [T32 AR56950]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Parts of this work were carried out using software provided by the University of Minnesota Supercomputing Institute. This work was presented in part at the 49 Annual Infectious Disease Society Meeting, October 20–23, 2011, Boston, MA (Abstract 923). th
© 2015 Frank et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.