Rifampicin enhances activity of daptomycin and vancomycin against both a polysaccharide intercellular adhesin (PIA)-dependent and -independent Staphylococcus epidermidis biofilm

Author:

Olson Michael E.1,Slater Shawn R.1,Rupp Mark E.2,Fey Paul D.12

Affiliation:

1. Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USA

2. Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-4031, USA

Abstract

Abstract Objectives and methods This study addressed the efficacy of daptomycin, vancomycin, rifampicin, daptomycin/rifampicin and vancomycin/rifampicin against a polysaccharide intercellular adhesin (PIA)-dependent and -independent Staphylococcus epidermidis biofilm using flow cell and guinea pig tissue cage models. Results The flow cell model of both PIA-dependent and -independent biofilms demonstrated that the viable cell count after treatment with daptomycin/rifampicin was significantly lower (P < 0.05) than after treatment with vancomycin, vancomycin/rifampicin, daptomycin or rifampicin alone. To validate these observations, a guinea pig tissue cage model was used. The results demonstrated that the addition of rifampicin to daptomycin or vancomycin sterilized 5/6 tissues cages colonized with S. epidermidis 1457 (PIA producing). Similar results were noted with S. epidermidis 1457 icaADBC::dhfr (non-PIA producing), where daptomycin/rifampicin and vancomycin/rifampicin sterilized 5/6 and 6/6 tissue cages, respectively. There was no statistical difference in comparison with the no-treatment control when both 1457 and 1457 icaADBC::dhfr were treated with vancomycin and daptomycin alone. Furthermore, treatment with rifampicin alone sterilized 5/6 and 3/6 1457 and 1457 icaADBC::dhfr tissue cages, respectively. Conclusions Interpretation of these data suggests that rifampicin is highly active against S. epidermidis biofilms and both vancomycin and daptomycin are effective at reducing the subpopulation of bacteria that develop rifampicin resistance.

Funder

NIH

Publisher

Oxford University Press (OUP)

Subject

Infectious Diseases,Pharmacology (medical),Pharmacology,Microbiology (medical)

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