An essential role for coagulase instaphylococcus aureusbiofilm development reveals new therapeutic possibilities for device-related infections
Zapotoczna, Marta ; McCarthy, Hannah ; Rudkin, Justine K. ; O'Gara, James P. ; O'Neill, Eoghan
Zapotoczna, Marta
McCarthy, Hannah
Rudkin, Justine K.
O'Gara, James P.
O'Neill, Eoghan
Publication Date
2015-06-04
Type
Article
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Zapotoczna, Marta; McCarthy, Hannah; Rudkin, Justine K. O'Gara, James P.; O'Neill, Eoghan (2015). An essential role for coagulase instaphylococcus aureusbiofilm development reveals new therapeutic possibilities for device-related infections. Journal of Infectious Diseases 212 (12), 1883-1893
Abstract
High-level resistance to antimicrobial drugs is a major factor in the pathogenesis of chronic Staphylococcus aureus biofilm-associated, medical device-related infections. Antimicrobial susceptibility analysis revealed that biofilms grown for <= 24 hours on biomaterials conditioned with human plasma under venous shear in iron-free cell culture medium were significantly more susceptible to antistaphylococcal antibiotics. Biofilms formed under these physiologically relevant conditions were regulated by SaeRS and dependent on coagulase-catalyzed conversion of fibrinogen into fibrin. In contrast, SarA-regulated biofilms formed on uncoated polystyrene in nutrient-rich bacteriological medium were mediated by the previously characterized biofilm factors poly-N-acetyl glucosamine, fibronectin-binding proteins, or autolytic activity and were antibiotic resistant. Coagulase-mediated biofilms exhibited increased antimicrobial resistance over time (>48 hours) but were always susceptible to dispersal by the fibrinolytic enzymes plasmin or nattokinase. Biofilms recovered from infected central venous catheters in a rat model of device-related infection were dispersed by nattokinase, supporting the important role of the biofilm phenotype and identifying a potentially new therapeutic approach with anti-microbials and fibrinolytic drugs, particularly during the early stages of device-related infection.
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Oxford University Press (OUP)
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Attribution-NonCommercial-NoDerivs 3.0 Ireland