| Autor: |
Beaudoin T; Translational Medicine, Research Institute, Hospital for Sick Children, 555 University Avenue, Toronto, M5G 1X8 Canada., Yau YCW; Division of Microbiology, Department of Pediatric Laboratory Medicine, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, M5G 1X8 Canada., Stapleton PJ; Division of Microbiology, Department of Pediatric Laboratory Medicine, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, M5G 1X8 Canada., Gong Y; Centre for the Analysis of Genome Evolution and Function, University of Toronto, Ontario, Canada., Wang PW; Centre for the Analysis of Genome Evolution and Function, University of Toronto, Ontario, Canada., Guttman DS; Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario Canada., Waters V; Translational Medicine, Research Institute, Hospital for Sick Children, 555 University Avenue, Toronto, M5G 1X8 Canada.; Division of Infectious Diseases, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, M5G 1X8 Canada. |
| Abstrakt: |
Antimicrobial resistance is a significant threat to the treatment of infectious disease. Multiple mechanisms of resistance to different classes of antibiotics have been identified and well-studied. However, these mechanisms are studied with bacteria in isolation, whereas often, infections have a polymicrobial basis. Using a biofilm slide chamber model, we visualized the formation and development of clinical Pseudomonas aeruginosa biofilms in the presence of secreted Staphylococcus aureus exoproducts, two bacteria that commonly co-infect pediatric patients with cystic fibrosis. We showed that, over time, certain isolates of P. aeruginosa can form different biofilm architecture in the presence of S. aureus exoproducts. We further determined that this interaction was dependent on Psl produced by P. aeruginosa and staphylococcal protein A from S. aureus . Importantly, we identified a mechanism of antibiotic resistance to tobramycin that is dependent on the polymicrobial interactions between these two bacteria. This interaction occurred in isolates of P. aeruginosa recovered from children with cystic fibrosis who failed to clear P. aeruginosa following inhaled tobramycin treatment. |
