Burkholderia cenocepacia-mediated inhibition of Staphylococcus aureus growth and biofilm formation.

Staphylococcus aureus asymptomatically colonizes the nasal cavity and pharynx of up to 60% of the human population and, as an opportunistic pathogen, can breach its normal habitat, resulting in life-threatening infections. S. aureus infections are of additional concern for populations with impaired immune function such as those with cystic fibrosis (CF) or chronic granulomatous disease. Multi-drug resistance is increasingly common in S. aureus infections, creating an urgent need for new antimicrobials or compounds that improve efficacy of currently available antibiotics. S. aureus biofilms, such as those found in the lungs of people with CF and in soft tissue infections, are notoriously recalcitrant to antimicrobial treatment due to the characteristic metabolic differences associated with a sessile mode of growth. In this work, we show that another CF pathogen, Burkholderia cenocepacia, produces one or more secreted compounds that can prevent S. aureus biofilm formation and inhibit existing S. aureus biofilms. The B. cenocepacia-mediated antagonistic activity is restricted to S. aureus species and perhaps some other staphylococci; however, this inhibition does not necessarily extend to other Gram-positive species. This inhibitory activity is due to death of S. aureus through a contact-independent mechanism, potentially mediated through the siderophore pyochelin and perhaps additional compounds. This works paves the way to better understanding of interactions between these two bacterial pathogens.IMPORTANCEStaphylococcus aureus is a major nosocomial pathogen responsible for infecting thousands of people each year. Some strains are becoming increasingly resistant to antimicrobials, and consequently new treatments must be sought. This paper describes the characterization of one or more compounds capable of inhibiting S. aureus biofilm formation and may potentially lead to development of a new therapeutic.