Interactions between S. aureus and Ps. aeruginosa promotes tobramicin resistance

Presence of Protein A from S. aureus changes Pseudomonas biofilm morphology and induces resistance.

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Oct 24, 2017
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A new study has revealed the molecular basis by which Staphylococcus aureus induces biofilm morphology change and tobramicin resistance in clinical isolates of Pseudomonas aeruginosa. The interaction of the S. aureus SpA and the Ps. aeruginosa Psl causes aggregation of bacterial cells that leaves them resistant to tobramicin. 

The resistance is thought to be an enhancement of the Pseudomonas Psl, a polysaccharide that has already been shown to confer resistance to a broad range of both cationic and anionic antibiotics. Like an umbrella, Psl also confers resistance to S. aureus and E. coli cells that integrated into the Ps. aeruginosa matrix (Billings et al. 2013).

In the current study, the authors show a correlation between resistance induced by S. aureus and Ps. aeruginosa strains that were not cleared in patients after tobramicin treatment.

Abstract

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.

Reference

T. Beaudoin, Y. C. W. Yau, P. J. Stapleton, Y. Gong, P. W. Wang, D. S. Guttman & V. Waters
npj Biofilms and Microbiomes 3, Article number: 25 (2017)
doi:10.1038/s41522-017-0035-0

Go to the profile of Ben Libberton

Ben Libberton

Communications Officer, MAX IV Laboratory

I'm a Communications Officer at MAX IV Laboratory in Lund, Sweden and the Community Editor for npj Biofilms and Microbiomes. I'm interested in how bacteria cause disease and look to technology to produce novel tools to study and ultimately prevent infection. Part of my current role is to find ways to use synchrotron radiation to study microorganisms.

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