Staphylococcus aureus interaction with Pseudomonas aeruginosa biofilm enhances tobramycin resistance

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.

Antibiotic treatment and stewardship in the era of microbiota-oriented diagnostics

“…For example, a tobramycin-susceptible Pseudomonas aeruginosa strain may unexpectedly show resistant behavior during treatment with tobramycin as a consequence of interaction with a co-colonizing Staphylococcus aureus strain [15]. Alternatively, resistance mechanisms such as antibiotic inactivation present in one bacterial (commensal) species can indirectly protect pathogenic bacteria living in the same niche from elimination by that therapeutic drug: a mechanism that has been suggested for protection of P. aeruginosa against cephalosporins mediated by the common intrinsic ESBL activity of Prevotella spp.…”

Evolution and Epidemiology of Antimicrobial Resistance: Staphylococcus aureus

“…They discovered that Staphylococcus aureus determines the structure of the biofilm Pseudomonas aeruginosa form. Such influence is the mechanism of resisting to antibiotics on the part of Pseudomonas aeruginosa isolates [15]. That same flaw is also exploring epidemic behavior of methilicin-resistant Staphylococcus aureus (MRSA) [16].…”

“…In the Hallin, et al [15], the researchers name them as the sporadic isolates [15,16]. Using the sample that contains 36 MRSA isolates, the research team identifies four distinct classes of the sporadic ones: The isolates with evolutionary history drastically different from healthcare associated MRSA clones and some characteristics of virulent MRSA strains; Isolates that have an ancestor susceptible to methicillin from whom epidemic isolates were derived, and an apparent type of staphylococcal cassette chromosome mec (SCCmec); Isolates that have the evolutionary history identical to the one the epidemic strains possess or are their closest descendants; Isolates that illustrate the transition from the ancestor of epidemic strains to them.…”

Dynamics of microbial competition, commensalism and cooperation and its implications for coculture and microbiome engineering

“…Novel synthetic biology tools, including cell signaling translator [11] and transcriptional factor-based biosensors [12, 13] have been recently developed to autonomously regulate culture composition and eliminate metabolic heterogeneity. In particular, microbial social interaction could define unique spatial patterns that are important for us to fabricate advanced biomaterials [14, 15], understand biofilm formation [16] and disarm antibiotic resistant superbugs [17].…”