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In the context of infection, Pseudomonas aeruginosaand Staphylococcus aureusare frequently co-isolated, particularly in cystic fibrosis (CF) patients. Within lungs, the two pathogens exhibit a range of competitive and coexisting interactions. In the present study, we explored the impact of S. aureuson the physiology of P. aeruginosain the context of coexistence. Transcriptomic analyses showed that S. aureussignificantly and specifically affects the expression of numerous genes involved in P. aeruginosacarbon and amino acid metabolism. In particular, 65% of the strains presented considerable overexpression of the genes involved in the acetoin catabolic (aco) pathway. We demonstrated that acetoin is (i) produced by clinical S. aureusstrains, (ii) detected in sputa from CF patients and (iii) involved in P. aeruginosa’s acosystem induction. Furthermore, acetoin is catabolized by P. aeruginosa, a metabolic process that improves the survival of both pathogens by providing a new carbon source for P. aeruginosaand avoiding the toxic accumulation of acetoin on S. aureus. Due to its beneficial effects on both bacteria, acetoin catabolism could testify to the establishment of trophic cooperation between S. aureusand P. aeruginosain the CF lung environment, thus promoting their persistence.

In the context of infection, Pseudomonas aeruginosaand Staphylococcus aureusare frequently co-isolated, particularly in cystic fibrosis (CF) patients. Within lungs, the two pathogens exhibit a range of competitive and coexisting interactions. In the present study, we explored the impact of S. aureuson the physiology of P. aeruginosain the context of coexistence. Transcriptomic analyses showed that S. aureussignificantly and specifically affects the expression of numerous genes involved in P. aeruginosacarbon and amino acid metabolism. In particular, 65% of the strains presented considerable overexpression of the genes involved in the acetoin catabolic (aco) pathway. We demonstrated that acetoin is (i) produced by clinical S. aureusstrains, (ii) detected in sputa from CF patients and (iii) involved in P. aeruginosa’s acosystem induction. Furthermore, acetoin is catabolized by P. aeruginosa, a metabolic process that improves the survival of both pathogens by providing a new carbon source for P. aeruginosaand avoiding the toxic accumulation of acetoin on S. aureus. Due to its beneficial effects on both bacteria, acetoin catabolism could testify to the establishment of trophic cooperation between S. aureusand P. aeruginosain the CF lung environment, thus promoting their persistence.

ABSTRACTSince the introduction of type b Haemophilus influenzaevaccination, noncapsulated H. influenzaehas become responsible for most cases of invasive H. influenzaediseases. In our two cases of septic arthritis, we isolated strains with ß-lactamase-positive amoxicillin-clavulanate resistance (BLPACR). Thus, the increasing prevalence of BLPACR should be taken into account when empirical therapy is chosen for septic arthritis.