Résumé
Cystic Fibrosis (CF) is a disease caused by mutation of the cftr gene (Cystic Fibrosis Transmembrane Conductance Regulator) resulting in a cellular ionic imbalance that is harmful to many organs including the lungs. This results in a change in mucociliary clearance and a viscous mucus conducive to bacterial stasis and colonization and respiratory infections. Staphylococcus aureus is the most frequently isolated species in patients with cystic fibrosis. Methicillin-resistant strains of S. aureus (MRSA) are also responsible for the deterioration of lung function in CF patients. In addition to their multiresistance to prescribes, the ability of these strains to form biofilm limits the effectiveness of antimicrobial therapies. In this context, we examined the ability of clinical strains of MRSA from CF patients to produce biofilm in the presence or absence of five known anti-MRSA agents: Linezolid, rifampicin, trimethoprim, ceftaroline and ceftobiprole. We used standardized methods: the BioFilm Ring test® (BRT®), the antibiofilmogram® and the BioFlux™ 200 system as well as the Artificial Sputum Medium (ASM) mimicking by its composition, the respiratory mucus of CF patients. A total of 63 MRSA strains isolated from 35 CF patients was selected.Seventeen strains (27%) showed strong adhesion, the initial step in biofilm production. Minimum Inhibitory Concentrations in biofilm (MICb) of the five antibiotics were determined for these 17 strains showing that the strongest inhibition of biofilm formation was observed for Linezolid, ceftaroline and ceftobiprole. This action was retained for strains adapted to the pulmonary environment after years of persistence (3 to 9 years). Finally, the study of the dynamics of biofilm formation showed that this was favored in ASM, justifying a wider use of this medium for studies of CF strains and that a marked and lasting inhibition of biofilm formation was observed for ceftaroline and ceftobiprole and, less markedly, for linezolid. This study provides new knowledge on the formation of biofilm by MRSA strains isolated from CF patients showing that it is frequent, strain-dependent, including within the same sample, and differentially influenced by antibiotics. The study of the anti-biofilm effect of a larger panel of antibiotics or even combinations of antibiotics should be considered in order to complete the data obtained in this work.