Antibiotics effect on S.aureus adhesion to human fibronectin
Abstract number: P1292
Dumitrescu O., Moulay A., Tristan A., Bes M., Vandenesch F., Etienne J., Lina G.
Background:Staphylococcus aureus is a human pathogen responsible of a large variety of severe infections. Its pathogenicity is strongly related to the production of many virulence factors. Among these, fibronectin binding molecules (FnBPA and FnBPB) are involved in the invasion and the intracellular passage of S. aureus, causing persistent infections non-responding to usual antibiotic treatment. Fibronectin binding molecules are major determinants of the pathogenesis of staphylococcal endocarditis and osteoarthritis. Unsuccessful outcome in these infections may be linked to the impaired diffusion of antibiotics at the infection site. In this work, we explored the effect of main anti-staphylococcal antibiotics, at subinhibitory concentrations, on S. aureus adhesion to human fibronectin.
Methods: We assayed for the adhesion to fibronectin of six different S. aureus strains by using a microplate adhesion test. Prior to the adhesion assay, the strains have been cultured in presence of subinhibitory concentrations of antibiotics (1/4 of the MIC). The antibiotics tested were: oxacillin, gentamicin, vancomycin, rifampicin, linezolid and moxifloxacin. By using relative quantitative RT-PCR, we also explored the effect of the antibiotics mentioned on the transcription of fnbA and fnbB genes coding for FnBPA and FnBPB.
Results: The results showed that the antibiotics differently modulate S. aureus adhesion to human fibronectin. Oxacilline, moxifloxacin and linezolid treatment led to the acquisition of a hyperadhesive phenotype consistent with the increased FnBPA and FnBPB mRNA levels after oxacilline, moxifloxacin and linezolid treatment. On the contrary, all the strains treated with rifampicin showed significantly decreased adhesion to fibronectin, while gentamicin and vancomycin had little impact on S. aureus adhesion to fibronectin.
Conclusion: Our results, showing an inhibitory effect of rifampicin on S. aureus adhesion to human fibronectin, support the use of rifampicin, in association with other anti-staphylococcal agents, for the treatment of severe S. aureus infections. Additionally, our observations may provide explanation for the poor outcome of staphylococcal infections in case of impaired antibiotics diffusion.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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