Staphylococcus aureus is a leading cause of implant-associated infections (IAI). The aim of this study was to identify bacterial and/or clinical features involved in the pathogenesis of S. aureus IAI. 57 IAI S. aureus and 31 nasal carriage (NC) S. aureus isolates were studied. S. aureus genetic background was obtained by microarray analysis. Multi-Locus Sequence Typing was performed to determine clonal complexes (CC). The ability of S. aureus isolates to produce biofilm was investigated by resazurin and crystal violet methods. Clinical data were retrospectively collected from the patient's medical records. Fifty-five IAI patients were included. Two of them had two different S. aureus IAI episodes. The median age was 73 years (range: 21–96 years) with 29 women (52.7%). The main diagnosis for arthroplasty was arthrosis (38%). Implants were hip prosthesis (n=35), knee prosthesis (n=18) and osteosynthesis (n=4). Infectious and nasal carriage isolates belonged respectively to 18 and 13 different sequence types (STs) without significant difference. Among IAI isolates, five strains were methicillin resistant. IAI isolates were classified as strong (14%), moderate (42.1%) and weak (43.9%) biofilm producers. For NC isolates, distribution was 12.9%, 25.8% and 61.3% for strong, moderate and weak, respectively. Staphylokinase gene was associated with the occurrence of S. aureus IAI (p<0.001). Patients’ ABO blood group phenotype was associated with IAI S. aureus genetic background (sasG, slpB, lukD and set12/ssl8) (p≤0.01). In vitro, CC8 S. aureus strains produce more biofilm than others (p≤0.0001). Two alleles of bbp gene were significantly associated with CC8 S. aureus strains (p≤0.0001). No specific CC involved in IAI compared to NC S. aureus isolates was revealed. Our results suggested that occurrence of IAI may depend on patients’ ABO blood group and staphylokinase gene detection. We also observed a strong biofilm producer phenotype in CC8 S. aureus. Further studies are needed to prove whether one bbp gene variant is correlated to this phenotype. This study was supported by a grant number WS1106649 from Pfizer, France and by the French “Ministère de l'Enseignement Supérieur et de la Recherche”.
