L'antibiogramme de Staphylococcus aureus

Staphylococcus aureus has acquired different types of resistance to antistaphylococcal agents. More than 80% of isolates produce a penicillinase. Oxacillin remains active against those isolates. However, hospital-associated staphylococci and, more recently, community-associated staphylococci have developed cross resistance between oxacillin and other beta-lactams by production of a penicillin-binding protein with low affinity for beta-lactams, PBP2a. This resistance is more readily detected by the cefoxitin test. Three enzymes are responsible for aminosides inactivation, each conferring a specific resistance spectrum. Glycopeptides, vancomycin and teicoplanin, are alternatives to oxacillin in case of resistance or intolerance. Strains with decreased susceptibility to glycopeptides that are difficult to detect are reported. Macrolide resistance is most often due to methylase production responsible for modification of the ribosomal site of these antibiotics. Two phenotypes, inducible and constitutive, can be distinguished by the disk-diffusion method. Quinolone resistance is related to mutations in topo-isomerases, the target of these antibiotics. New antistaphylococcal agents were recently commercialized, linezolid, daptomycin and tigecycline. Resistance to these drugs are already reported but still rare. Resistances are mostly combined in methicillin-resistant S. aureus (MRSA). Currently, methicillin resistance is associated in approximately 90% of cases of hospital-associated MRSA to resistance to fluoroquinolone and to the phenotype of aminoglycoside resistance, Kanamycin-Tobramycin. By contrast, community-associated MRSA, are only resistant to kanamycin, fusidic acid and often tetracyclines, in addition to methicillin.