MSSA

Nearly all S. aureus produce penicillinase, so plain penicillin fails; the antistaphylococcal penicillins nafcillin, oxacillin, and dicloxacillin resist that enzyme by steric hindrance of their bulky side chain. Methicillin resistance arises from acquisition of the mecA gene on the SCCmec cassette, encoding an altered penicillin-binding protein PBP2a with low affinity for all beta-lactams, which confers resistance to the whole class including cephalosporins other than ceftaroline. The clinically important point, frequently examined, is that vancomycin is inferior to beta-lactams for MSSA bacteraemia and endocarditis, with slower clearance and higher failure and mortality; so once susceptibility is known, therapy should be de-escalated from vancomycin to nafcillin or cefazolin. S. aureus is a catalase-positive, coagulase-positive gram-positive coccus in clusters, causing skin and soft tissue infection, acute endocarditis on normal valves, osteomyelitis, septic arthritis, pneumonia after influenza, and toxin-mediated disease including toxic shock syndrome, scalded skin syndrome, and preformed-toxin food poisoning.