Staphylococcus aureus is present on the skin of approximately
30% of normal people, and may be carried by up to 25% of hospital staff.
Its ability to rapidly develop resistance to antimicrobial agents, and
its propensity to establish a reservoir by colonizing hospital inpatients
and staff, contribute to its success as a pathogen.
There are three known resistance mechanisms in MRSA:
alteration of penicillin-binding proteins (PBPs), termed intrinsic
resistance, is most common. Found in the bacterial cell wall, PBPs are
the structures to which beta-lactams bind, thereby inhibiting cell wall
synthesis. The PBPs of methicillin-resistant organisms have only a low
affinity for methicillin, thereby conferring high level resistance
hyperproduction of penicillinase, first described in 1984, confers
borderline methicillin-resistance; and
organisms which have normal PBPs with a decreased affinity for lactams,
are classed as modified resistant strains.