Staphylococcus aureus is a common cause of both community- and hospital-acquired infections, ranging from
simple skin pustules to wound abscesses, systemic infection with toxic shock, and
death [
[1]
]. Resistance to penicillin G developed soon after its introduction due to staphylococcal
β-lactamase production. This was followed by development of resistance in the 1960s
to all currently available β-lactams through altered penicillin binding protein (PBP)
2a encoded by the mecA gene [
2
,
3
,
4
]. Such strains are referred to as methicillin-resistant S aureus (MRSA) based on resistance to methicillin, the first β-lactamase stable penicillin
derivative introduced into clinical use. Current estimates are that up to 50% of S aureus in the United States are MRSA [
[5]
]. Until recently, MRSA was predominantly a problem of institutions such as acute and
chronic care hospitals, but it is now also a problem in other institutions, such as
jails and child care centers, and is increasingly community acquired, for example
by competitive contact sports participants [
[6]
].To read this article in full you will need to make a payment
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