ABSTRACT
Throughout the modern antibiotic era, Staphylococcus aureus has
remained a formidable and adaptable pathogen. Through the production
of penicillinase, S. aureus has averted the effect of penicillin G and
congeners (1). Through a penicillin-binding protein 2 alteration (PBP-2a),
the pathogen has overcome semisynthetic penicillins and first-generation
cephalosporins (2). Infections caused by this altered form of S. aureus
have been shown to cause increased morbidity and mortality and are more
expensive to care for than methicillin-susceptible S. aureus (MSSA)
strains (3). While often referred to as methicillin-resistant S. aureus
(MRSA), this term does not reflect contemporary susceptibility testing
procedures that are now performed with oxacillin not methicillin, so the
more suitable term would be oxacillin-resistant S. aureus (ORSA) (4).
Some investigators have promoted cefoxitin as the best b-lactam substrate for identifying S. aureus with a PBP-2a and a cefoxitin disk along
with an oxacillin minimum inhibitory concentration (MIC) is recommend
by the CLSI as the standard testing procedure for MRSA/ORSA (4).
Additionally, the presence of MRSA can now be confirmed using various
gene probe tests that determine the presence of mecA, the gene respon-
sible for the alteration of PBP-2. Borderline-resistant S. aureus (BORSA)
are hyper-b-lactamase-producing strains that are mecA negative and can be misinterpreted to be MRSA in antibiotic susceptibility testing (2).
