RESISTANCE of Staphylococcus aureus and S epidermidis organisms to penicillin is known to be mediated by several different mechanisms. Resistance due to production of β-lactamase (penicillinase) resulting in penicillin inactivation was recognized with S aureus in the early 1960s.1 "Intrinsic" resistance to the penicillinase-resistant penicillins (PRPs) has been observed in both S aureus and S epidermidis for more than ten years.2 Recently, strains of S aureus described as "tolerant" to PRPs have been reported.3 This tolerance is manifested by a wide disparity between the concentration of penicillin required to inhibit growth of the organism and that required for killing it. Routine antibiotic sensitivity testing shows these strains to be sensitive to PRPs. The minimal inhibitory concentration (MIC) is well within the therapeutic range of these drugs, but the minimal bactericidal concentration (MBC) is 32 times the MIC or greater, indicating a required therapeutic level not practically achievable
Arthur JD, Bass JW, Keiser JF, Harden LB, Brown SL. Nafcillin-Tolerant Staphylococcus epidermidis Endocarditis. JAMA. 1982;247(4):487–488. doi:10.1001/jama.1982.03320290033026
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