McDougal L K, Thornsberry C
J Clin Microbiol. 1986 May;23(5):832-9. doi: 10.1128/jcm.23.5.832-839.1986.
We showed that most Staphylococcus aureus strains that have borderline or intermediate susceptibility to the penicillinase-resistant penicillins (PRPs) react this way because of the activity of their beta-lactamase on these antimicrobial agents. These strains produced large amounts of staphylococcal beta-lactamase that rapidly hydrolyzed penicillin and partially hydrolyzed the PRPs. Susceptibility to hydrolysis was penicillin greater than oxacillin greater than cephalothin greater than methicillin. The borderline results and the hydrolysis could be prevented by the beta-lactamase inhibitors clavulanic acid and sulbactam. For intrinsically methicillin-resistant (heteroresistant) S. aureus, the inhibitors reduced the penicillin MICs, but the strains remained resistant to all the beta-lactam antimicrobial agents, including penicillin. We conclude that the borderline in vitro susceptibility or resistance to PRPs in most of these S. aureus strains is mediated by beta-lactamase and they are not heteroresistant or intrinsically resistant. We do not know whether this in vitro resistance is expressed clinically.
我们发现，大多数对耐青霉素酶青霉素（PRPs）具有临界或中度敏感性的金黄色葡萄球菌菌株之所以有这种反应，是因为其β-内酰胺酶对这些抗菌药物有活性。这些菌株产生大量葡萄球菌β-内酰胺酶，能迅速水解青霉素并部分水解PRPs。对水解的敏感性顺序为青霉素大于苯唑西林大于头孢噻吩大于甲氧西林。β-内酰胺酶抑制剂克拉维酸和舒巴坦可防止临界结果和水解现象。对于固有耐甲氧西林（异质性耐药）的金黄色葡萄球菌，抑制剂降低了青霉素的最低抑菌浓度（MIC），但这些菌株对所有β-内酰胺类抗菌药物（包括青霉素）仍具有耐药性。我们得出结论，大多数这些金黄色葡萄球菌菌株对PRPs的体外临界敏感性或耐药性是由β-内酰胺酶介导的，它们并非异质性耐药或固有耐药。我们尚不清楚这种体外耐药性在临床上是否会表现出来。
