Ingerman M, Pitsakis P G, Rosenberg A, Hessen M T, Abrutyn E, Murray B E, Levison M E
J Infect Dis. 1987 Jun;155(6):1226-32. doi: 10.1093/infdis/155.6.1226.
We used a beta-lactamase-producing (beta L+) strain of Streptococcus faecalis that also had high levels of resistance to all aminoglycosides to induce experimental endocarditis in rats. The rats were treated for five or 10 days with procaine penicillin, vancomycin, gentamicin, rifampin, or ciprofloxacin (alone or in various combinations), or with penicillin plus clavulanic acid. The levels of penicillin in serum and vegetations declined rapidly in the beta L+-infected rats treated with procaine penicillin alone, unlike the sustained levels of penicillin in either beta L- -infected rats treated with procaine penicillin or beta L+-infected rats treated with penicillin plus clavulanic acid. For the beta L+-infected rats, the enterococcal counts in vegetations were significantly reduced (greater than 3 log10 cfu/g) only by vancomycin and by penicillin plus clavulanic acid. The efficacy of the latter regimen probably resulted from the inhibition of penicillin inactivation by clavulanic acid in vegetations infected with the beta L+ strain. Our in vivo findings document the biologic significance of beta-lactamase production.
我们使用一株产β-内酰胺酶（βL+）的粪肠球菌，该菌株对所有氨基糖苷类抗生素也具有高水平耐药性，以诱导大鼠发生实验性心内膜炎。用普鲁卡因青霉素、万古霉素、庆大霉素、利福平或环丙沙星（单独使用或联合使用），或青霉素加克拉维酸对大鼠进行5天或10天的治疗。单独用普鲁卡因青霉素治疗的βL+感染大鼠血清和赘生物中的青霉素水平迅速下降，这与用普鲁卡因青霉素治疗的βL-感染大鼠或用青霉素加克拉维酸治疗的βL+感染大鼠中青霉素的持续水平不同。对于βL+感染的大鼠，仅万古霉素和青霉素加克拉维酸能使赘生物中的肠球菌计数显著降低（大于3 log10 cfu/g）。后一种治疗方案的疗效可能是由于克拉维酸抑制了感染βL+菌株的赘生物中青霉素的失活。我们的体内研究结果证明了β-内酰胺酶产生的生物学意义。
