Stevens D L, Yan S, Bryant A E
Department of Medicine, University of Washington School of Medicine, Seattle.
J Infect Dis. 1993 Jun;167(6):1401-5. doi: 10.1093/infdis/167.6.1401.
Mechanisms to explain the "inoculum effect" have not been elucidated in gram-positive infections. A mouse model of group A streptococcal myositis was used to compare the efficacies of two beta-lactams, penicillin and ceftriaxone, and a protein synthesis inhibitor, clindamycin, at three different inoculum sizes. beta-lactams were more susceptible to inoculum effects than was clindamycin both in vivo and in vitro (P < .05). The large inocula were hypothesized to reach stationary phase of growth sooner than smaller inocula both in vitro and in vivo. The penicillin-binding protein (PBP) patterns from membrane proteins isolated from mid-log-phase and stationary-phase cultures of Streptococcus pyogenes were compared. Binding of radiolabeled penicillin by all PBPs was decreased in stationary cells; however, PBPs 1 and 4 were undetectable at 36 h. Thus, the loss of certain PBPs during stationary-phase growth in vitro may be responsible for the inoculum effect observed in vivo and may account for the failure of penicillin in both experimental and human cases of severe streptococcal infection.
解释革兰氏阳性菌感染中“接种量效应”的机制尚未阐明。利用A组链球菌性肌炎小鼠模型,比较了两种β-内酰胺类药物(青霉素和头孢曲松)以及一种蛋白质合成抑制剂(克林霉素)在三种不同接种量下的疗效。在体内和体外,β-内酰胺类药物比克林霉素对接种量效应更敏感(P < 0.05)。据推测,无论是在体外还是体内,大接种量比小接种量更早进入生长稳定期。比较了从化脓性链球菌对数中期和稳定期培养物中分离的膜蛋白的青霉素结合蛋白(PBP)模式。在稳定期细胞中,所有PBP与放射性标记青霉素的结合均减少;然而,在36小时时无法检测到PBP 1和PBP 4。因此,体外稳定期生长过程中某些PBP的缺失可能是体内观察到的接种量效应的原因,也可能是青霉素在严重链球菌感染的实验和临床病例中失效的原因。