Giesbrecht P, Kersten T, Maidhof H, Wecke J
Robert Koch-Institut, D-13 353 Berlin, Germany.
Microbiol Mol Biol Rev. 1998 Dec;62(4):1371-414. doi: 10.1128/MMBR.62.4.1371-1414.1998.
The primary goal of this review is to provide a compilation of the complex architectural features of staphylococcal cell walls and of some of their unusual morphogenetic traits including the utilization of murosomes and two different mechanisms of cell separation. Knowledge of these electron microscopic findings may serve as a prerequisite for a better understanding of the sophisticated events which lead to penicillin-induced death. For more than 50 years there have been controversial disputes about the mechanisms by which penicillin kills bacteria. Many hypotheses have tried to explain this fatal event biochemically and mainly via bacteriolysis. However, indications that penicillin-induced death of staphylococci results from overall biochemical defects or from a fatal attack of bacterial cell walls by bacteriolytic murein hydrolases were not been found. Rather, penicillin, claimed to trigger the activity of murein hydrolases, impaired autolytic wall enzymes of staphylococci. Electron microscopic investigations have meanwhile shown that penicillin-mediated induction of seemingly minute cross wall mistakes is the very reason for this killing. Such "morphogenetic death" taking place at predictable cross wall sites and at a predictable time is based on the initiation of normal cell separations in those staphylococci in which the completion of cross walls had been prevented by local penicillin-mediated impairment of the distribution of newly synthesized peptidoglycan; this death occurs because the high internal pressure of the protoplast abruptly kills such cells via ejection of some cytoplasm during attempted cell separation. An analogous fatal onset of cell partition is considered to take place without involvement of a detectable quantity of autolytic wall enzymes ("mechanical cell separation"). The most prominent feature of penicillin, the disintegration of bacterial cells via bacteriolysis, is shown to represent only a postmortem process resulting from shrinkage of dead cells and perturbation of the cytoplasmic membrane. Several schematic drawings have been included in this review to facilitate an understanding of the complex morphogenetic events.
本综述的主要目的是汇编葡萄球菌细胞壁的复杂结构特征以及一些不寻常的形态发生特性,包括壁体的利用和两种不同的细胞分裂机制。了解这些电子显微镜观察结果可能是更好地理解导致青霉素诱导死亡的复杂事件的先决条件。五十多年来,关于青霉素杀死细菌的机制一直存在争议。许多假说试图从生化角度解释这一致命事件,主要是通过细菌溶解。然而,尚未发现青霉素诱导葡萄球菌死亡是由于整体生化缺陷或溶菌性胞壁质水解酶对细菌细胞壁的致命攻击。相反,据称能触发胞壁质水解酶活性的青霉素,却损害了葡萄球菌的自溶壁酶。与此同时,电子显微镜研究表明,青霉素介导的看似微小的横壁错误诱导是导致这种杀伤的真正原因。这种在可预测的横壁部位和可预测的时间发生的“形态发生死亡”,是基于在那些横壁的完成因局部青霉素介导的新合成肽聚糖分布受损而受阻的葡萄球菌中正常细胞分裂的启动;这种死亡发生是因为原生质体的高内部压力在细胞试图分裂期间通过排出一些细胞质而突然杀死这些细胞。类似的致命细胞分裂开始被认为是在没有可检测量的自溶壁酶参与的情况下发生的(“机械性细胞分裂”)。青霉素最显著的特征,即通过细菌溶解使细菌细胞解体,被证明只是死亡细胞收缩和细胞质膜扰动导致的死后过程。本综述中包含了几幅示意图,以帮助理解复杂的形态发生事件。