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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of microbiology 131 (1982), S. 116-123 
    ISSN: 1432-072X
    Keywords: Cell wall ; Wall degradation ; Lysozyme ; Autolysines ; Electron microscopy ; Staphylococcus aureus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In contrast to former findings lysozyme was able to attack the cell walls ofStaphylococcus aureus under acid conditions. However, experiments with14C-labelled cell walls and ribonuclease indicated that, under these conditions, lysozyme acted less as an muralytic enzyme but more as an activator of pre-existing autolytic wall enzymes. Electron microscopic studies showed that under these acid conditions the cell walls were degraded by a new mechanism (i.e. “attack from the inside”). This attack on the cell wall started asymmetrically within the region of the cross wall and induced the formation of periodically arranged lytic sites between the cytoplasmic membrane and the cell wall proper. Subsequently, a gap between the cell wall and the cytoplasmic membrane resulted and large cell wall segments became detached and suspended in the medium. The sequence of lytic events corresponded to processes known to take place during wall regeneration and wall formation. In the final stage of lysozyme action at pH 5 no cell debris but “stabilized protoplasts” were to be seen without detectable alterations of the primary shape of the cells. At the same time long extended ribbon-like structures appeared outside the bacteria. The origin as well as the chemical nature of this material is discussed. Furthermore, immunological implications are considered.
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  • 2
    ISSN: 1432-072X
    Keywords: Bacteriolysis ; Penicillin ; Autolysis ; Cell wall ; Electron microscopy ; Staphylococcus aureus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The actual reason for the penicillin-induced bacteriolysis of staphylococci was shown to be the “punching” of one or a few minute holes into the peripheral cell wall at predictable sites. These perforations were the result of the lytic activity of novel, extraplasmatic vesicular structures, located exclusively within the bacterial wall material, which we have named “murosomes”. In untreated staphylococci the punching of holes into the peripheral wall is a normal process which follows cross wall completion and represents the first visible step of cell separation. Under penicillin, however, analogous holes are punched by the murosomes at sites of presumptive cell separation even if no sufficient cross wall material had been assembled before at this site (but had rather been deposited at other sites). Consequently, because of the internal pressure of the protoplast, lytic death is the inevitable result of this perforation of the protective peripheral wall. Hence, the real mechanism of penicillin-induced bacteriolysis in staphylococci is considered to be mainly the result of a special morphogenetic wall defect: bacteriolysis is taking place regularly when a cell separation process is no longer preceeded by sufficient cross wall assembly at the correct place. However, hypotheses which are based purely on some variations of overall biochemical processes like total wall enzyme activities or total wall synthesis are not regarded to be sufficient to explain this type of lytic death.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Archives of microbiology 121 (1979), S. 103-110 
    ISSN: 1432-072X
    Keywords: Staphylococcus aureus ; Cell wall ; Turnover ; Zero order kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Cells exponentially grown from four strains ofS. aureus (SG 511, H, 52A5G, and248 PN-1) and uniformly labeled in their walls with3H-N-acetylglucosamine, were found to turn over their old walls at constant rates of up to 25% per generation. Wall turnover was not observed to follow first order kinetics, thus ruling out the implication that maintenance of normal wall thickness was achieved by a random distribution of new wall components in the old wall. Instead, wall turnover in all cases strictly followed zero order kinetics, indicating that newly synthesized wall material was placed layer by layer beneath the inner surface of the old cell wall. This finding correlates with evidence obtained from earlier electron microscopic investigations into the regeneration of the staphylococcal cell wall after chloramphenicol treatment. Based on the experimental data presented, a simplified model for wall turnover of the growing staphylococcal cell was proposed. The model also takes into account the finding, derived from additional experiments with strainSG 511, that the total cell wall turned over at a somewhat higher rate than the old portions of the wall. The rates of cell wall turnover found inS. aureus SG 511 are the highest reported to date for pathogenic bacteria. The medical implications of this finding were discussed.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Archives of microbiology 135 (1983), S. 120-124 
    ISSN: 1432-072X
    Keywords: Staphylococcus aureus ; Chloramphenicoltreatment ; Cell wall ; Wall degradation ; Lysozyme ; Autolysins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The effectiveness of host defence against staphylococcal infections depends on the capability of phagocytes to degrade the bacterial cell walls. Treatment with bacteriostatic agents like chloramphenicol could cause problems since under these drugs staphylococcal walls will be substantially thickened. This study presents evidence that the additional wall material built in the presence of chloramphenicol could moreover be rendered more resistant to lysosomal enzymes: In vitro at pH 5.6, lysozyme from hen egg-white proved to degrade the chloramhenicol-wall material at a velocity reduced to 20% of that of the normal wall. Thus, during the degradation of chloramphenicol-treated staphylococcal cell walls the phagocytes have to deal not only with a quantitative but also with a qualitative problem. Possible reasons for the reduced degradability as to chloramphenicol-induced alterations of the wall composition as well as to activating effects of lysozyme on cell wall autolysins are discussed in view of microbiological and medical implications.
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  • 5
    ISSN: 1432-072X
    Keywords: Mechanism of penicillin action ; Staphylococci ; Cross-wall welding ; Bacteriolysis ; Morphogenetic resistance system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In log-phase cells of staphylococci, cultivated under high, “non-lytic” concentrations of penicillin G, there occurred a novel killing process hitherto hidden behind seemingly bacteriostatic effects. Two events are essential for the apprearance of this “hidden death”: (i) the failure of the dividing cell to deposit enough fibrillar cross-wall material to be welded together, and (ii) a premature ripping up of incomplete cross walls along their splitting system. “Hidden death” started as early as 10–15 min after drug addition, already during the first division cycle. It was the consequence of a loss of cytoplasmic constituents which erupted through peripheral slit-like openings in the incomplete cross walls. The loss resulted either in more or less empty cells or in cell shrinkage. These destructions could be prevented by raising the external osmotic pressure. In contrast, the conventional “non-hidden death” occurred only much later and exclusively during the second division cycle and mainly in those dividing cells, whose nascent cross walls of the first division plane had been welded together. These welding processes at nascent cross walls, resulting in tough connecting bridges between presumptive individual cells, were considered as a morphogenetic tool which protects the cells, so that they can resist the otherwise fatal penicillin-induced damages for at least an additional generation time (“morphogenetic resistance system”). Such welded cells, in the virtual absence of underlying cross-wall material, lost cytoplasm and were killed via ejection through pore-like wall openings or via explosions in the second division plane and after liberation of their murosomes, as it was the case in the presence of low, “lytic” concentrations of penicillin. Bacteriolysis did not cause any of the hitherto known penicillin-induced killing processes.
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  • 6
    ISSN: 1432-072X
    Keywords: staphylococci ; Cell wall organization ; Cytoplasmic membrane organization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract By disintegration of the cell wall of staphylococci a definite interlayer located between the cytoplasmic membrane and the cell wall proper could be demonstrated for the first time (=MW-interlayer). This MW-interlayer contains a sort of “cloddy” material in which clusters of embedded ring-like disks are hexagonally arranged in a crystal-like manner. The ring-like disks, approximately 40 Å in diameter and with center-to-center spacings of approximately 75 Å, lie in direct contact either with a rhombically arranged fibrillar network of the outer parts of the cytoplasmic membrane or they themselves are part of (or interconnected by) such an apparently rhombical network. The crystal-like arranged ring-like disks of the interlayer between the cytoplasmic membrane and the cell wall shall be called MW-particles in order to differentiate them from intramembrane particles and particles on the outer surface of the cell wall. At present, nothing more than speculation on the function of the MW-particles located within the space where final processes of the cell wall polymerization are taking place is possible.
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  • 7
    ISSN: 1432-072X
    Keywords: Bacteriolysis ; Staphylococci ; Penicillin ; Cell wall ; Autolysins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In contrast to what has been postulated, penicillin G at its optimal lytic concentration of 0.1 μg per ml did not lead to a detectable activation of autolytic wall processes in staphylococci in terms of the release of uniformly labelled wall fragments from cells pretreated with the drug for 1 h. Rather a considerable inhibition of this release was observed. A similarly profound inhibition of the release of peptidoglycan fragments occurred when staphylococci pretreated for 1 h with 0.1 μg penicillin per ml acted as a source of crude autolysins on peptidoglycan isolated from labelled normal cells of the same strain. This clearly demonstrated that the overall inhibition of autolytic wall processes caused by penicillin was mainly due to a decreased total autolysin action rather than to an altered wall structure. Furthermore, no substantial penicillin-induced inhibition of the incorporation of 14C-N-acetylglucosamine into the staphylococcal wall could be observed before bacteriolysis started, i. e., approximately during the first 80 min of penicillin action. These results are not consistent with any of the models hitherto proposed for the action of penicillin.
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  • 8
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract l-[4,5-3H]isoleucine was introduced to label anteiso-fatty acid (AIFA)-containing lipids in Staphylococcus aureus SG 511. After an overnight incubation in peptone broth in the presence of 37 kBq l-[4,5-3H]isoleucine/ml, 8.5–13% of the total radioactivity applied was found to be incorporated into the cells. 22.4–25.6% of the incorporated radioactivity was found in AIFA-containing lipids extracted by chloroform-methanol-water (2:1:02, v/v/v) at pH 2. The interphase contained 70–75% of the incorporated radioactivity. Lipoteichoic acid, extracted by phenol-water 80:20, w/v) contained less than 1% of the incorporated radioactivity, as measured after purification by hydrophobic interaction chromoatography on octyl sepharose gel. Within 1 h after addition of 10μg/ml penicillin G to exponentially growing cultures of S. aureus, that led to non-lytic death of the cells, 11.9–18.1% of the incorporated l-[4,5-3H] isoleucine label were released. Lipids containing AIFA were excreted to 5.4–8.4% of total incorporated activity; this amount represents more than 1/4 of the labeled cellular lipids.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 43 (1956), S. 89-90 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 51 (1964), S. 46-46 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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