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PubMed2005

Mode of action of piscicocin CS526 produced by Carnobacterium piscicola CS526.

AIMS: Piscicocin CS526 is a unique class IIa bacteriocin produced by Carnobacterium piscicola CS526. The mode of action against the sensitive strain Listeria monocytogenes IID581 was evaluated. METHODS AND RESULTS: Piscicocin CS526 was adsorbed on both sensitive and insensitive gram-positive and gram-negative bacterial cells. Treatment of L. monocytogenes cells with trypsin, lipase and Triton X-100 did not reduce subsequent adsorption of piscicocin CS526. The activity of piscicocin CS526 against L. monocytogenes cells was bactericidal rather than bacteriostatic, but did not cause bacteriolysis. Piscicocin CS526 induced the efflux of K+ ions from the target cells which cause dissipation of the transmembrane potential (DeltaPsi) of the cell membrane. Moreover, after exposure to piscicocin CS526, intracellular adenosine 5'-triphosphate (ATP) level of the target cells rapidly reduced without leakage of ATP from the cells, indicating that ATP depletion occurred in the cells. CONCLUSIONS: Pore formation by piscicocin CS526 caused a rapid efflux of small molecules such as K+ from the indicator cells and dissipation of proton motive force (PMF), which lead to the cell death. SIGNIFICANCE AND IMPACT OF THE STUDY: Molecular mechanism of action of piscicocin CS526 is very similar to that of other pediocin-like bacteriocins, although piscicocin CS526 possesses a unique N-terminal sequence in which Val is substituted for by Leu in the amino acid at position 7.

Adenosine Triphosphate↗

PubMed1993

Recent approaches to the chemotaxonomy of the Actinobacillus-Haemophilus-Pasteurella group (family Pasteurellaceae).

Many members of the Actinobacillus-Haemophilus-Pasteurella group (family Pasteurellaceae) have been misclassified. This article reviews the chemotaxonomic characters that recently have been provided to improve the taxonomy of Pasteurellaceae. These include fatty acids of whole cells, of lipopolysaccharides and of single colonies, together with sugar contents of whole cells, of whole defatted cells, of lipopolysaccharides and of single colonies. This article also reviews taxonomy aided by distribution of proteins in whole cells and outer membranes, distribution of enzymes in outer membrane vesicles and in whole cells, bacteriolysis induced by ethylenediaminetetraacetic acid and hen eggwhite lysozyme and the distribution of respiratory quinones. Furthermore, an overview of characters obtained through studies on genetic transformation, restriction enzyme analysis, restriction fragment length polymorphism, DNA-DNA hybridization, DNA-rRNA hybridization, and 16S rRNA sequencing is given.

Aggregatibacter actinomycetemcomitans↗

PubMed1999

Can we learn from the pathogenetic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae?

The purpose of this review-hypothesis is to discuss the literature which had proposed the concept that the mechanisms by which infectious and inflammatory processes induce cell and tissue injury, in vivo, might paradoxically involve a deleterious synergistic 'cross-talk', among microbial- and host-derived pro-inflammatory agonists. This argument is based on studies of the mechanisms of tissue damage caused by catalase-negative group A hemolytic streptococci and also on a large body of evidence describing synergistic interactions among a multiplicity of agonists leading to cell and tissue damage in inflammatory and infectious processes. A very rapid cell damage (necrosis), accompanied by the release of large amounts of arachidonic acid and metabolites, could be induced when subtoxic amounts of oxidants (superoxide, oxidants generated by xanthine-xanthine oxidase, HOCl, NO), synergized with subtoxic amounts of a large series of membrane-perforating agents (streptococcal and other bacterial-derived hemolysins, phospholipases A2 and C, lysophosphatides, cationic proteins, fatty acids, xenobiotics, the attack complex of complement and certain cytokines). Subtoxic amounts of proteinases (elastase, cathepsin G, plasmin, trypsin) very dramatically further enhanced cell damage induced by combinations between oxidants and the membrane perforators. Thus, irrespective of the source of agonists, whether derived from microorganisms or from the hosts, a triad comprised of an oxidant, a membrane perforator, and a proteinase constitutes a potent cytolytic cocktail the activity of which may be further enhanced by certain cytokines. The role played by non-biodegradable microbial cell wall components (lipopolysaccharide, lipoteichoic acid, peptidoglycan) released following polycation- and antibiotic-induced bacteriolysis in the activation of macrophages to release oxidants, cytolytic cytokines and NO is also discussed in relation to the pathophysiology of granulomatous inflammation and sepsis. The recent failures to prevent septic shock by the administration of only single antagonists is disconcerting. It suggests, however, that since tissue damage in post-infectious syndromes is caused by synergistic interactions among a multiplicity of agents, only cocktails of appropriate antagonists, if administered at the early phase of infection and to patients at high risk, might prevent the development of post-infectious syndromes.

Animals↗

PubMed1984

Influence of bacterial cell concentration and inorganic anions on lysis of Streptococcus mutans BHT by salivary lysozyme.

The aim of this work was to study the influence of bacterial cell concentrations and inorganic anions on lysis of Streptococcus mutans BHT by human salivary lysozyme (HSL). HSL was partly purified from saliva by ion exchange chromatography. The bacteria were grown in a synthetic medium containing 3H-thymidine to monitor DNA release. The experiments demonstrated that release of 3H-thymidine was dependent on the bacterial cell concentration and an apparent Km-value corresponding to approximately 2.9 X 10(8) cells/ml was calculated. The influence of I-, Br-, Cl-, F-, HCO3- and SCN- on bacteriolysis was studied. All anions tested were slightly inhibitory on the action of HSL. The inhibition varied from 7 to 76% depending on the ion and ionic strength. The order of addition of HSL and sodium chloride caused different lytic responses. This was reflected by the amount of HSL adsorbed by the bacteria.

Animals↗

PubMed1980

Events leading to cell death and lysis of Neisseria meningitidis in low concentrations of penicillin G.

Neisseria meningitidis SD1C exhibited a low tolerance to penicillin G (0.03 microgram/ml). Loss of viability in the absence of polyvinylpyrrolidone-40 and horse serum was independent of the concentration of antibiotic above the minimum inhibitory concentration, whereas the rate of bacteriolysis was concentration dependent. Penicillin-induced lysis was a secondary event in this organism. At low levels of penicillin G, growth characteristics, i.e., absorbancy changes, respiratory rate, and uptake of Mg2+, appeared normal during the first 90 min in penicillin; however, viability dropped dramatically. Additionally, total cell numbers remained constant while cell mass continued to increase at a rate normal for the population. The increase in cellular mass in the absence of cell division could be observed microscopically. Only one ultrastructural change induced by penicillin correlated with the loss in viability: the loss in continuity of the outer membrane with the peptidoglycan but only at the site of septum formation. This lesion did not occur when cells were grown in media supplemented with the protective agents polyvinylpyrrolidone-40 and horse serum. Under these conditions of growth and with relatively high levels of penicillin, constant viability was maintained, but cell division no longer occurred. Cell populations treated with penicillin in the presence of the protective agents became increasingly more dependent on the presence of these agents for total viability even in the absence of penicillin in the culture.

Blood↗

PubMed1992

Effect of inoculum size on bacteriolytic activity of cefminox and four other beta-lactam antibiotics against Escherichia coli.

MICs and turbidimetric experiments revealed a negligible inoculum effect with two Escherichia coli strains exposed to cefminox and cefoxitin, whereas a marked inoculum effect was revealed after exposure to cefotaxime, ceftizoxime, and imipenem. The activities of the cephamycins were associated with spheroplast formation and bacteriolysis at concentrations close to the MIC, whereas the other agents induced the formation of filaments or, in the case of imipenem, rounded cells.

Anti-Bacterial Agents↗

PubMed1976

Bacteriological study on effects of beta-lactam group antibiotics in high concentrations.

The growth and viability of Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa exposed to various concentrations of a number of beta-lactam group antibiotics were determined. In S. aureus, the bacteriolytic and bactericidal activity of these drugs was lower at very high drug concentrations than that occurring at low concentrations, but these phenomena were not observed in E. coli and P. aeruginosa. Under phase-contrast and scanning electron microscopy, S. aureus treated with high concentrations of beta-lactam group antibiotics revealed a lower frequency of bacteriolysis than at low drug concentrations, and similarly by transmission electron microscopy fewer cells were transformed into spheroplasts at high drug concentrations. However, swelling of the cell wall septum was seen in many cells. Spheroplast formation occurred with the highest frequency at drug levels near the minimum inhibitory concentration and became less frequent as drug concentrations were increased.

Anti-Bacterial Agents↗

PubMed2000

Lactic acid permeabilizes gram-negative bacteria by disrupting the outer membrane.

The effect of lactic acid on the outer membrane permeability of Escherichia coli O157:H7, Pseudomonas aeruginosa, and Salmonella enterica serovar Typhimurium was studied utilizing a fluorescent-probe uptake assay and sensitization to bacteriolysis. For control purposes, similar assays were performed with EDTA (a permeabilizer acting by chelation) and with hydrochloric acid, the latter at pH values corresponding to those yielded by lactic acid, and also in the presence of KCN. Already 5 mM (pH 4.0) lactic acid caused prominent permeabilization in each species, the effect in the fluorescence assay being stronger than that of EDTA or HCl. Similar results were obtained in the presence of KCN, except for P. aeruginosa, for which an increase in the effect of HCl was observed in the presence of KCN. The permeabilization by lactic and hydrochloric acid was partly abolished by MgCl(2). Lactic acid sensitized E. coli and serovar Typhimurium to the lytic action of sodium dodecyl sulfate (SDS) more efficiently than did HCl, whereas both acids sensitized P. aeruginosa to SDS and to Triton X-100. P. aeruginosa was effectively sensitized to lysozyme by lactic acid and by HCl. Considerable proportions of lipopolysaccharide were liberated from serovar Typhimurium by these acids; analysis of liberated material by electrophoresis and by fatty acid analysis showed that lactic acid was more active than EDTA or HCl in liberating lipopolysaccharide from the outer membrane. Thus, lactic acid, in addition to its antimicrobial property due to the lowering of the pH, also functions as a permeabilizer of the gram-negative bacterial outer membrane and may act as a potentiator of the effects of other antimicrobial substances.

Cell Membrane↗

PubMed2006

Alpha-2,3-sialyltransferase enhances Neisseria gonorrhoeae survival during experimental murine genital tract infection.

The addition of host-derived sialic acid to Neisseria gonorrhoeae lipooligosaccharide is hypothesized to be an important mechanism by which gonococci evade host innate defenses. This hypothesis is based primarily on in vitro assays of complement-mediated and phagocytic killing. Here we report that a nonpolar alpha-2,3-sialyltransferase (lst) mutant of N. gonorrhoeae was significantly attenuated in its capacity to colonize the lower genital tract of 17-beta estradiol-treated female BALB/c mice during competitive infection with the wild-type strain. Genetic complementation of the lst mutation restored recovery of the mutant to wild-type levels. Studies with B10.D2-HC(o)H2(d)H(2)-T18c/OSN (C5-deficient) mice showed that attenuation of the lst mutant was not due to increased sensitivity to complement-mediated bacteriolysis, a result that is consistent with recently reported host restrictions in the complement cascade. However, Lst-deficient gonococci were killed more rapidly than sialylated wild-type gonococci following intraperitoneal injection into normal mice, which is consistent with sialylation conferring protection against killing by polymorphonuclear leukocytes (PMNs). As reported for human PMNs, sialylated gonococci were more resistant to killing by murine PMNs, and sialylation led to reduced association with and induction of a weaker respiratory burst in PMNs from estradiol-treated mice. In summary, these studies suggest sialylation confers a survival advantage to N. gonorrhoeae in mice by increasing resistance to PMN killing. This report is the first direct demonstration that alpha-2,3-sialyltransferase contributes to N. gonorrhoeae pathogenesis in an in vivo model. This study also validates the use of experimental murine infection to study certain aspects of gonococcal pathogenesis.

Animals↗

PubMed1981

Bactericidal capacity of newborn phagocytes against group B beta-hemolytic streptococci.

The bactericidal capacity of mononuclear and polymorphonuclear phagocytes obtained from normal newborn infants and from healthy adults was evaluated in vitro, using two group B beta-hemolytic streptococci (GBBHS) serotypes (GBBHS-Ia-SS-615/28 and GBBHS-III-SS-620/50) and uniform opsonic conditions. No intertype differences in bacteriolysis of these two serotypes were observed among leukocytes from newborns or adults. As group, only polymorphonuclear phagocytes from newborns disclosed a significantly lower mean bactericidal capacity than their adult cellular counterpart, and only with respect to GBBHS-III-SS-620/50. On the other hand, 4 or 16 polymorphonuclear samples from newborns tested revealed significantly low bactericidal capacities against both GBBHS serotypes, and an additional sample revealed a bactericidal capacity against GBBHS-III-SS-620/50 alone. Interstrain variations in the intrinsic bactericidal capacity of polymorphonuclear phagocytes from newborns against GBBHS-III may exist, as suggested by a single observation made by using four clinical isolates of GBBHS-III. Such deviant phagocytic capacities of polymorphonuclear phagocytes from newborns may constitute an additional selective risk factor in the genesis of GBBHS sepsis of the newborn.

Adult↗

PubMed1984

Cytotoxicity of human peripheral blood and colostral leukocytes against Shigella species.

We examined the ability of human peripheral blood leukocytes to kill strains of Shigella sonnei and Shigella flexneri by using a modified bactericidal assay. Antibody-dependent cellular cytotoxicity (ADCC) was demonstrated in the presence of specific rabbit immune serum directed against S. sonnei. With peripheral blood leukocytes from adults, ADCC was found only in the mononuclear cell and purified lymphocyte populations. Monocyte-macrophages and polymorphonuclear leukocytes were unable to demonstrate ADCC. Lymphocyte ADCC, which was not affected by the addition of phenylbutazone (an inhibitor of phagocytosis), was mediated by a non-T, Fc receptor-positive, HNK-1- cell. ADCC (using antiserum directed against virulent S. sonnei) was demonstrated against virulent S. sonnei but not against virulent S. sonnei or virulent S. flexneri. In contrast to leukocytes from adults, both mononuclear and polymorphonuclear cells from neonatal cord blood and from a patient with chronic granulomatous disease mediated anti-Shigella ADCC. Breast milk leukocytes (BMLs) collected 1 to 3 days postpartum were used as effector cells against virulent S. sonnei. The entire BML population, BMLs which did not adhere to plastic and BMLs which passed through nylon wool columns mediated both natural killer cytotoxicity and ADCC. In paired experiments, natural killer cytotoxicity and ADCC were significantly lower (30 to 45% inhibition) but not ablated, when phenylbutazone was added to BMLs and nylon wool-purified BMLs (P less than 0.05). These experiments suggest that colostral leukocytes mediated both extracellular and intracellular bacteriolysis in the presence and absence of specific antiserum. These mechanisms may be active in vivo in protection against shigellosis.

Age Factors↗

PubMed1987

Physical heterogeneity of neisserial lipooligosaccharides reflects oligosaccharides that differ in apparent molecular weight, chemical composition, and antigenic expression.

We studied the oligosaccharides (OS) of outer membrane lipooligosaccharides (LOS) of Neisseria gonorrhoeae and Neisseria meningitidis. OS from the LOS of an individual neisserial strain always eluted from Sephadex G-50S as multiple peaks; the polyacrylamide gel elution profiles were nearly identical to the polyacrylamide gel electrophoresis profiles of the sodium dodecyl sulfate-disaggregated native LOS from which the OS were derived. Neisserial OS coeluted with Dex14 to Dex27 dextran oligomers (Mr, 2,210 to 4,320). Monosaccharide composition varied among the several OS released from the LOS of a single strain. The two OS of a gonococcal strain sensitive to normal human serum (NHS) bacteriolysis (sers) varied in their ability to inhibit the binding of NHS immunoglobulin M to their parental LOS. The OS that was rich in hexosamines inhibited NHS immune lysis of its parent strain; the OS that was poor in hexosamines did not. We conclude that structural differences in their OS account for the Mr heterogeneity of the LOS of a strain.

Acetates↗

PubMed1999

Differences in surface expression of NspA among Neisseria meningitidis group B strains.

NspA is a highly conserved membrane protein that is reported to elicit protective antibody responses against Neisseria meningitidis serogroups A, B and C in mice (D. Martin, N. Cadieux, J. Hanel, and B. R. Brodeur, J. Exp. Med. 185:1173-1183, 1997). To investigate the vaccine potential of NspA, we produced mouse anti-recombinant NspA (rNspA) antisera, which were used to evaluate the accessibility of NspA epitopes on the surface of different serogroup B strains by an immunofluorescence flow cytometric assay and by susceptibility to antibody-dependent, complement-mediated bacteriolysis. Among 17 genetically diverse strains tested, 11 (65%) were positive for NspA cell surface epitopes and 6 (35%) were negative. All six negative strains also were resistant to bactericidal activity induced by the anti-rNspA antiserum. In contrast, of the 11 NspA surface-positive strains, 8 (73%; P < 0.05) were killed by the antiserum and complement. In infant rats challenged with one of these eight strains, the anti-rNspA antiserum conferred protection against bacteremia, whereas the antiserum failed to protect rats challenged by one of the six NspA cell surface-negative strains. Neither NspA expression nor protein sequence accounted for differences in NspA surface accessibility, since all six negative strains expressed NspA in outer membrane preparations and since their predicted NspA amino acid sequences were 99 to 100% identical to those of three representative positive strains. However, the six NspA cell surface-negative strains produced, on average, larger amounts of group B polysaccharide than did the 11 positive strains (reciprocal geometric mean titers, 676 and 224, respectively; P < 0.05), which suggests that the capsule may limit the accessibility of NspA surface epitopes. Given these strain differences in NspA surface accessibility, an rNspA-based meningococcal B vaccine may have to be supplemented by additional antigens.

Amino Acid Sequence↗

PubMed2002

Sequential immunization with vesicles prepared from heterologous Neisseria meningitidis strains elicits broadly protective serum antibodies to group B strains.

The capsular polysaccharide of Neisseria meningitidis group B is an autoantigen, whereas noncapsular antigens are highly variable. These factors present formidable challenges for development of a broadly protective and safe group B vaccine. Mice and guinea pigs were sequentially immunized with three doses of micovesicles or outer membrane vesicles prepared from three meningococcal strains that were each antigenically heterologous with respect to the two major porin proteins, PorA and PorB, and the group capsular polysaccharide. The resulting antisera conferred passive protection against meningococcal group B bacteremia in infant rats and elicited complement-mediated bactericidal activity against genetically diverse group B strains that were either homologous or heterologous with respect to PorA of the strains used to prepare the vaccine. By using knockout strains, a portion of the bactericidal antibody was directed against the highly conserved protein, neisserial surface protein A (NspA). Further, an anti-NspA monoclonal antibody elicited by the sequential immunization was highly bactericidal against strains that were previously shown to be resistant to bacteriolysis by anti-NspA antibodies produced by immunization with recombinant NspA. Sequential immunization with heterologous vesicle preparations offers a novel approach to eliciting broadly protective immunity against N. meningitidis strains. An NspA-based vaccine prepared from protein expressed by Neisseria also may be more effective than the corresponding recombinant protein made in Escherichia coli.

Animals↗

PubMed2003

Disparity in functional activity between serum anticapsular antibodies induced in adults by immunization with an investigational group A and C Neisseria meningitidis-diphtheria toxoid conjugate vaccine and by a polysaccharide vaccine.

Polysaccharide-protein conjugate vaccines elicit higher concentrations of serum anticapsular antibody in infants and children than do unconjugated polysaccharide vaccines. The conjugate-induced antibodies also have higher avidity and complement-mediated bactericidal activity. Similar vaccine-related differences in the magnitude or functional activity of antibody are observed infrequently in immunized adults. We compared the antibody responses of adults immunized with an investigational group A and C meningococcal conjugate vaccine to those elicited by an unconjugated meningococcal polysaccharide vaccine. Although there were no significant differences between the respective geometric mean bactericidal titers of the two vaccine groups, it took, on average, three- to fourfold higher concentrations of polysaccharide-induced serum anticapsular antibody to achieve 50% complement-mediated bacteriolysis than conjugate-induced antibody (P < 0.001 for groups A and C). At limiting doses, the polysaccharide-induced anticapsular antibodies also were less effective in conferring passive protection against meningococcal bacteremia in infant rats challenged with a group C strain (P < 0.04). The avidity index of the group C antibodies was higher in the conjugate vaccine group than in the polysaccharide vaccine group (P < 0.005). The disparities in the functional activity of the anticapsular antibodies elicited in adults by the two vaccines imply fundamental differences in the respective B-cell populations stimulated.

Adult↗

PubMed2004

Naturally acquired passive protective activity against Neisseria meningitidis Group C in the absence of serum bactericidal activity.

The hallmark of immunity to meningococcal disease is a bactericidal titer in serum of > or =1:4 measured with human complement, but this threshold titer may underestimate the extent of protection. We used the infant rat model of meningococcal bacteremia to measure group C passive protective activity in serum samples from 91 unimmunized adults living in California. A total of 35 sera (38.5%) had passive protective activity. Sera with complement-mediated bactericidal titers of > or =1:4 were 3.4-fold more likely to confer protection (89%) than nonbactericidal sera (26%; P < 0.0001). Thus, bactericidal titers of > or =1:4 are a marker of protection, but this threshold lacks sensitivity for predicting protective activity. We investigated the 73 sera with bactericidal titers of <1:4 to determine the basis of protective activity. The 19 sera with protective activity had a higher geometric mean group C anticapsular antibody concentration (0.72 microg/ml) than the 54 sera that lacked protective activity (0.16 microg/ml; P < 0.001). Thus, protective activity in the absence of bactericidal activity was associated with higher concentrations of anticapsular antibodies, but not all sera with anticapsular antibodies conferred protection. Of 18 nonbactericidal sera with anticapsular antibody concentrations between 0.31 and 0.99 microg/ml, the 11 sera that conferred protection had a higher mean antibody avidity constant (21.9 nM(-1)) than the 7 nonprotective sera (14.6 nM(-1); P < 0.03). Thus, in sera with titers of <1:4, protective activity is associated with higher-avidity group C anticapsular antibodies, which are present in concentrations insufficient to elicit complement-mediated bacteriolysis in vitro but sufficient to confer protection in an in vivo bacteremia model.

Animals↗

PubMed1992

A new mercury-penicillin V derivative as a probe for ultrastructural localization of penicillin-binding proteins in Escherichia coli.

The precise ultrastructural localization of penicillin-binding protein (PBP)-antibiotic complexes in Escherichia coli JM101, JM101 (pBS96), and JM101(pPH116) was investigated by high-resolution electron microscopy. We used mercury-penicillin V (Hg-pen V) as a heavy-metal-labeled, electron-dense probe for accurately localizing PBPs in situ in single bacterial cells grown to exponential growth phase. Biochemical data derived from susceptibility tests and bacteriolysis experiments revealed no significant differences between Hg-pen V and the parent compound, penicillin V, or between strains. Both antibiotics revealed differences in the binding affinities for PBPs of all strains. Deacylation rates for PBPs were slow despite the relatively low binding affinities of antibiotics. Cells bound most of the Hg-pen V added to cultures, and the antibiotic-PBP complex could readily be seen by electron microscopy of unstained whole mounts as distinct, randomly situated electron-dense particles. Fifty to 60% of the antibiotic was retained by cells during processing for conventional embedding so that thin sections could also be examined. These revealed similar electron-dense particles located predominantly on the plasma membrane and less frequently in the cytoplasm. Particles positioned on the plasma membranes were occasionally shown to protrude into the periplasmic space, thereby reflecting the high resolution of the Hg-pen V probe. Moreover, some particles were observed free in the periplasm, suggesting, for the first time, that a proportion of PBPs may not be restricted to the plasma membrane but may be tightly associated with the peptidoglycan for higher efficiency of peptidoglycan assembly. All controls were devoid of the electron-dense particles. The presence of electron-dense particles in cells of the wild-type JM101, demonstrated that our probe could identify PBPs in naturally occurring strains without inducing PBP overproduction.

Anti-Bacterial Agents↗

PubMed1992

Fan-shaped ejections of regularly arranged murosomes involved in penicillin-induced death of staphylococci.

Electron microscopic research into the murosomes of staphylococci has shown that the number of murosomes involved in penicillin-induced death varies depending on the experimental conditions employed. With 0.1 micrograms of penicillin G per ml, only 1 of a total of about 20 murosomes, the "killing murosome," completely perforated the pressure-stabilized peripheral cell wall during a three-step process. This strictly localized event was mainly attributed to a mechanical effect being comparable to the process of aneurysm formation. Wall perforation was also considered to mark the very moment of penicillin-induced death ("nonlytic killing event"), while bacteriolysis started only postmortem. By varying the osmolarity of the growth medium, the number of murosomes involved in penicillin-induced killing increased considerably, which resulted in the ejection of a fan-shaped row of murosomes at the second division plane. These data are compatible with the finding that, in untreated or chloramphenicol-treated staphylococci, the activation of the murosomes resulted in (i) the formation of regularly arranged "blebs" on the cell surface, containing traces of disintegrated wall material, and (ii) the subsequent liberation of the murosomes lying underneath, leaving behind their former sites in the peripheral wall as a row of regularly arranged "pores" in every division plane. The number, distribution, and positioning of these blebs corresponded with those of the pores and the original murosomes. The significance of wall autolysins liberated from the first division plane for penicillin-induced wall perforation at the second division plane is discussed.

Cell Division↗