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At least 1,117 records · Page 62Linked to original sources
PubMed1975

Isolation and characterization of Gal E mutant Ty 21a of Salmonella typhi: a candidate strain for a live, oral typhoid vaccine.

A gal E mutant of Salmonella typhi was isolated; results obtained with Salmonella typhimurium and the mouse as a model for human typhoid fever indicated that this mutant has the potential for use as a live, oral typhoid vaccine. The mutant, Ty 21a, took up galactose from exogenous sources and accumulated sufficient quantities of galactose-1-phosphate and uridine diphosphate galactose to cause lysis of the cells, an event that resulted in the avirulence of the strain. Galactose was incorporated sufficiently into the cell wall of Ty 21a to allow the synthesis of smooth-type lipopolysaccharides, which are necessary for the proper immunogenicity. Cells of strain Ty 21a, when given intraperitoneally, protected mice against lethal challenge with strain Ty 2 of S. typhi.

Animals↗
PubMed1977

Mechanism of action of tetracaine hydrochloride against Pseudomonas aeruginosa.

The mode of action of tetracaine hydrochloride in vitro on Pseudomonas aeruginosa was investigates. The inhibitory and bactericidal action of tetracaine hydrochloride in vitro was adversely affected by magnesium ions. Observation of cellular lysis, leakage of intracellular materials, dehydrogenase activity, and a higher sensitivity of spheroplasts than of whole cells to tetracaine led to the conclusion that tetracaine acts by damaging the cell membrane. The lytic action of lysozyme was potentiated by tetracaine; this finding indicates enhanced permeability of the cell wall. Alteration of cell wall permeability was demonstrated by the finding that the cells exposed to subinhibitory amounts of tetracaine became susceptible to otherwise ineffective erythromycin.

Bacteriolysis↗
PubMed1986

Role of lipopolysaccharide and capsule in the serum resistance of bacteremic strains of Escherichia coli.

To define the relative roles of capsule and lipopolysaccharide in the virulence of Escherichia coli obtained from blood, we compared the behavior of K1- and K5-encapsulated strains in serum bactericidal and rat virulence assays. Unencapsulated isogenic mutants selected from five parent strains of E. coli O12:K1, but not of O18:K1 or O7:K1 (all rough-specific phage insensitive), were lysed by normal human sera. In contrast, isogenic mutants from strains of serotypes O6:K5 and O18:K5 retained the serum resistance of the parent strains. There was a greater than 10(5) difference in LD50 in newborn rats between K1-positive and K1-negative pairs of E. coli serotypes O18 and O7 and a greater than 1 log difference between isogenic pairs of serotype O12; however, the K5 isogenic pairs had a similar LD50. Some non-O6 O serotypes, however, required the K5 capsule for serum resistance. We conclude that some O serotypes require encapsulation for optimal virulence but that other O serotypes may not.

Animals↗
PubMed1987

Nonsteroidal anti-inflammatory agents in the therapy for experimental pneumococcal meningitis.

An increased inflammatory mass in the subarachnoid space during bacterial meningitis may correlate with a poor outcome of disease. Using a rabbit model of pneumococcal meningitis, we sought to reduce this inflammatory process. The ability of the pneumococcal cell wall to cause death and to generate leukocytosis and abnormal chemistry in cerebrospinal fluid was prevented when animals were treated with inhibitors of cyclooxygenase pathway of arachidonate metabolism. Bacterial lysis by ampicillin led to release of cell wall that caused a significant, transient increase in meningeal inflammation. This inflammatory burst was also prevented by administering cyclooxygenase inhibitors concurrently with the antibiotic.

Ampicillin↗
PubMed1988

Penicillin resistance and defective lysis in clinical isolates of pneumococci: evidence for two kinds of antibiotic pressure operating in the clinical environment.

Seventy percent of clinical isolates of penicillin-resistant pneumococci also exhibit defective lysis when treated with penicillin exceeding the minimal inhibitory concentration (MIC). To provide a possible explanation for the frequent association of these two traits, we exposed penicillin-susceptible pneumococci to two kinds of antibiotic pressures in the laboratory. Treatment of cultures with cycles of high concentrations of penicillin (20 X MIC) followed by growth of the survivors in drug-free medium selected for lysis-defective mutants that died only slowly during antibiotic treatment but had unchanged MICs. Exposure to sustained, low levels of penicillin produced resistant mutants, with elevated MICs, that lysed normally with penicillin. We suggest that the cyclic antibiotic exposure generally used in the clinical setting may select primarily for enhanced survival. From these survivors a second type of antibiotic exposure--sustained antibiotic concentrations just above the MIC (concentrations that may be restricted to the tail-end trough of a dosing interval)--selects for penicillin-resistant mutants.

Bacteriolysis↗
PubMed1988

Microbiological and clinical significance of a new property of defective lysis in clinical strains of pneumococci.

A pneumococcal isolate that caused relapsing meningitis in a patient infected with human immunodeficiency virus (HIV) was found to display an unusual response to penicillin--rapid death but a striking lack of cellular lysis. This lytic defect was also detected in all four pneumococcal isolates from three additional HIV-infected patients and in more than half of the clinical isolates from patients with bacteremia. In a rabbit model of meningitis, the lysis-defective strain remained cryptic, with a delay of 5 h in the onset of leukocytosis in cerebrospinal fluid. A marked burst of leukocytosis was associated with ampicillin-induced lysis of a lysis-sensitive strain but not of a lysis-defective strain. Pneumococcal clinical isolates have different lytic responses to penicillin; defective lysis may adversely affect the course of meningitis, an observation suggesting that autolysins play a role in modulating infectious diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Inducible resistance to vancomycin in Enterococcus faecium D366.

Strain D366, a clinical isolate of Enterococcus faecium, is resistant (minimum inhibitory concentration [MIC] 32 mg/L) to vancomycin. When exponential-phase cultures were exposed to half the MIC of vancomycin, a lag of 3-4 h occurred before growth resumed. Cells preexposed to 1/2 MICs of vancomycin did not show any lag. Pregrowth of D366 with vancomycin caused resistance to all glycopeptides tested. Pregrowth in vancomycin resulted in synthesis of a 3.95-kDa cytoplasmic-membrane-associated protein. This protein was correlated with resistance in mutants with high-level resistance, in the presence of NaCl, which inhibited the activity of vancomycin, and when several glycopeptides with varying activities were tested. Vancomycin-grown cells appeared abnormal and lysed at a much slower rate than did normal cells. We conclude that (1) vancomycin resistance in D366 is inducible; (2) resistance is correlated with the synthesis of 39.5-kDa cytoplasmic membrane protein; and (3) this protein play an additional role in the inhibition of normal lytic functions.

Aged↗
PubMed1990

The vir locus affects the response of Bordetella pertussis to antibiotics: phenotypic tolerance and control of autolysis.

Eradication of Bordetella pertussis from the respiratory tract occurs slowly even when bactericidal antibiotics are used. The rate of killing of B. pertussis was found to be proportional to growth rate: virulent, slowly growing strains were killed over days, while rapidly growing strains (either avirulent or virulent modulated by growth conditions to avirulent) were killed over hours. Minimum inhibitory concentrations and binding of antibiotics to membrane targets were equivalent in virulent and avirulent cells, suggesting differences in antibiotic response might reflect differences in activities of the autolytic cascade. This was supported by the finding that cell wall degradation was less than 40% per day in virulent strains and greater than 70% per day in avirulent strains. Penem antibiotics, known to rapidly kill even slowly growing bacteria, demonstrated a more-than-twofold greater rate of killing of slowly growing virulent strains compared with ampicillin or erythromycin. This suggests the potential for improved therapeutic efficacy in vivo. Thus, the vir locus, which determines phase transition in B. pertussis, is apparently the first example of a sensor-transducer system controlling phenotypic tolerance and antibiotic-induced autolytic activity.

Anti-Bacterial Agents↗
PubMed1993

Triggering of pneumococcal autolysis by lysozyme.

Lysozyme had no effect on the rate of multiplication of growing cultures of Streptococcus pneumoniae, but it greatly reduced the lag period that precedes autolysis of these bacteria in stationary phase. Several experiments were done to understand the mechanism of this effect. Lysozyme had no hydrolytic activity on intact cell walls, and cell walls of pneumococci grown with or without lysozyme had identical composition and susceptibility to the pneumococcal autolysin. The acceleration of stationary-phase autolysis by lysozyme involved triggering of the pneumococcal autolytic enzyme since lysozyme had no detectable effect on nonautolysing (LytA-) mutants and heat-inactivated lysozyme completely lacking enzymatic activity was as effective as the nondenatured enzyme in facilitating stationary-phase autolysis. The role of lysozyme in host defense against pneumococcal infection remains elusive.

Animals↗
PubMed1987

Trimethoprim-induced structural alterations in Staphylococcus aureus and the recovery of bacteria in drug-free medium.

Bacteriostatic concentrations of trimethoprim, which possibly acts as a DNA-inhibitor, induced the swelling of staphylococci and affected their cell walls, their cytoplasmic membrane and part of their autolytic wall system. Trimethoprim proved to be the first growth-inhibiting drug that did not induce the formation of thickened cell walls in staphylococci. An ultrastructurally important effect of trimethoprim treatment was the appearance of mesosome-like structures which were not fixation artefacts. Additionally, trimethoprim led to the formation of incomplete cross walls, while cross wall initiation continued virtually unaffected. After removal of trimethoprim, extremely fast growth restoration occurred with the formation of new cell wall material underlying the old wall. Afterwards, the old wall material was disintegrated by autolytic processes.

Bacteriolysis↗