PubMed Health⌕ Search

Biomedical subjects

W H Traub

Publications and source records attributed to W H Traub.

At least 55 records · Page 3Linked to original sources
PubMed1987

Active immunization of NMRI mice against Serratia marcescens. II. K-antigen extracts.

The minimal active immunogenic doses (intraperitoneal administration) of crude K-antigen extracts of Serratia marcescens for NMRI mice were 80 ng. Following ultracentrifugation (300,000 x g, 16 h), supernatant fluids of three K-antigen extracts were free of contaminating DNA, RNA, and 2-keto-3-deoxy-D-manno-octonic acid (KDO), and the contents of Limulus amoebocyte lysate-reactive lipopolysaccharide (LPS) had been reduced from 100- to 1000-fold. The minimal active immunogenic doses of two ultracentrifuged K-antigen extracts were 2 and 10 micrograms, respectively. A mucoid strain of S. marcescens (SM 20-M; serotype O6/O14:H12) yielded nonmucoid (= SM 29-NM) variants that had lost most of the O6/O14 O-antigen (LPS) and all of the SM 29-M K-antigen extract reactivity (ELISA test) and which were ca. 5-fold less mouse-virulent. Crude K-antigen extracts from S. marcescens strain SM 29-M and variant SM 29-NM failed to protect NMRI mice against strain SM 29-M.

Animals↗
PubMed1987

Growth curves of Clostridium perfringens in Schaedler and brain heart infusion broths.

Four Clostridium perfringens strains recovered from clinical specimens, four strains obtained from faecal specimens of healthy adults, and control strain ATCC 13124 were inoculated into Schaedler and Brain Heart Infusion broths, respectively, and incubated anaerobically at 35 degrees C for 24 h. The exponential growth phase usually lasted from 2 to 6 h following inoculation; the generation times averaged 23 min at 2 to 4 h and 27 min between 4 and 6 h of incubation. The early stationary growth phase (generation time between 6 and 8 h = 89 min) was reached at 8 h following inoculation. All strains displayed essentially identical in vitro growth rates, even though they differed in murine virulence.

Animals↗
PubMed1987

Active immunization of NMRI mice against Serratia marcescens. I. Phenol-water lipopolysaccharide fractions and purified metalloproteases.

The minimal intraperitoneal (i.p.) immunogenic doses of phenol-hot water lipopolysaccharide (P-W- LPS) preparations from three strains of Serratia marcescens for juvenile NMRI mice ranged from 3.2 to 16 ng following i.p. challenge infection with homologous strains. Dual autoclaving (121 degrees C, 15 min) abolished the cross-immunogenicity of two selected P-W LPS extracts. Four purified metalloproteases from S. marcescens strains SF 178, SH 186, SV O1, and SE 182 shared the following properties: a) inhibition of proteolytic (azocasein hydrolysis) activity by 50 mM of EDTA; b) heat-lability (60 degrees C, 15 min); c) identical molecular weights (54,000 Daltons = 54 K) as documented with the SDS-PAGE procedure; d) close serologic relatedness (ELISA technique, polyclonal rabbit immune sera); and e) uniform reactivity of the 54 K polypeptide bands with polyclonal rabbit anti-metalloprotease immune sera (Western blots). The minimal immunogenic dose of metalloprotease SF 178, the sole significantly murine immunogenic enzyme, was 1000 ng = 1 microgram.

Animals↗
PubMed1987

Interactions of purified Serratia marcescens metalloproteases with fresh human serum and with purified human serum proteins.

Exposure of fresh human serum to two purified metalloproteases of S. marcescens strains SF 178 and SH 186 (both of serotype O6/O14:H12) at 35 degrees C, 3 h, resulted in altered electrophoretic mobility of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin, alpha 2-HS-glycoprotein, and complement (C) components C1q, C1s, C3a, C3c, C4, C5, and C9, but not C6, C7, C8, and properdin, as determined with electroimmunoassays (Laurell technique). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) documented the partial degradation of the heavy (H) chain of purified human immunoglobulin IgG by the metalloproteases of S. marcescens strains SF 178 and SV O1 (serotype O13/O19:H1), but not by the metalloproteases of strains SH 186 and SE 182 (serotype O9B:H11) following extended incubation (35 degrees C, 22 h). Human IgA and IgM were refractory. Purified human C components, C3, C4, C5, C6, C7, C8, and C9, as well as purified human alpha 1-antitrypsin, alpha 2-macroglobulin, transferrin, and lactoferrin were attacked by the S. marcescens metalloproteases SF 178 and SH 186 at 35 degrees C for 5 h, as demonstrated with the SDS-PAGE procedure; haptoglobin and C-reactive protein were resistant.

Acute-Phase Proteins↗
PubMed1987

Outer membrane protein alterations in Serratia marcescens resistant against aminoglycoside and beta-lactam antibiotics.

Six isolates of Serratia marcescens were recovered sequentially from the respiratory tract of a single patient. The first three isolates were of the 'opaque' (wild-type) colony type and were susceptible to amikacin, cefotaxime, and lamoxactam. The following three isolates were of the small, 'gray' colony variety, significantly less susceptible to the three antibiotics, and revealed three altered outer membrane proteins, as determined with the SDS-PAGE procedure.

Aminoglycosides↗
PubMed1987

Comparative disk and broth dilution susceptibility test results with ticarcillin and timentin against Pseudomonas aeruginosa and Pseudomonas maltophilia.

A total of 500 clinical isolates of Pseudomonas aeruginosa and 14 isolates of Pseudomonas maltophilia were examined for susceptibility to ticarcillin and timentin (ticarcillin plus clavulanic acid). Clavulanic acid enhanced the activity of ticarcillin against only 34 of 500 isolates of P. aeruginosa. Among 23 isolates of P. aeruginosa, that had yielded divergent disk diffusion results, there were 3 major discrepancies (3 = ticarcillin-resistant by disk diffusion, but susceptible by broth dilution test criteria) and 1 very major discrepancy (timentin-susceptible by disk diffusion, but resistant by broth dilution test criteria). Clavulanic acid enhanced the activity of ticarcillin against 12 of 14 isolates of P. maltophilia; there were 2 major discrepancies (ticarcillin resistance in terms of disk diffusion, but susceptibility according to ticarcillin MICs). Consequently, it was decided to continue employing timentin disks alone, rather than add ticarcillin disks in our Bauer-Kirby test battery for Pseudomonadaceae.

Clavulanic Acids↗
PubMed1987

Gentamicin- and methicillin-resistant Staphylococcus aureus: in vitro susceptibility to antimicrobial drugs.

Thirteen nosocomially significant, gentamicin- and methicillin-resistant (GRMR) Staphylococcus aureus isolates, all of phage group III/M (lysotype 42E/47/53/54/75/77/83A/84/85/94/96), were uniformly resistant against augmentin, erythromycin, fosfomycin, gentamicin, methicillin, oxacillin, penicillin G, tetracycline, and tobramycin, but differed in susceptibility to cefamandole, ciprofloxacin, clindamycin, imipenem, josamycin, the synthetic chinolone Ro 23-6240, and ofloxacin. All isolates were susceptible to chloramphenicol, coumermycin, fusidic acid, novobiocin, rifampin, teicoplanin, trimethoprim-sulfamethoxazole (cotrimoxazole), and vancomycin. One isolate was of intermediate susceptibility to netilmicin. On a weight-for-weight basis, the 7 most active drugs were rifampin, coumermycin, cotrimoxazole, novobiocin, teicoplanin, fusidic acid, and vancomycin (in decreasing order) in terms of minimal inhibitory concentrations. With regard to minimal bactericidal concentrations, coumermycin, rifampin, vancomycin, teicoplanin, cotrimoxazole, ofloxacin, and ciprofloxacin (in decreasing order) were the 7 most potent antimicrobial drugs. Freshly defibrinated human blood [65% (v/v)] combined with chloramphenicol and rifampin, respectively, resulted in a weak additive effect (time kill curves). Indifferent effects were observed following combination of blood with ciprofloxacin, cotrimoxazole, coumermycin, fusidic acid, imipenem, netilmicin, novobiocin, ofloxacin, compound Ro 23-6240, teicoplanin, and vancomycin. Rifampin combined with novobiocin, teicoplanin, and vancomycin, respectively, in the presence of 65% (v/v) human blood, resulted in an additive effect. Combinations of rifampin with 9 other antimicrobial drugs in blood yielded essentially indifferent effects.

Anti-Bacterial Agents↗
PubMed1987

Tentative inhibition zone criteria (Bauer-Kirby agar disk diffusion method) for rifampin against staphylococci.

Two of 359 (0.6%) clinical isolates of Staphylococcus aureus and 12 of 218 (5.5%) clinical isolates of coagulase-negative staphylococci were resistant or of intermediate susceptibility against rifampin as based on minimal inhibitory concentration (MIC) breakpoints obtained with the agar dilution method: MIC greater than or equal to 2 micrograms/ml = resistant; MIC 0.25-1 microgram/ml = intermediate susceptible; MIC less than 0.125 microgram/ml = susceptible. The following inhibition zone criteria with 2 micrograms rifampin disks were proposed for staphylococcal isolates utilizing the Bauer-Kirby agar disk diffusion test: diameter of inhibition zones less than or equal to 13 mm = resistant; diameter 14-21 mm = intermediate susceptible; diameter greater than or equal to 22 mm = susceptible.

Drug Resistance, Microbial↗
PubMed1986

In vitro additive effect of imipenem combined with vancomycin against multiple-drug resistant, coagulase-negative Staphylococci.

Imipenem combined with vancomycin resulted in a marked additive effect in vitro against 9 clinical isolates of multiple-drug resistant (MDR), coagulase-negative staphylococci, including strains resistant against imipenem. The additive effect was documented with the aid of checkerboard MIC determinations and with time kill curve experiments. In contrast, imipenem combined with vancomycin merely yielded weak additive or indifferent effects against 10 MDR isolates of Staphylococcus aureus, all of which were susceptible to imipenem.

Coagulase↗
PubMed1986

Intraphagocytic bactericidal activity of ofloxacin compared with that of aztreonam and ceftriaxone against Serratia marcescens.

Addition of phenylbutazone (2 mg/ml) to 55 vol % of fresh defibrinated human blood permitted leukocytic ingestion of serum-resistant Serratia marcescens bacteria, but blocked phagocytic killing activity. The group A (phage tail) bacteriocin bA+ 16 served to kill extraphagocytic test bacteria. At greater than or equal to 2 X MBC, the DNA gyrase inhibitor ofloxacin revealed potent intraphagocytic bactericidal activity against S. marcescens test bacteria (99% kill; 3 h observation period) which corresponded to that of the control drug rifampin (97% kill). The monobactam aztreonam (11% kill) and the third generation cephalosporin ceftriaxone (14% kill) corresponded to cefotaxime (26% kill) in terms of suboptimal intraphagocytic activity. Ofloxacin and aztreonam yielded additive effects following combination of supra-(2 X MIC) and inhibitory (MIC), but not sub-inhibitory (0.5 X MIC) concentrations with 55 vol % of defibrinated human blood against S. marcescens and Escherichia coli control strain ATCC 25922; sub- and inhibitory concentrations of ceftriaxone yielded indifferent effects.

Aztreonam↗
PubMed1986

Clostridium perfringens type A. Comparison of in vitro and in vivo activity of twelve antimicrobial drugs.

Penicillin G and imipenem (N-formimidoyl thienamycin) in vitro were the most active of twelve examined antimicrobial drugs against clinical and fecal isolates of Clostridium perfringens type A. However, vancomycin and fosfomycin, which revealed suboptimal in vitro bactericidal activity, proved as efficacious as penicillin G and imipenem in an experimental mode of murine gas gangrene. Thus, conventional in vitro tests were not uniformly predictive for in vivo (murine) chemotherapeutic efficacy.

Animals↗
PubMed1986

Streptococcus faecalis: in vitro susceptibility to antimicrobial drugs, single and combined, with and without defibrinated human blood.

Ampicillin, fusidic acid, gentamicin, imipenem, mezlocillin, ofloxacin, penicillin G, piperacillin, and vancomycin were examined for inhibitory and bactericidal activity in various broth media against 7 clinical isolates of Streptococcus faecalis. On a weight-for-weight basis, ampicillin, imipenem, mezlocillin, and ofloxacin proved to be more efficacious. All enterococcal isolates were resistant against gentamicin; fusidic acid and vancomycin lacked bactericidal activity. The combinations of either ampicillin, imipenem, mezlocillin, ofloxacin, piperacillin, or vancomycin with a subinhibitory concentration (4 micrograms/ml) of gentamicin, with or without added 65% (v/v) fresh defibrinated human blood, respectively, yielded additive effects against all enterococcal isolates. The addition of fresh human blood failed to enhance the antienterococcal activity of 4 micrograms/ml of gentamicin; in contrast, addition of 65% (v/v) fresh or heat-inactivated (56 degrees C, 30 min) normal rabbit, bovine, and human sera augmented the activity of gentamicin, an effect that was ablated through the addition of either 0.005 M DTT or 0.01 M MgCl2 + 0.01 M EGTA + 0.01 M CaCl2, supplements known to antagonize human serum beta-lysin, but not lysozyme activity.

Animals↗
PubMed1986

Josamycin: interpretation of inhibition zones with the Bauer-Kirby agar disk diffusion test as compared with erythromycin.

A total of 432 clinical isolates of Staphylococcus aureus (128), coagulase-negative staphylococci (123), group A and B beta-hemolytic streptococci (61), group D streptococci (30), Streptococcus penumoniae (29), Haemophilus influenzae (19), Haemophilus parainfluenzae (12), and Legionella pneumophila (30) were examined with the agar dilution and Bauer-Kirby agar disk diffusion tests for susceptibility to josamycin as compared with erythromycin. On a weight-for-weight basis, erythromycin was more active than josamycin against all bacterial species, including L. pneumophila. Josamycin inhibited 18 of 23 S. aureus and 11 of 16 coagulase-negative staphylococcal strains resistant to erythromycin. Utilizing minimal inhibitory concentrations (MIC) breakpoints of less than or equal to 2 micrograms/ml (sensitive), 4 microgram/ml (intermediate) and of greater than or equal to 8 micrograms/ml (resistant), and inhibition zone criteria of greater than or equal to 18 mm diameter (sensitive), 14-17 mm (intermediate), and less than or equal to 13 mm (resistant), and excluding L. pneumophila, there was good correlation between erythromycin MIC and corresponding disk diffusion data for staphylococci and streptococci, but not for Haemophilus species. In comparison, josamycin yielded a significant number of minor discrepant data for group D streptococci and Haemophilus species. It is suggested that erythromycin and josamycin should not be tested against Haemophilus species, and that josamycin should be excluded from test batteries against enterococci. Erythromycin-resistant staphylococci require separate testing with josamycin.

Anti-Bacterial Agents↗
PubMed1986

Susceptibility of Clostridium perfringens type A to 23 antimicrobial drugs.

A total of 106 strains of Clostridium perfringens type A, that had been isolated very recently from faecal cultures of healthy adults, were examined for susceptibility to 23 antimicrobial drugs (agar dilution method). All strains were susceptible to ampicillin, cefazolin, cefotaxime, cefotetan, cefoxitin, ceftriaxone, ciprofloxacin, fusidic acid, imipenem, metronidazole, mezlocillin, ofloxacin, penicillin G, piperacillin, teicoplanin, and vancomycin. Teicoplanin and imipenem were the most active, whereas fosfomycin and tetracycline were the least active drugs. Three of the 106 strains revealed multiple drug resistance against clindamycin, erythromycin, josamycin, tetracycline, and, in one instance, against chloramphenicol.

Anti-Bacterial Agents↗
PubMed1986

Passive protection of NMRI mice with commercial, intravenously applicable human immunoglobulin IgG preparations against Serratia marcescens.

Three commercial, intravenously applicable human immunoglobulin IgG preparations (Gamma-Venin, Polyglobin, and Sandoglobulin) revealed low-titered O-agglutinins against the majority of 22 O-antigen reference strains of Serratia marcescens The three IgG preparations passively protected NMRI mice against intraperitoneal challenge with 8 of 19 selected, serologically defined O-antigen reference strains and clinical, nosocomially significant isolates of S. marcescens.

Agglutinins↗
PubMed1985

Active immunization of NMRI mice against Serratia marcescens.

Phenol-hot water lipopolysaccharide (LPS) extracts of Serratia marcescens strains CDC O3:H1, CDC O6:H3, NEW CDC O14:H12, and SH 186 (serotype O6/O14:H12) significantly protected NMRI mice against intraperitoneal challenge with the more mouse virulent homologous strains; overall, there was moderate cross-protection against the minority of heterologous challenge strains. Trichloroacetic acid LPS extracts and K-antigen extracts of strains NEW CDC O14:H12 and SH 186 also proved protective antigens. The purified metalloproteases of strains SH 186 and SF 178 (serotype O6/O14:H12) effected active murine immunization. Neither active nor passive immunization of NMRI mice with E. coli Rc mutant J5 afforded significant protection against various challenge strains of S. marcescens.

Animals↗