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W H Traub

Publications and source records attributed to W H Traub.

At least 73 records · Page 4Linked to original sources

Incomplete cross-resistance of nalidixic and pipemidic acid-resistant variants of Serratia marcescens against ciprofloxacin, enoxacin, and norfloxacin.

Spontaneous and selected variants of Serratia marcescens with resistance against chloramphenicol, cotrimoxazole, nalidixic acid, and pipemidic acid, revealed moderately reduced susceptibility for enoxacin and norfloxacin, and slightly diminished susceptibility for ciprofloxacin. Therefore, urinary tract infections due to S. marcescens strains showing this nonspecific resistance mechanism still might be amenable to judicious chemotherapy with these three novel bacterial DNA gyrase inhibitors, particularly ciprofloxacin.

Anti-Infective Agents, Urinary↗

Chemotherapy of systemic murine infection due to beta-lactam antibiotic 'tolerant' and non-'tolerant' Staphylococcus aureus.

Two in vitro beta-lactam antibiotic (oxacillin, cefotaxime) 'tolerant' (MBC:MIC ratios = greater than 32) strains of Staphylococcus aureus served to intraperitoneally infect cyclophosphamide-pretreated (leukopenic) NMRI mice. With larger bacterial inocula (approximately 5 X 10(8) CFU) neither oxacillin nor gentamicin or netilmicin yielded optimal chemotherapeutic results. Only combination chemotherapy, in particular oxacillin combined with netilmicin, consistently reduced mouse mortality significantly (p less than 0.001). In contrast, moderate 'tolerant' staphylococcal inocula (approximately 2 X 10(8) CFU) were amenable to chemotherapy with either oxacillin or netilmicin, but not with cefotaxime or gentamicin. Oxacillin combined with either gentamicin or netilmicin resulted in significantly lowered murine mortality rates (p less than 0.001). Cefotaxime combined with either aminoglycoside antibiotic gave less satisfactory results. Systemic murine infections due to three non-'tolerant' strains of S. aureus were amenable to chemotherapy with oxacillin, cefotaxime or netilmicin alone and to combination chemotherapy. It is recommended that cases of life-threatening S. aureus infection, not complicated by acute endocarditis, initially be treated with oxacillin plus netilmicin until availability of laboratory results (antibiogram, documentation of 'tolerance').

Animals↗

Divergent disk susceptibility of coagulase-negative staphylococci to penicillinase-resistant penicillins and augmentin (amoxycillin/clavulanic acid).

30 representative intrinsically penicillin-resistant coagulase-negative staphylococcal (CONS) isolates yielded discrepant agar disk diffusion test (Bauer-Kirby) results for augmentin. Clavulanic acid (2.5 micrograms/ml) enhanced the activity of amoxycillin from 8- to greater than or equal to 128-fold (mean = 26-fold); MICs of amoxycillin (combined with 2.5 micrograms/ml clavulanate) ranged from 1-16 (mean = 3) micrograms/ml. It is recommended that clinical microbiology laboratories withhold 'susceptible' augmentin disk tests results from their reports regarding intrinsically penicillin-resistant CONS isolates. No such discrepancies were encountered among clinical isolates of Staphylococcus aureus.

Amoxicillin↗

Multiple drug-resistant Corynebacteriaceae: in vitro and in vivo (murine) studies.

Five multiple-drug-resistant (MDR) Corynebacterium isolates, which differed in several biochemical traits, were sensitive to rifampin, vancomycin and ciprofloxacin; ciprofloxacin was more active than enoxacin and norfloxacin. The MDR Corynebacterium isolates uniformly were resistant against fresh human serum, but varied in susceptibility to fresh, defibrinated human blood. In combined blood plus antimicrobial drug assays, vancomycin was more active than rifampin, which in turn was more active than ciprofloxacin. Outbred NMRI mice essentially were resistant against the MDR Corynebacterium isolates, as were mice pretreated with cyclophosphamide (leukopenia), type II Carrageenan (blockade of macrophages), or zymosan (depletion of complement), or with the combination of cyclophosphamide plus zymosan. However, mice pretreated with cyclophosphamide plus type II Carrageenan proved somewhat more susceptible.

Actinomycetales↗

Gentamicin- and methicillin-resistant, clinical isolates of Staphylococcus aureus: comparative in vitro and in vivo efficacy of alternative antimicrobial drugs.

Six representative clinical isolates of gentamicin- and methicillin-resistant (GRMR) Staphylococcus aureus, constituting phage groups II and III, were susceptible only to amikacin, cefamandole, clindamycin, fosfomycin, fusidic acid, netilmicin, nitrofurantoin, trimethoprim-sulfamethoxazole, and vancomycin (Bauer-Kirby test). With few exceptions, the minimal bactericidal concentrations of the beta-lactam and aminoglycoside antibiotics tested, fusidic acid, and irregularly those of vancomycin, but not those of fosfomycin and rifampin, exceeded minimal inhibitory concentrations values by at least 8-fold. In vitro, combinations of rifampin with cefamandole, cefazolin, cefotaxime, erythromycin, fosfomycin, fusidic acid, netilmicin, and vancomycin yielded indifferent effects. The GRMR S. aureus strains were refractory against 50, 65, and 80 vol% of fresh defibrinated blood; following reduction of viable counts at 2 h (greater than or equal to 90%), rebound growth invariably occurred within 4 h after exposure. Combined human blood (55 vol%)-antibiotic assays revealed rifampin as the most effective drug, followed by vancomycin, fusidic acid, and cefamandole, in that order. Blood plus cefotaxime, cefazolin, or netilmicin yielded indifferent effects; fosfomycin failed in vitro. In terms of speed of recovery and survival data (chi 2 test), cyclophosphamide-pretreated, i.e., leukopenic NMRI mice responded best to chemotherapy with rifampin, followed by vancomycin, cefamandole, netilmicin, and fosfomycin, in that order; cefazolin yielded variable results.

Animals↗

Chemotherapeutic efficacy of cefotaxime and failure of fosfomycin in murine Salmonella typhimurium infection.

Six clinical isolates and 1 reference strain of Salmonella typhimurium were sensitive to conventional antibiotics (ampicillin, chloramphenicol, cotrimoxazole), cefotaxime (CTX), and fosfomycin ( FOSFO ). All 7 strains carried a 55 megadalton plasmid ( Birnboim - Doly agarose gel electrophoresis technique) and were of comparable virulence for outbred NMRI mice (LD50 values = range of 1.7 X 10(5)-1.0 X 10(6) CFU; intraperitoneal route). CTX (5 mg/25 g mouse/day, divided into 2 doses; duration = 7 days) proved efficacious against 3 selected strains (No. H 8800, 14, and 20) of S. typhimurium (p less than 0.01). FOSFO (same therapeutic regimen) failed in this regard; following transitory improvement of diseased animals (days 2-4), the mortality of treated animals eventually approached that of untreated control animals. Administration of 15 mg FOSFO /mouse/day likewise failed to enhance murine survival. Reisolated S. typhimurium bacteria of these 3 assay strains still were susceptible to FOSFO . In vitro, CTX likewise surpassed FOSFO in bactericidal activity against the same 3 S. typhimurium strains on a weight-for-weight basis in various biological fluids (human midstream urine; human defibrinated blood; murine thioglycolate-induced macrophage-rich peritoneal exudate).

Animals↗

In vitro antibiotic susceptibility of Legionellaceae: search for alternative antimicrobial drugs.

Reference strains of Legionella pneumophila (serotypes 1-4, and 6), Legionella micdadei , and Legionella bozemanii proved susceptible (agar dilution test, buffered charcoal yeast extract agar) to erythromycin, rifampin, augmentin (amoxycillin plus clavulanic acid), cefotaxime, cefoxitin, enoxacin , fusidic acid, and norfloxacin; cefamandole was less active. The strains varied in susceptibility to fosfomycin.

Anti-Bacterial Agents↗

Characterization of two clinical, multiple-drug-resistant isolates of Enterobacter cloacae.

Two multiple drug resistant Enterobacter cloacae isolates (Nos. 460 and 493) varied phenotypically in bacteriocin susceptibility in the absence of significant O antigen variation. Both isolates were susceptible to chloramphenicol, nitrofurantoin, polymyxin B, nalidixic acid, norfloxacin, and enoxacin only. One isolate carried a non-conjugative resistance (R) plasmid, whereas the other isolate contained a conjugative, 'curable' R plasmid and a cryptic plasmid. Both wild-type isolates constitutively produced a chromosomal cephalosporinase (nitrocefin hydrolysis); 'cured' variants of E. cloacae isolate No. 493, which had become susceptible for lamoxactam, produced a cefazolin-inducible beta-lactamase. The two E. cloacae isolates, including their 'cured' variants, were of low-grade virulence for outbred NMRI mice. Both isolates differed somewhat in susceptibility to defibrinated human blood. Inhibitory (0.25 microgram/ml), but not subinhibitory (0.125 microgram/ml) concentrations of norfloxacin and enoxacin combined with human blood yielded additive effects against both E. cloacae isolates.

Adult↗

Intraphagocytic bactericidal activity of bacterial DNA gyrase inhibitors against Serratia marcescens.

Addition of phenylbutazone (2 mg/ml) to 55 vol% of fresh defibrinated human blood permitted leukocytic ingestion of Serratia marcescens bacteria, but blocked phagocytic killing activity. The group A (phage tail) bacteriocin bA+ 16 served to kill extraphagocytic test bacteria. Five bacterial DNA gyrase inhibitors (ciprofloxacin, enoxacin, norfloxacin, nalidixic acid and pipemidic acid) revealed intraphagocytic bactericidal activity against ingested S. marcescens bacteria of three test strains; the extent of intraphagocytic activity of these drugs approximated that of rifampin. Following combination with unmodified defibrinated human blood (55 vol%), ciprofloxacin, enoxacin, norfloxacin and pipemidic acid yielded additive effects against 3 assay strains of S. marcescens and Escherichia coli strain ATCC 25922; nalidixic acid was inferior in this regard. These data might guide chemotherapy of parenchymatous urinary tract infections.

Blood Bactericidal Activity↗

Purification and characterization of two Serratia marcescens proteases.

The exocellular proteases of two Serratia marcescens strains (strains SF 178 and SH 186; both of serotype 06/014:H12 and bacteriocin type 18) were separated from the culture supernatants through precipitation with ammonium sulfate, followed by hydroxylapatite adsorption chromatography, Sephadex G-100 gel filtration, and DEAE-Sephadex A-25 ion exchange chromatography. The molecular weights amounted to 54,400 Daltons (SDS-PAGE electrophoresis). Both enzymes contained 1 g-atom of zinc and 7 g-atoms of calcium per mol. The amino acid sequences were essentially identical. Serologically, both enzymes cross-reacted strongly, suggesting similar antigenic determinants. The two enzymes were microheterogeneous; isoelectric focusing revealed two protein bands at pH 5.4 and 5.5, respectively. The optimal temperature for hydrolysis of azocasein was 30 degrees C. Both proteases revealed 2 optimal pH values (SF 178 = pH 6-7 and pH 8-10; SH 186 = pH 7 and pH 9).

Amino Acids↗

Failure of the commercial human IgG immunoglobulin preparation Polyglobin to enhance combined phagocytic and serum bactericidal activity of normal blood against Serratia marcescens.

The IgG immunoglobulin preparation Polyglobin failed to enhance the combined phagocytic and serum bactericidal activity of 65 vol% of fresh defibrinated human blood from health adults against representative test strains of Serratia marcescens, despite documented O-agglutinin activity of Polyglobin against every test strain employed. It was concluded that pooled human IgG immunoglobulin, i.e. 'natural' IgG antibodies, would not be expected to exert a beneficial effect against S. marcescens in patients with sufficient residual, functional 'natural' antibodies and complement.

Blood Bactericidal Activity↗

Interactions of antimicrobial drugs and combined phagocytic/serum bactericidal activity of defibrinated human blood against Serratia marcescens. III. beta-Lactam antibiotics and fosfomycin.

Neither cefoperazone, cefotaxime, mezlocillin nor piperacillin significantly killed intraphagocytic bacteria of representative assay strains of Serratia marcescens, as determined with 55 vol% of fresh defibrinated human blood treated with 2 mg/ml of phenylbutazone, which permitted phagocytic ingestion of bacteria, but selectively inhibited the microbicidal activity of peripheral blood leukocytes. Extraphagocytic bacteria were killed with group A (phage tail) bacteriocins of S. marcescens. However, minimal bactericidal concentrations of fosfomycin displayed intraphagolysosomal bactericidal activity which approximated that of rifampin. Inhibitory and subinhibitory concentrations of cefoperazone, cefotaxime, fosfomycin, mezlocillin, and piperacillin combined with 55 vol% of defibrinated human blood, respectively, yielded additive effects against all test strains of S. marcescens utilized and Escherichia coli control strain ATCC 25922.

Anti-Bacterial Agents↗

Interactions of antimicrobial drugs and combined phagocytic/serum bactericidal activity of defibrinated human blood against Serratia marcescens. IV. N-formimidoyl thienamycin.

Minimal bactericidal concentrations of thienamycin revealed moderate intraphagolysosomal bactericidal activity against pseudo-(PSR) and genuinely serum-resistant (NSS) assay strains of Serratia marcescens. Combinations of inhibitory and subinhibitory concentrations of thienamycin with 55 vol% of defibrinated human blood resulted in additive effects against all PSR and NSS test strains of S. marcescens and against the NSS Escherichia coli control strain ATCC 25922.

Anti-Bacterial Agents↗

Plasmid-independent resistance of 'gray' colony variants of a strain of Serratia marcescens resistant to amikacin, cefotaxime and lamoxactam.

A multiple-drug-resistant strain of Serratia marcescens (serotype O14:H12; bacteriocin type 18), which was recovered repeatedly from the respiratory tract of an intensive care unit patient, yielded 'gray' colony phenotypic variants which were greater than or equal to four-fold less susceptible to amikacin, cefotaxime, and lamoxactam, but not to netilmicin and N-formimidoyl thienamycin, as compared with 'opaque' (wild-type) colony variants. The 'gray' variants proved phenotypically highly unstable and displayed comparable low virulence for NMRI mice (intraperitoneal route). The 'opaque' and 'gray' variants of this strain carried a nonconjugative, 46-megadalton resistance (R) plasmid, as determined by DNA agarose gel electrophoresis. The R-plasmid-mediated resistance against chloramphenicol, gentamicin, kanamycin, mezlocillin, piperacillin, triple sulfonamides, and cotrimoxazole, as demonstrated with 'curing' experiments. The mechanism of the novel amikacin-beta-lactam antibiotic resistance phenomenon remained undetermined.

Amikacin↗

Combined defibrinated human blood and antimicrobial drug activities against Enterobacter cloacae.

The combinations of 11 antimicrobial drugs and fresh human defibrinated blood were examined for potential additive effects against several isolates of Enterobacter cloacae recovered from patients with bacteremia or meningitis. Aminoglycosides (amikacin, gentamicin, netilmicin) proved most efficacious, followed by cephalosporins (lamoxactam, cefotaxime, ceftizoxime) and ureidopenicillins (mezlocillin, piperacillin). Nalidixic acid, nitrofurantoin, and cotrimoxazole yielded indifferent effects. The E. cloacae isolates displayed low virulence for outbred NMRI mice.

Animals↗