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W H Traub

Publications and source records attributed to W H Traub.

At least 91 records · Page 5Linked to original sources
PubMed1983

Passive protection of NMRI mice against Serratia marcescens: comparative efficacy of commercial human IgG immunoglobulin preparations and rabbit anti-O, -H, -K, -life cell and -protease immune sera.

Three commercial, intravenously applicable human IgG preparations passively protected NMRI mice against intraperitoneal challenge with 11 of 19 selected, serologically defined O-antigen reference strains and clinical, nosocomially significant isolates of Serratia marcescens. Conventional anti-O and anti-H, but not anti-K and anti-protease, rabbit immune sera revealed passive protective capacity against homologous challenge strains; however, anti-O rabbit immune sera failed to invariably protect against heterologous test strains that carried identical serogroup O-antigens. The passive protective efficacy of anti-live cell immune sera, derived from rabbits following recovery from experimental septicemia, was abolished through dual absorption with homologous O-cells. It was concluded that antibodies directed against O-antigens, i.e., lipopolysaccharide moieties, of the challenge strains of S. marcescens afforded passive protection.

Agglutination Tests↗
PubMed1983

Resistance-plasmid- and protease-independent murine virulence of a multiple-drug-resistant strain of Serratia marcescens.

The multiple-drug-resistant Serratia marcescens isolate SH 186 (serotype 06/014:H12, bacteriocin type 18) carried a 44 megadalton, nonconjugative resistance (R-) plasmid as demonstrated with 'curing' experiments and the DNA agarose gel electrophoresis technique. 'Cured' variants, which had lost part of or the entire R-plasmid, proved as virulent for outbred NMRI mice (intraperitoneal route) as the wild-type parent strain. Therefore, the virulence of this S. marcescens strain was plasmid-independent. Protease-deficient variants of this strain as well as protease-negative variants of two additional S. marcescens strains displayed comparable murine virulence. None of 19 representative S. marcescens strains, including isolate SH 186, gave rise to guinea pig keratoconjunctivitis (negative Anton-Sereny tests), i.e., were non-invasive; NMRI mice pretreated with either cyclophosphamide (leukopenia), type II carrageenan (blockade of macrophages) or with zymosan (depletion of complement) revealed essentially unaltered susceptibility to S. marcescens. However, mice pretreated with cyclophosphamide followed by zymosan were significantly more susceptible for 4 tests strains of S. marcescens, including isolate SH 186. Thus, neutrophil granulocytes and complement were required for murine defense against intraperitoneal infection with S. marcescens.

Animals↗
PubMed1983

Hydrogen peroxide-mediated antagonism against serratia marcescens by Streptococcus mitis.

The alpha-hemolytic Streptococcus mitis strain no. 17-1, isolated from the oral cavity of an healthy female adult, antagonized the growth of all 24 test strains of Serratia marcescens examined; furthermore, this strain inhibited the growth of various strains of Staphylococcus aureus, S. epidermidis, Streptococcus pyogenes, S. agalactiae, S. pneumoniae, Haemophilus influenzae, Listeria monocytogenes, and Corynebacterium diphtheriae. However, strans of Escherichia coli, Enterobacter cloacae, Klebsiella pneumoniae, and Pseudomonas aeruginosa proved refractory. The mechanism of microbial antagonism was due to production and release of hydrogen peroxide under aerobic atmospheric conditions, which was neutralized through incorporation of bovine liver catalase into the solid assay medium.

Adult↗
PubMed1983

Bactericidal activity of antimicrobial drugs in simulated urine specimens at various temperatures of incubation.

A total of 23 antimicrobial drugs were examined for bactericidal activity in midstream-urine against Escherichia coli ATCC 25922, Pseudomonas aeruginosa ATCC 27853, Staphylococcus aureus ATCC 25923, or Streptococcus faecalis ATCC 29212 at incubation temperatures of 35, 22, and 7 degrees C, respectively. The majority of chemotherapeutic agents significantly reduced bacterial inocula within 2 h at 35 degrees C. At room temperature, most drugs required 4 h for significant killing activity to ensue. At 7 degrees C only nitrofurantoin, polymyxin B, and rifampin were significantly active within 2 to 4 h following exposure. Following prolonged (overnight) incubation at 7 degrees C, however, 10 of 23 drugs (amikacin, cefotaxime, chloramphenicol, gentamicin, nalidixic acid, netilmicin, nitrofurantoin, polymyxin B, rifampin, and vancomycin) effected reduction of bacterial colony counts of greater than or equal to 50%. On the basis of these data it is recommended that urine specimens from patients with known antibacterial chemotherapy should not be refrigerated for longer than 2 to 4 h following collection.

Adult↗
PubMed1982

Bacteriocin typing of clinical isolates of Enterobacter cloacae.

A total of 16 selected bacteriocins of Enterobacter cloacae were characterized presumptively. They proved to be noninfectious, sedimentable (105,000 X g), resistant against chloroform and trypsin, and nonfilterable. The host ranges were essentially species specific. Based on susceptibility to one or more of these 16 bacteriocins, 242 of 308 (78.6%) clinical E. cloacae isolates were typed and assigned to 52 provisional bacteriocin types. Several outbreaks of nosocomial cross-infection were discerned retrospectively. Thus, bacteriocin typing of E. cloacae isolates may prove useful for controlling hospital infection.

Bacteriocins↗
PubMed1982

Simple screening method for gram-positive bacterial beta-lactam antibiotic tolerance on routine laboratory Bauer-Kirby antibiogram plates.

A simple screening method served to detect beta-lactam antibiotic-tolerant variants of clinical isolates and laboratory control strains of staphylococcus aureus, S. epidermis, group B beta-hemolytic streptococci, and Listeria monocytogenes. The beta-lactamase(s) of a multiple drug-resistant strain of Enterobacter cloacae (isolate No. 19) yielded most consistent results as compared with several other beta-lactamase producers; the E. cloacae beta-lactamase(s) was neutralized by clavulanic acid. Spot inocula of E. cloacae isolate No. 19, following overnight "induction" with 1 microgram/ml of ampicillin and 3 microgram/ml of cephalothin in tryptic soya broth, were applied centrally to beta-lactam antibiotic inhibition zones of Bauer-Kirby antibiogram plates (Mueller-Hinton agar, MHA, and diagnostic sensitivity test agar, DSTA) following removal of the appropriate disks. The spot-inoculated plates were incubated overnight at 35 degrees C and inspected for satellite growths of tolerant variants around the E. cloacae spot inocula. Satellite growths of less than or equal to 10 colonies were interpreted to indicate tolerance of the relevant cell wall synthesis inhibitor. The method readily permitted detection of variants tolerant for ampicillin, cephalothin, penicillin G, piperacillin, azlocillin, and mezlocillin. However, strains documented by minimal inhibitory and minimal bactericidal concentrations to be tolerant for cefotaxime, cefoxitin, fosfomycin, and vancomycin only rarely gave rise to respective satellite growths. DSTA proved superior to MHA with respect to "rescue" of inhibited tolerant staphylococcal variants; furthermore, the diameters of inhibition zones obtained on DSTA correlated well with those on MHA. Therefore, DSTA was adopted as the routine test medium for clinical staphylococcal isolates.

Anti-Bacterial Agents↗
PubMed1982

Agar (disk) diffusion test susceptibility of clinical isolates of Pseudomonas aeruginosa to azlocillin, cefotaxime, cefsulodin, lamoxactam, mezlocillin, and piperacillin.

The standardized Bauer-Kirby agar diffusion test served to examine 100 clinical isolates of Pseudomonas aeruginosa against various recently introduced broad-spectrum penicillins and cephalosporins. Neither cefotaxime nor lamoxactam displayed significant activity against this microorganism. Azlocillin, cefsulodin, and piperacillin were significantly more effective (p less than 0.0001) than mezlocillin against the majority of isolates. When compared individually, azlocillin and piperacillin displayed comparable in vitro activity; the same was true for cefsulodin compared with piperacillin. On the other hand, cefsulodin was somewhat more active than azlocillin (p less than 0.05, greater than 0.01) against P. aeruginosa. These data should enable diagnostic laboratories to curtail the number of antimicrobial drugs routinely utilized to examine clinical isolates of P. aeruginosa for antibiotic susceptibility, i.e., piperacillin exclusively.

Azlocillin↗
PubMed1982

Combined serum bactericidal and phagocytic activities of defibrinated human blood against Serratia marcescens. Use of phenylbutazone to selectively block phagocytic killing activity and of Group A (phage tail) bacteriocins to kill extraphagocytic bacteria.

Fresh, defibrinated human blood (65 vol%) from normal adults reduced cell inocula of Serratia marcescens, comprising 'delayed serum-sensitive', 'pseudo-serum-resistant', and 'non-serum-sensitive' human serum susceptibility categories, by up to approximately 3 log10 units, provided cell inocula did not significantly exceed 10(5) colony-forming units/ml at 0 time. Phenylbutazone (2 mg/ml) antagonized neither serum bactericidal activity nor the biological activity of group A (phage tail) bacteriocins bA+ 16 and bA+ 18. These bacteriocins were suitable for killing extraphagocytic S. marcescens cells, since they were not internalized by peripheral blood leukocytes. Phenylbutazone at 2 mg/ml failed to interfere with ingestion of S. marcescens by leukocytes; however, this drug inhibited intraphagocytic killing of ingested S. marcescens bacteria. Pilot experiments, utilizing this latter system, disclosed that rifampin effectively killed intraphagolysosomal bacteria.

Adult↗
PubMed1982

Polymyxin B-induced cocarde growth phenomenon of Serratia marcescens due to cationic detergent-like activity of polymyxin B.

14 of 74 test strains of Serratia marcescens yielded reproducible cocarde-like growths (coc+) around 30-micrograms disks of polymyxin B (PB) on Müller-Hinton, brain heart infusion and tryptic soy agar. The coc+ phenomenon was not due to nutrient effects of growth medium nor did it correlate with either group A (phage tail) bacteriocinogeny or colicinogeny as determined with 32 selected test strains; mitomycin C failed to give rise to coc+ growths. The anionic bile salts of MacConkey agar as well as aqueous sodium deoxycholate neutralized the coc+ activity of PB. Benzalkonium chloride, chlorhexidine digluconate, and cetyltrimethylammonium bromide by themselves did not produce cocardes. Rather, these cationic detergents enhanced PB activity somewhat against selected coc+ and coc- strains of S. marcescens. It was concluded that the PB-induced growth phenomenon of S. marcescens was due to the cationic detergent-like activity of this polypeptide antibiotic.

Culture Media↗
PubMed1982

Interactions of antimicrobial drugs and combined phagocytic/serum bactericidal activity of defibrinated human blood against Serratia marcescens. I. Cotrimoxazole, nalidixic acid, nitrofurantoin, and trimethoprim.

Minimal bactericidal concentrations of trimethoprim, nalidixic acid, and nitrofurantoin revealed effective intraphagolysosomal bactericidal activity against several assay strains of Serratia marcescens as determined with phenylbutazone-treated (2 mg/ml) fresh defibrinated human blood (55 vol%), following killing of extraphagocytic test bacteria with group A (phage tail) bacteriocins of S. marcescens. The degree of intraphagocytic killing activity of trimethoprim, nalidixic acid, and nitrofurantoin approximated that of rifampin. Inhibitory and subinhibitory concentrations of cotrimoxazole or trimethoprim combined with 55 vol% of defibrinated blood, respectively, yielded additive effects against all test strains of S. marcescens. However, combinations of nalidixic acid and nitrofurantoin with blood, respectively, resulted in essentially indifferent effects against S. marcescens.

Anti-Bacterial Agents↗
PubMed1982

Interactions of antimicrobial drugs and combined phagocytic/serum bactericidal activity of defibrinated human blood against Serratia marcescens. II. Aminoglycosides: amikacin, gentamicin, and netilmicin.

Minimal bactericidal concentrations of the aminoglycoside antibiotics amikacin, gentamicin, and netilmicin killed intraphagolysosomal test bacteria of selected assay strains of Serratia marcescens, though not as efficiently as rifampin. The system employed consisted of 55 vol% of fresh defibrinated human blood treated with 2 mg/ml of phenylbutazone which permitted ingestion of bacteria, but selectively inhibited microbicidal activity of the peripheral blood leukocytes. Extraphagocytic bacteria were killed with the aid of group A (phage tail) bacteriocins of S. marcescens. Inhibitory and subinhibitory concentrations of amikacin, gentamicin, and netilmicin combined with 55 vol% of defibrinated blood, respectively, yielded additive effects against all test strains of S. marcescens utilized and against Escherichia coli control strain ATCC 25922.

Amikacin↗
PubMed1982

Proteolytic activity of selected clinical isolates of Serratia marcescens against human serum proteins.

Six representative clinical isolates of Serratia marcescens were examined for proteolytic activity against various proteins of normal fresh human serum. The extent of proteolytic activity was screened with micro-scale immunoelectrophoresis and quantitatively documented with the aid of Laurell's rocket electroimmuno assay. The 6 S. marcescens strains regularly altered, albeit to varying degrees, complement components C3a, C3c, C4, C5, and C9, and haptoglobin. Apolipoprotein and immunoglobulin A, the latter derived from human colostrum, were attacked by 5 and 4 isolates, respectively. Two isolates altered alpha 1-antitrypsin, whereas only one isolate interacted with alpha 2-macroglobulin and transferrin. In contrast, alpha 2-HS-glycoprotein, alpha 1-antichymotrypsin, and serum IgA, IgG, and IgM immunoglobulins were not affected by the test strains.

Alpha-Globulins↗
PubMed1982

Virulence of nosocomial isolates of Serratia marcescens for NMRI mice: correlation with O-antigens O6 and O14.

Nosocomially significant Serratia marcescens strains with O-antigens O6 or O14, or the serogroup complex O6/O14, proved somewhat more virulent for juvenile NMRI mice following intraperitoneal injection, than strains carrying other O-antigens. There was no correlation between virulence and extent of casein proteolytic activity or resistance against fresh normal human serum.

Animals↗
PubMed1982

Opsonization requirements of Serratia marcescens.

Dextran-separated human peripheral blood leukocytes (55 vol%) from healthy adults served to delineate the opsonic requirements of various serologically defined assay strains of Serratia marcescens. 'Natural' antibodies of three commercial IgG immunoglobulin preparations (25 vol%), in the absence of complement (C), did not opsonize all 19 test strains, in particular certain strains carrying O-antigens O6 and/or O14, despite documented (ELISA technique) contents of anti-O6 and -O14 IgG antibodies. The 'natural' IgG opsonins proved O-antigen specific. Several of 13 selected assay strains of S. marcescens differed in opsonic requirements for 'classically' or 'alternatively' activated human C; opsonization was optimal with intact fresh human serum (25 vol%). All 13 tested strains activated both pathways of C. Anti-live cell rabbit immune sera (RIS) surpassed conventional anti-O and anti-H RIS (25 vol%) in terms of opsonizing activity, which proved partially heat-labile and O-antigen specific for two, but not for two other test strains. Isolated IgM immunoglobulin fractions of anti-live cell RIS either totally lacked or displayed inferior opsonizing activity in the absence of C, although O-agglutinin activity was only from 4- to 8-fold lower than that of unfractionated anti-live cell RIS. Human and rabbit 'natural' IgM antibodies opsonized moderately. Added guinea pig C (10 vol%) failed to enhance opsonizing activity of 'natural' and 'immune' rabbit IgM and 'natural' human IgG and IgM antibodies.

Animals↗
PubMed1981

Perinatal listeriosis. Tolerance of a clinical isolate of Listeria monocytogenes for ampicillin and resistance against cefotaxime.

A strain of Listeria monocytogenes isolated from a case of early onset, generalized, fatal, perinatal listeriosis in a premature infant was found to be tolerant for ampicillin and resistant against cefotaxime. A laboratory control strain of L. monocytogenes and Staphylococcus aureus control strain ATCC 25923 proved tolerant for both beta-lactam antibiotics, respectively. The combinations of ampicillin with gentamicin and cefotaxime with gentamicin resulted in additive bactericidal activity against both strains of L. monocytogenes. Based on these findings and those of the literature, it is suggested that cases of systemic listeriosis be treated with a combination of a beta-lactam antibiotic, preferably ampicillin, with an appropriate aminoglycoside, such as gentamicin.

Ampicillin↗
PubMed1981

Variable tolerance of a clinical isolate of Staphylococcus epidermidis from an infected hydrocephalus shunt for several beta-lactam antibiotics, vancomycin and fosfomycin.

A strain of Staphylococcus epidermidis isolated from an infected hydrocephalus shunt with associated ventriculitis in a 3-month-old infant proved variably tolerant for the beta-lactam antibiotics ampicillin, cephalothin, cefotaxime, cefoxitin, oxacillin, penicillin G, as well as vancomycin and fosfomycin. In contrast, Staphylococcus aureus control strain ATCC 25923 was regularly tolerant to the above stated beta-lactam antibiotics; however, this latter strain displayed variable tolerance for vancomycin and fosfomycin. The beta-lactam tolerance of both strains proved inoculum sizes. Penicillin G-tolerant variants were detected more readily among cells of the S. epidermidis strain in the stationary than in the logarithmic growth phase; in contrast, the yield of penicillin G-tolerant variants from S. aureus ATCC 25923 was independent of the growth phase. Tolerant variants of both staphylococcal strains failed to survive more than three successive passages in Mueller-Hinton broth with added beta-lactam antibiotics at concentrations identical to those which had originally served to select these tolerant variants. Gentamicin combined with vancomycin displayed additive bactericidal activity against both staphylococcal strains; conversely, the combination of rifampin plus vancomycin showed inadequate bactericidal activity against both strains.

Anti-Bacterial Agents↗