Walter H. Traub
University of Erlangen-Nuremberg
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Featured researches published by Walter H. Traub.
Chemotherapy | 1976
Walter H. Traub; Georg Acker; Ingrid Kleber
Exposure of Serratia marcescens cells to 10, 5, and 2.5 mug/ml of polymyxin B resulted in outer cell surface alterations that consisted of coarse, pleomorphic projections which revealed a double-contoured membrane structure. In contrast, fresh, but not heat-inactivated human serum caused the deposition of very fine, thread-like aggregates on the outer cell surface of exposed cells. The combination of polymyxin B and fresh human serum caused clearly discernible ultrastructural changes of the polymyxin and the fresh serum type, respectively.
Chemotherapy | 1977
Walter H. Traub; Ingrid Kleber
Combined resistance against chloramphenicol (CHLOR), nalidixic acid (NA), and trimethoprim (TMP) was demonstrated in isolates and variants of a nosocomially significant, multiple-drug-resistant, nonconjugative strain of Serratia marcescens (bacteriocin type 18), either as a spontaneous event or after exposure of isolates and variants derived therefrom to increasing concentrations of CHLOR, NA, and TMP, respectively. This phenomenon was also noted among several selected mutants of two control strains of S. marcescens. The level of resistance was not absolute; the combined resistant mutants and variants were inhibited by 100–200 μg/ ml of CHLOR, 25–50 μg/ml of NA, and 12.5–25 μg/ml of TMP. However, the phenomenon of combined triple-resistance occurred irregularly with respect to the strain or variant of S. marcescens employed, and with regard to the selective drug utilized. Selection of mutants with CHLOR yielded a larger number of combined CHLOR-NA-TMP resistant mutants than selection with NA or TMP. Preliminary data obtained with spontaneously ‘cured’ variants of the multiple-drug-resistant strain of S. marcescens that had lost resistance against CHLOR, NA, TMP, penicillins, and aminoglycoside antibiotics, and which subsequently were shown to yield spontaneous mutants with combined triple-resistance against CHLOR, NA, and TMP, seem to indicate that this resistance phenomenon is not mediated extra-chromosomally, but rather chromosomally, and subject to phenotypic variation. The precise nature of this novel, unusual resistance mechanism against these three unrelated antimicrobial drugs remains to be elucidated.
Chemotherapy | 1975
Walter H. Traub; Ingrid Kleber
Two of twelve examined S. marcescens strains were promptly killed by 80% (v/v) fresh human serum (within 20 min), analogous to a serum-sensitive control strain of Escherichia coli; ten strains, however, were killed by fresh serum only after extended incubation (2-4 h). The combination of therapeutically achievable concentrations of polymyxin B (range 5 to 1.25 mug/ml) and fresh, but not heat-inactivated human serum was found to exert an accelerated, additive effect against 9 of 10 delayed serum-sensitive isolates of S. marcescens, an organism that is characterized by intrinsic resistance against polymyxins. The combination of 80% (v/v) fresh, defibrinated human blood and polymyxin B likewise resulted in an additive effect. Polymyxin B treatment of S. marcescens strains caused a prompt, marked, though reversible bile salt susceptibility of the cells; in contrast, the effect induced by fresh serum was slight and not apparent until several hours after exposure.
Antimicrobial Agents and Chemotherapy | 1975
Walter H. Traub; Ingrid Kleber
The combination of polymyxin B and rifampin resulted in an additive effect against all 12 clinical isolates of Serratia marcescens examined, including multiple-drug-resistant isolates.
Pathobiology | 1974
Walter H. Traub; Ingrid Kleber
Thirty-three of 35 clinical isolates of Serratia marcescens examined displayed fibrinolytic activity, whereas only 5 isolates elaborated a weakly active elastase. All strains liquef
Chemotherapy | 1976
Walter H. Traub; Ingrid Kleber; Alfred Pühler; Hans-Joachim Burkardt
A multiple drug-resistant strain of Serratia marcescens (bacteriocin type 18) was isolated from three clinical patients. The isolates were found to carry a conjugally nontransferable, nonmobilizeable resistance plasmid (R-plasmid) with resistance-(r)-determinants against ten antimicrobial drugs: ampicillin, carbenicillin, chloramphenicol, gentamicin, kanamycin, neomycin, streptomycin, tobramycin, triple sulfonamides, cotrimoxazole, and--possibly--nalidixic acid, as determined with exposure to curing agents (ethidium bromide, acridine orange, and sodium dodecyl sulfate) and by the high rate of spontaneous loss of r-determinants. Dyebuoyant density centrifugation allowed recovery of R-plasmid DNA that measured roughly 24 mum in contour length; after curing with concomitant loss of 9 r-determinants, the contour length of the R-plasmid DNA of one isolate (No. SE 154) had decreased to roughly 15 mum, and none was detected in the sole variant of the isolate that spontaneously had lost 11 r-determinants.
Chemotherapy | 1974
Walter H. Traub; Ingrid Kleber
A total of 109 clinical isolates of Staphylococcus aureus as well as 2 isolates of S.epidermidis , 11 isolates of group A β -hemolytic streptococ
Pathobiology | 1977
Walter H. Traub
13 isolates of Serratia marcescens of various human serum-susceptibility categories and Escherichia coli strain ATCC 25922 were not inhibited by 80 or 50 vol% of
Chemotherapy | 1992
Walter H. Traub; Birgit Leonhard
Bacillus subtilis strain ATCC 6633 was examined for susceptibility to 30 additional antimicrobial drugs, the majority of which had been released during the 1980s. The data served to update previous findings with regard to the suitability of this assay strain for the detection of chemotherapeutic agents in fluid clinical specimens.
Pathobiology | 1975
Walter H. Traub; Ingrid Kleber
Two H2S producing, multiple drug-resistant variants of Escherichia coli were isolated from clinical urine specimens. Both isolates transferred, eleven resistance determinants to recipient strains of E. coli K 12 and nine r-determinants to Klebsiella pneumoniae recipients; in no instance was transfer of the curing-refractory H2S marker demonstrable.