Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PSEUDOMONAS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

The metabolism of tryptophan and 7-chlorotryptophan in Pseudomonas pyrrocinia and Pseudomonas aureofaciens.

Pseudomonas pyrrocinia ATCC 15958 and a mutant strain (ACN) of Pseudomonas aureofaciens ATCC 15926 possess a mechanism for the degradation of the tryptophan side chain. Indole, indole-3-carboxylic acid, indole-3-acetic acid and the corresponding compounds chlorinated or brominated at position 7, as well as indole-3-pyruvate and 7-chloroindole-3-pyruvate, were isolated from bacterial cultures. The chlorinated indole derivatives were isolated after the addition of 7-chloro-DL-tryptophan to cultures of P. pyrrocinia whereas their bromo analogues were found in the culture medium of the mutant strain ACN of P. aureofaciens, grown in the presence of sodium bromide. Enzymatic studies show that tryptophan is transaminated to indole-3-pyruvate, which is transformed to indole-3-acetaldehyde. Dehydrogenation of indole-3-acetaldehyde leads to indole-3-acetic acid, which is further metabolized to indole-3-carboxaldehyde, and converted by dehydrogenation to indole-3-carboxylic acid. Indole is formed by the spontaneous decarboxylation of indole-3-carboxylic acid.

Amino Acid Isomerases↗
PubMed1991

Microbial metabolism of quinoline and related compounds. X. The molybdopterin cofactors of quinoline oxidoreductases from Pseudomonas putida 86 and Rhodococcus spec. B1 and of xanthine dehydrogenase from Pseudomonas putida 86.

The bis(carboxamidomethyl) derivatives of the molybdenum cofactors in three eubacterial molybdo-iron/sulphur-flavoproteins were examined. The quinoline oxidoreductases from Pseudomonas putida 86 and Rhodococcus spec. B1 contain molybdopterin cytosine dinucleotide. In xanthine dehydrogenase from Pseudomonas putida 86, however, only molybdopterin was found. The bis(carboxamidomethyl) derivatives of all three enzymes were treated with nucleotide pyrophosphatase, but only those of the quinoline oxidoreductases were cleaved into [bis(carboxamidomethyl)]molybdopterin and CMP, whereas that of xanthine dehydrogenase remained unchanged. Dephosphorylation by alkaline phosphatase yielded dephospho-[bis(carboxamidomethyl)]molybdopterin and cytidine from the cleaved molybdopterin cytosine dinucleotide. The bis(carboxamidomethyl) derivative from xanthine dehydrogenase was converted to dephospho-[bis(carboxamidomethyl)]molybdopterin by alkaline phosphatase. Acid hydrolysis of the purified enzymes and analysis of the hydrolysate by HPLC confirmed that compared with the xanthine dehydrogenase both quinoline oxidoreductases contain CMP.

Alkaline Phosphatase↗
PubMed1975

Pseudomonas cytochrome c peroxidase XI. Kinetics of the peroxidatic oxidation of Pseudomonas respiratory chain components.

The steady state kinetics of cytochrome c peroxidase from Pseudomonas aeruginosa (PaCCP) has been studied by initial velocity techniques using several cytochromes c (550 and 555 P. aeruginosa; 551 P. fluorescens) and Pseudomonas azurin as electron donors and hydrogen peroxide as electron acceptor. From the initial velocity patterns a sequential mechanism with compulsory substrate-binding order is proposed for PaCCP. A comparative kinetic study of the peroxidatic oxidation of cytochrome c-551 (P. aeruginosa) by yeast cytochrome c peroxidase was made to evaluate the significance of electrostatic interactions in complex formation between the enzyme and substrates.

Animals↗
PubMed1988

[Antigenic polysaccharides of bacteria. 26. Structure of O-specific polysaccharides from Pseudomonas cerasi 467 and Pseudomonas syringae pv. syringae strains 218 and P-55 belonging to serogroups II and III].

Serologically active O-specific polysaccharides were obtained on mild acid hydrolysis of lipopolysaccharides from Pseudomonas cerasi 467 and Pseudomonas syringae pv. syringae strains 218 and P-55. On the basis of 1H- and 13C-NMR analysis, it was concluded that the P. cerasi polysaccharide has the following structure: ----3)-alpha-D-Rhap-(1----3)-alpha-D-Rhap-(1----2)-alpha-D-+ ++Rhap-(1---- which is identical to that of O-specific polysaccharide from P. syringae pv. morsprunorum C28 (Smith A. R. W. et al. Eur. J. Biochem., 1985, V. 149, No 1, p. 73-78). The polysaccharides from P. syringae pv. syringae strains possess the same backbone but differ by the presence of D-fucose as monosaccharide branches. Methylation and 1H- and 13C-NMR analysis revealed the following structure of these polysaccharides: (Formula: see text). The degree of substitution of the backbone trisaccharide units by the fucofuranose residues is about 35% for the strain 218 and about 85% for the strain P-55.

Antigens, Bacterial↗
PubMed1988

[Antigenic polysaccharides of bacteria. 27. Structure of the O-specific polysaccharide chain of lipopolysaccharides from Pseudomonas syringae pv. atrofaciens 2399, phaesolica 120a and Pseudomonas holci 8299 belonging to serotype VI].

Lipopolysaccharides from Pseudomonas syringae pvs atrofaciens 2399. phaseolicola 120a and Pseudomonas holci 8299, belonging to serogroup VI. possess an identical polysaccharide chain composed of D-rhamnose and D-fucose. On the hasis of methylation, partial acid hydrolysis, 1H- and 13C-NMR data, it was concluded that the backbone of the polysaccharide represents D-rhamnan built up of tetrasaccharide repeating units and alpha-D-fucofuranose residues are attached to the backbone as the monosaccharide branches. The following structure of the repeating unit is established: (Formula: see text).

Antigens, Bacterial↗
PubMed1988

[Antigenic bacterial polysaccharides. 28. The structure of the O-specific lipopolysaccharide chain of Pseudomonas syringae pv. atrofaciens K-1025 and Pseudomonas holci 90a (serogroup II)].

Lipopolysaccharides of serologically related strains of Pseudomonas syringae pv. atrofaciens K-1025 and Pseudomonas holci 90a possess the identical O-specific polysaccharide chains, representing a homopolymer of D-rhamnose. On the basis of methylation, partial and complete Smith degradation, and analysis by 1H- and 13C-NMR-spectroscopy, it was concluded that the repeating unit of the polysaccharide is a branched pentasaccharide of the following structure: (formula; see text)

Antigens, Bacterial↗
PubMed1979

Experimental Pseudomonas infection in mice: effect of single cyclophosphamide administration on Pseudomonas infection.

The kinetic effect of cyclophosphamide (CY) was investigated using the immune response to sheep red blood cells (SRBC), activation of the mononuclear macrophage system and altered susceptibity to pseudomonas infection. The level of delayed type hypersensitivity (DTH) was enhanced with suppressed antibody formation, when antigenic stimulation was given about 3 days after CY administration. In contrast, antibody formation increased markedly when challenged with antigen about 10 days after CY administration. Activity of macrophage system as measured by rate of carbon clearance and spreading of peritoneal macrophage was decreased within 6 days after CY, therefore increased to a peak at the 13th day of CY administration. CY increased a susceptibility to pseudomonas infection at the early time of its administration such as the 3rd day, whereas more increased resistance was observed at the later time such as the 13th day. These results indicated that B-lymphocyte depletion included by administration of sublethal dose of CY (200mg/kg) was followed by vigorous hyperplasia of B-lymphocyte.

Animals↗
PubMed1984

Immunoserology of Pseudomonas aeruginosa infections in man. III. Site of infection, duration of the presence of Pseudomonas aeruginosa and antibody response.

In 39 patients of a respiratory intensive care unit the intensity of the serological response to the purified LPS of the causative Pseudomonas aeruginosa was found to change according to the site of infection. The highest titres were found in septic cases, when the antigenic assault reached all the immune-competent cells in the body. Short presence (only one positive bacteriological culture) of P. aeruginosa at the site of inflammation resulted in a low or moderate rise in antibody titre. Ten days were enough for the development of a maximum total antibody (approximately IgM) response, while IgG type antibodies moderately grew further when the presence of P. aeruginosa lasted more than 10 days. Only a 16-fold increase in total antibodies per se or a 4-fold rise in both total (approximately IgM) and IgG antibodies confirmed the pseudomonas infection.

Adolescent↗
PubMedDate not supplied

[Nucleoside catabolism study of Pseudomonas putida and Pseudomonas trifolii].

No activity of specific nucleoside phosphorylases was detected in Pseudomonas putida; as the result, its cells cannot grow on various nucleosides using them as carbon sources. Insignificant growth on ribonucleosides, viz. inosine and uridine, should be attributed to the activity of hydrolases in the cell. In contrast, Pseudomonas trifolii is capable of normal growth on various nucleosides using them as a sole source of carbon. Accordingly, the cell extracts display the activities of enzymes involved in the catabolism of nucleosides, namely, the so-called deo enzymes. Methods developed for E. coli were used to obtain mutants in the genes dra, tpp and drm as well as in regulatory loci negatively controlling the activity of deo genes in Ps. trifolii. Like in E. coli, cytidine and thymidine induce the activity of deo genes in Ps. trifolii.

Culture Media↗
PubMed1996

General pharmacology of a Pseudomonas vaccine prepared from outer-membrane fractions of Pseudomonas aeruginosa.

CFC-101 is a novel Pseudomonas vaccine with high effectiveness against Pseudomonas infection and is currently under clinical evaluation. The general pharmacological properties of this vaccine were evaluated in mice, rats, guinea pig ileum, and dogs. In vivo doses of 0.2, 2.0 and 20 mg/kg given by intramuscular route, or in vitro concentrations up to 50 micrograms/ml were used. Intramuscular administration of CFC-101 vaccine had no effect on the central nervous system except that the body temperature of rats was slightly decreased at the highest dose, 20 mg/kg. CFC-101 vaccine did not affect the function of smooth muscles, gastrointestinal system, and cardiovascular and respiratory systems. In water and electrolytes excretion test, a decrease in urine output and an elevation of the excretion of Na+, Cl- and total protein at the highest dose (20 mg/kg) were observed. In summary, CFC-101 vaccine had no pharmacological effect in these studies even up to the 100-fold clinical dose, 2 mg/kg.

Animals↗
PubMed1996

[Conjugative transfer and expression of R plasmids of the genus Pseudomonas in the cells of Pseudomonas mallei C-5].

Conjugative transfer of the incompatibility group plasmids Inc P-2, Inc P-3, Inc P-4 and Inc P-5 as well as the plasmids of Pseudomonas sp. of an unknown incompatibility group to the cells of Pseudomonas mallei C-5 was shown possible for the first time. The inheritance of the transferred plasmids and the expression of the markers of resistance to antibacterial drugs were stable. Clones with reserved virulence, lowered virulence and no virulence were detected among the transconjugants. The results of the immunization by the avirulent cells of P. mallei C-5 (RP4) were evident of low immunogenic capacity of the microbe.

Animals↗
PubMed1997

[Creation of genomic DNA libraries for Pseudomonas mallei and Pseudomonas pseudomallei].

The genomic libraries of P. mallei and P. pseudomallei species were constructed in Escherichia coli. The chromosomal DNA of P. pseudomallei C-141 strain has been cloned into the cosmid vector pHC79 and the broad host range plasmid vector pES154. The chromosomal DNA of P. mallei [symbol: see text]-5 strain has been cloned into the plasmid vector pSUP202. The recombinant clones of the genomic libraries were screened by the enzyme-linked immunoadsorbent assay (ELISA) to detect the production of Pseudomonas antigens: 28 clones were positive. Twelve recombinant strains demonstrated specific antigenic determinants of P. mallei and P. pseudomallei by immunoblotting. Cloned proteins of P. mallei and P. pseudomallei have molecular weights from 30 to 70 kD. A new method for introducing foreign genes into Pseudomonas genomes is offered. P. mallei strains with the chromosomally integrated plasmids pSM are universal recipients for ColEI-based cloning vectors.

Burkholderia pseudomallei↗
PubMed1979

Pseudomonas aeruginosa keratitis treated with ticarcillin and tobramycin.

A corneal ulcer, infected with Pseudomonas aeruginosa and complicated by conjunctivitis and endophthalmitis, was treated successfully with systemic administration of ticarcillin and topical application of tobramycin. It is unlikely that carbenicillin, to which the organism was much less sensitive, would have attained sufficient tissue levels to control the infection.

Aged↗
PubMed1987

[Significance of Pseudomonas aeruginosa virulence factors for acute and chronic Pseudomonas aeruginosa infections].

The virulence of Pseudomonas aeruginosa is multifactorial and caused by several extracellular enzymes and other substances. The importance of these virulence factors for the pathogenesis of human P. aeruginosa infections is dependent on the type of infection. For acute, systemic infections in immunocompromised patients, exotoxin A, alkaline protease and elastase are essential virulence factors. In localized infections (e. g., cystic fibrosis) they seem to be of minor importance, since they are neutralized by specific antibodies in immune complexes, and in the case of exotoxin A cleavage by proteinases from polymorphonuclear leukocytes occurs. The rhamnolipid of P. aeruginosa which has been detected in sputa of patients with cystic fibrosis evades the host's immune response and has to be regarded as a potential virulence factor together with the phenazine pigments, also in chronic P. aeruginosa infections.

ADP Ribose Transferases↗
PubMedDate not supplied

[Significance of Pseudomonas aeruginosa virulence factors in acute and chronic Pseudomonas aeruginosa infections].

The virulence of Pseudomonas aeruginosa is multifactorial and caused by several extracellular enzymes and other substances. The importance of these virulence factors for the pathogenesis of human P. aeruginosa infections is dependent on the type of infection. For acute, systemic infections in immunocompromised patients, exotoxin A, alkaline protease and elastase are essential virulence factors. In localized infections (e.g., cystic fibrosis) they seem to be of minor importance, since they are neutralized by specific antibodies in immune complexes, and in the case of exotoxin A cleavage by proteinases from polymorphonuclear leukocytes occurs. The rhamnolipid of P. aeruginosa which has been detected in sputa of patients with cystic fibrosis evades the host's immune response and has to be regarded as a potential virulence factor together with the phenazine pigments, also in chronic P. aeruginosa infections.

ADP Ribose Transferases↗
PubMed2001

Survey of antibiotic resistance in Pseudomonas aeruginosa by The Tokyo Johoku Association of Pseudomonas Studies.

Pseudomonas aeruginosa resistance (minimum inhibitory concentration [MIC], > or =16 microg/ml defined as resistant) to meropenem, imipenem, panipenem, piperacillin, ceftazidime, cefozopran, cefoperazone, sulbactam/cefoperazone, amikacin, and tobramycin, as well as cross-resistance profiles, were investigated in P. aeruginosa strains isolated at eight hospitals in the Johoku area, Tokyo, during November 1998. Overall, 8.3% of isolates were imipenem-resistant and 4.6% were ceftazidime-resistant. However, the incidence of antibiotic-resistant P. aeruginosa was distinctly different at each hospital. P. aeruginosa resistance to imipenem ranged from (MIC) 1 to 64 microg/ml (MIC90 32 microg/ml), and its resistance to ceftazidime ranged from 2 to more than 128 microg/ml (MIC90, 64 microg/ml). Meropenem (MIC range, < or =0.25 to 16 microg/ml) was more active than panipenem (MIC range, 2 to 64 microg/ml). Cefozopran was more active than piperacillin, cefoperazone, or sulbactam/cefoperazone, but many strains were resistant to cefoperazone (17/57). Our analysis found cross-resistance to many beta-lactams, but the degree of cross-resistance was very variable.

Anti-Bacterial Agents↗
PubMedDate not supplied

Synergy of new C-3 substituted cephalosporins and tobramycin against Pseudomonas aeruginosa and Pseudomonas cepacia.

The effects of the combination of E-1040, a new cephalosporin, ceftazidime, cefpirome, or cefepime with tobramycin against 40 Pseudomonas aeruginosa and 16 P. cepacia isolates from cystic fibrosis patients were examined. Synergy fractional inhibitory concentration less than or equal to 0.5 was found against P. aeruginosa when tobramycin was combined with E-1040 32%, cefpirome 32%, cefepime 22%, and ceftazidime 22%. Fifty-two percent of isolates showed an additive response for E-1040, 60% for cefpirome, 45% cefepime, and 55% ceftazidime, p greater than 0.05. The differences were not statistically significant. Synergy was not more likely to be achieved if the isolates were susceptible or resistant to either the aminoglycoside or cephalosporin. None of the E-1040-resistant isolates, all of which were tobramycin-resistant, became susceptible when tested with an aminoglycoside, whereas 15 of 34 cefpirome-resistant, 13 of 30 cefepime-resistant, and seven of 14 ceftazidime-resistant isolates became susceptible. Synergy of aminoglycoside and the cephalosporins against P. cepacia was found for 25% with E-1040, 44% with cefpirome, 38% with cefepime, and 31% with ceftazidime. These differences were not statistically significant.

Cephalosporins↗
PubMed2003

Prevention of Yersinia enterocolitica, Pseudomonas fluorescens, and Pseudomonas putida outgrowth in deliberately inoculated blood by a novel pathogen-reduction process.

BACKGROUND: Yersinia enterocolitica, Pseudomonas fluorescens, and P. putida are responsible for a significant amount of the bacterial sepsis cases attributed to RBC transfusions. INACTINE is a pathogen-reduction process for RBCs, which consists of incubation of RBCs with PEN110 (proprietary compound) followed by automated washing of the RBCs. INACTINE is an electrophilic agent, which inactivates a wide range of viruses and WBCs by disruption of nucleic acid replication. The present study investigated the effect of the PEN110 process on Y. enterocolitica, P. fluorescens, and P. putida. STUDY DESIGN AND METHODS: Identical units of reduced CPD/ADSOL additive solution (AS-1) or CP2D/Nutricel additive solution (AS-3) RBCs were inoculated with 10 to 100 CFU per mL of either Y. enterocolitica, P. fluorescens, or P. putida. The control units were put on storage immediately after the bacterial spike. The test units were subjected to the PEN110 process and then stored. Sham control units were processed the same way as test units without addition of PEN110. Bacterial titer in all units was monitored during the 6-week storage period. RESULTS: No bacteria were detected in any of the RBC units (n = 9 for each microorganism) prepared using the PEN110 process throughout 6 weeks of storage. Substantial bacterial growth occurred in all control and in a majority of sham control units (11 out of 15 experiments). The bacterial inactivation by the INACTINE process was found to be equally effective in CPD/AS-1 and CP2D/AS-3 RBC units. CONCLUSION: The INACTINE process effectively prevented the outgrowth of Y. enterocolitica, P. fluorescens, and P. putida deliberately inoculated into WBC-reduced CPD/AS-1 and CP2D/AS-3 RBCs. The results demonstrated the crucial bactericidal role of PEN110 in the INACTINE process.

Anti-Bacterial Agents↗