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FEMS Microbiology Letters Jan 1991Pyrimidine catabolism in Pseudomonas aeruginosa was investigated. It was found that the pyrimidine bases uracil and thymidine as well as their respective reductive...
Pyrimidine catabolism in Pseudomonas aeruginosa was investigated. It was found that the pyrimidine bases uracil and thymidine as well as their respective reductive catabolic products could be utilized as sole sources of nitrogen. Reductive degradation of the pyrimidine bases was noted. The reductive catabolic pathway enzymes dihydropyrimidine dehydrogenase, dihydropyrimidinase and N-carbamoyl-beta-alanine amidohydrolase were all detected in minimal medium grown cells. Induction of pyrimidine catabolism by uracil was observed in this pseudomonad. Pyrimidine degradation in P. aeruginosa was not subject to catabolite repression.
Topics: Amidohydrolases; Chloramphenicol; Dihydrouracil Dehydrogenase (NADP); Kinetics; Oxidation-Reduction; Oxidoreductases; Pseudomonas aeruginosa; Pyrimidines
PubMed: 1903745
DOI: 10.1016/0378-1097(91)90547-n -
Journal of Clinical Microbiology May 1982Colonial variants of Pseudomonas aeruginosa have received renewed interest because of their occurrence in sputum cultures of patients with cystic fibrosis. We...
Colonial variants of Pseudomonas aeruginosa have received renewed interest because of their occurrence in sputum cultures of patients with cystic fibrosis. We encountered 11 strains of P. aeruginosa from various body sites of non-cystic fibrosis patients. The strains showed two to three colonial variants, including smooth, rough, and iridescent morphotypes that arose from subculture of a single colony of P. aeruginosa originating from a primary source. The colonial segregants differed in antibiotic susceptibility (resistance to gentamicin, carbenicillin, chloramphenicol, and tetracycline), presence or absence of exoenzymes (gelatinase and elastase), degree of proteolytic activity (caseinase), pigmentation, and antigenicity. These observations suggest that in vivo dissociation with concomitant changes in enzymatic and surface properties might greatly enhance invasiveness. Concurrent differences in antimicrobial susceptibility among the colonial variants could account in some instances for the failure of antibiotic treatment in P. aeruginosa infections in which one would anticipate a positive therapeutic response.
Topics: Carbenicillin; Chloramphenicol; Gentamicins; Humans; Microbial Sensitivity Tests; Penicillin Resistance; Pseudomonas aeruginosa; Serotyping; Surface Properties; Tetracycline
PubMed: 6808021
DOI: 10.1128/jcm.15.5.926-930.1982 -
FEMS Microbiology Reviews Jul 2014Members of the Pseudomonas genus produce diverse secondary metabolites affecting other bacteria, fungi or predating nematodes and protozoa but are also equipped with the... (Review)
Review
Members of the Pseudomonas genus produce diverse secondary metabolites affecting other bacteria, fungi or predating nematodes and protozoa but are also equipped with the capacity to secrete different types of ribosomally encoded toxic peptides and proteins, ranging from small microcins to large tailocins. Studies with the human pathogen Pseudomonas aeruginosa have revealed that effector proteins of type VI secretion systems are part of the antibacterial armamentarium deployed by pseudomonads. A novel class of antibacterial proteins with structural similarity to plant lectins was discovered by studying antagonism among plant-associated Pseudomonas strains. A genomic perspective on pseudomonad bacteriocinogeny shows that the modular architecture of S pyocins of P. aeruginosa is retained in a large diversified group of bacteriocins, most of which target DNA or RNA. Similar modularity is present in as yet poorly characterized Rhs (recombination hot spot) proteins and CDI (contact-dependent inhibition) proteins. Well-delimited domains for receptor recognition or cytotoxicity enable the design of chimeric toxins with novel functionalities, which has been applied successfully for S and R pyocins. Little is known regarding how these antibacterials are released and ultimately reach their targets. Other remaining issues concern the identification of environmental triggers activating these systems and assessment of their ecological impact in niches populated by pseudomonads.
Topics: Anti-Bacterial Agents; Bacterial Secretion Systems; Deoxyribonucleases; Peptides; Pseudomonas aeruginosa; Pyocins
PubMed: 24923764
DOI: 10.1111/1574-6976.12079 -
The Journal of Biological Chemistry 2021Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen whose virulence is dependent on quorum sensing (QS). DksA1, an RNA polymerase-binding transcriptional...
Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen whose virulence is dependent on quorum sensing (QS). DksA1, an RNA polymerase-binding transcriptional regulator, plays a role in determining a number of phenotypes, including QS-mediated virulence. We therefore envisioned that DksA1 inhibitors may help to control P. aeruginosa infection. Here, we screened a library of 6970 chemical compounds and identified two compounds (henceforth termed Dkstatins) that specifically suppressed DksA1 activity. Treatment with these two compounds also substantially decreased the production of elastase and pyocyanin, dominant virulence determinants of P. aeruginosa, and protected murine hosts from lethal infection from a prototype strain of P. aeruginosa, PAO1. The Dkstatins also suppressed production of homoserine lactone (HSL)-based autoinducers that activate P. aeruginosa QS. The level of 3-oxo-C12-HSL produced by Dkstatin-treated wildtype PAO1 closely resembled that of the ΔdksA1 mutant. RNA-Seq analysis showed that transcription levels of QS- and virulence-associated genes were markedly reduced in Dkstatin-treated PAO1 cells, indicating that Dkstatin-mediated suppression occurs at the transcriptional level. Importantly, Dkstatins increased the antibiotic susceptibilities of PAO1, particularly to protein synthesis inhibitors, such as tobramycin and tetracycline. Co-immunoprecipitation assays demonstrated that these Dkstatins interfered with DksA1 binding to the β subunit of RNA polymerase, pointing to a potential mechanism of action. Collectively, our results illustrate that inhibition of P. aeruginosa QS may be achieved via DksA1 inhibitors and that Dkstatins may serve as potential lead compounds to control infection.
Topics: Animals; Anti-Bacterial Agents; Bacterial Proteins; Cell Line; Conserved Sequence; Mice; Mutation; Pseudomonas aeruginosa; Quorum Sensing; Virulence
PubMed: 33757766
DOI: 10.1016/j.jbc.2021.100576 -
Microbial Biotechnology Jul 2012Pseudomonas aeruginosa is becoming recognized as an important pathogen in the gastrointestinal (GI) tract. Here we demonstrate that adenosine, derived from hydrolysis of...
Pseudomonas aeruginosa is becoming recognized as an important pathogen in the gastrointestinal (GI) tract. Here we demonstrate that adenosine, derived from hydrolysis of ATP from the eucaryotic host, is a potent interkingdom signal in the GI tract for this pathogen. The addition of adenosine nearly abolished P. aeruginosa biofilm formation and abolished swarming by preventing production of rhamnolipids. Since the adenosine metabolite inosine did not affect biofilm formation and since a mutant unable to metabolize adenosine behaved like the wild-type strain, adenosine metabolism is not required to reduce pathogenicity. Adenosine also reduces production of the virulence factors pyocyanin, elastase, extracellular polysaccharide, siderophores and the Pseudomonas quinolone signal which led to reduced virulence with Caenorhabditis elegans. To provide insights into how adenosine reduces the virulence of P. aeruginosa, a whole-transcriptome analysis was conducted which revealed that adenosine addition represses genes similar to an iron-replete condition; however, adenosine did not directly bind Fur. Therefore, adenosine decreases P. aeruginosa pathogenicity as an interkingdom signal by causing genes related to iron acquisition to be repressed.
Topics: Adenosine; Animals; Biofilms; Caenorhabditis elegans; Gene Expression Profiling; Glycolipids; Pseudomonas aeruginosa; Signal Transduction; Survival Analysis; Virulence; Virulence Factors
PubMed: 22414222
DOI: 10.1111/j.1751-7915.2012.00338.x -
Antimicrobial Agents and Chemotherapy May 2019High-throughput screening of transposon insertion libraries is a useful strategy for unveiling bacterial genes whose inactivation results in an altered susceptibility to...
High-throughput screening of transposon insertion libraries is a useful strategy for unveiling bacterial genes whose inactivation results in an altered susceptibility to antibiotics. A potential drawback of these studies is they are usually based on just one model antibiotic for each structural family, under the assumption that the results can be extrapolated to all members of said family. To determine if this simplification is appropriate, we have analyzed the susceptibility of mutants of to four aminoglycosides. Our results indicate that each mutation produces different effects on susceptibility to the tested aminoglycosides, with only two mutants showing similar changes in the susceptibility to all studied aminoglycosides. This indicates that the role of a particular gene in the resistome of a given antibiotic should not be generalized to other members of the same structural family. Five aminoglycoside-hypersusceptible mutants inactivating , , , , and were chosen for further analysis in order to elucidate if lower aminoglycoside susceptibility correlates with cross-hypersusceptibility to other antibiotics and with impaired virulence. Our results indicate that inactivation leads to increased cross-susceptibility to different antibiotics. The mutant in this gene is strongly impaired in virulence traits such as pyocyanin production, biofilm formation, elastase activity, and swarming motility and the ability to kill Thus, GlnD might be an interesting target for developing antibiotic coadjuvants with antiresistance and antivirulence properties against .
Topics: Aminoglycosides; Anti-Bacterial Agents; Biofilms; Microbial Sensitivity Tests; Pseudomonas aeruginosa; Virulence
PubMed: 30858210
DOI: 10.1128/AAC.00185-19 -
MicrobiologyOpen Dec 2014Lectin-like bacteriocins of the LlpA family, originally identified in plant-associated bacteria, are narrow-spectrum antibacterial proteins composed of two tandemly...
Lectin-like bacteriocins of the LlpA family, originally identified in plant-associated bacteria, are narrow-spectrum antibacterial proteins composed of two tandemly organized monocot mannose-binding lectin (MMBL) domains. The LlpA-like bacteriocin of Pseudomonas aeruginosa C1433, pyocin L1, lacks any similarity to known P. aeruginosa bacteriocins. The initial interaction of pyocin L1 with target cells is mediated by binding to d-rhamnose, present in the common polysaccharide antigen of lipopolysaccharides (LPS), but the actual cytotoxic mechanism is unknown. In this study, we characterized the activity range of pyocin L1 and two additional L pyocins revealed by genome mining, representing two highly diverged LlpA groups in P. aeruginosa. The recombinant proteins exhibit species-specific antagonistic activities down to nanomolar concentrations against clinical and environmental P. aeruginosa strains, including several multidrug-resistant isolates. The overlap in target strain spectrum between two close homologues of the pyocin L1 group is only minimal, contrasting with the considerable spectral redundancy of LlpA proteins reported for other Pseudomonas species. No correlation was found between L pyocin susceptibility and phylogenetic relatedness of P. aeruginosa isolates. Sensitive strains were retrieved in 13 out of 15 O serotypes tested, excluding the possibility that the highly variable and immunogenic O serotype antigen of the LPS coating would represent a dominant susceptibility-discriminating factor.
Topics: Anti-Bacterial Agents; Bacterial Proteins; Models, Molecular; Phylogeny; Protein Structure, Tertiary; Pseudomonas aeruginosa; Pyocins; Serogroup
PubMed: 25224846
DOI: 10.1002/mbo3.210 -
Journal of Infection in Developing... Oct 2019Pseudomonas aeruginosa is an ubiquitous bacterium causes various community-acquired and nosocomial infections. In this investigation, we aimed to screen the antibiotic...
INTRODUCTION
Pseudomonas aeruginosa is an ubiquitous bacterium causes various community-acquired and nosocomial infections. In this investigation, we aimed to screen the antibiotic susceptibility patterns and the prevalence of virulence factor genes in a set of Pseudomonas aeruginosa isolated from nosocomial and community-acquired infections in the Northwestern of Morocco.
METHODOLOGY
A total of 155 of Pseudomonas aeruginosa strains were collected (January 2015 - December 2016) from nosocomial and community-acquired infections at hospital centers and clinical laboratories in the Northwestern of Morocco. Antimicrobial susceptibility test was performed by the standard disk diffusion method. In addition, PCR assays were used for screening five virulence encoding genes (lasB, algD, plcH, exoA, and exoS).
RESULTS
Our results revealed that high level of antimicrobial resistance was detected towards aztreonam (27.1%) followed by meropenem (14.2%). The resistance to imipenem was significantly higher in strains isolated from nosocomial infections (12.7%) than strains isolated from community-acquired infections (1.5%). The results highlighted that lasB (98.7%) and exoS (98.7%) were the most frequent virulence genes.
CONCLUSIONS
This survey provides data about phenotypic and genotypic properties of Pseudomonas aeruginosa emerged in the Northwestern of Morocco. It could be helpful for the health workers to improve infection control measures and to establish a surveillance system.
Topics: Anti-Bacterial Agents; Genes, Bacterial; Humans; Microbial Sensitivity Tests; Morocco; Pseudomonas Infections; Pseudomonas aeruginosa; Virulence; Virulence Factors
PubMed: 32084019
DOI: 10.3855/jidc.10675 -
Archives de Pediatrie : Organe Officiel... Oct 2006Pseudomonas aeruginosa antibiotic resistance mechanisms are both innate and acquired, different according to the considered antibiotic; epidemiological follow-up of AB... (Review)
Review
Pseudomonas aeruginosa antibiotic resistance mechanisms are both innate and acquired, different according to the considered antibiotic; epidemiological follow-up of AB resistance for this pathogen is managed through ONERBA network (www.onerba.org); therapeutic approaches must limit resistant strains diffusion and resistant mutants emergence.
Topics: Drug Resistance, Bacterial; Pseudomonas aeruginosa; beta-Lactam Resistance
PubMed: 17370389
DOI: No ID Found -
Journal of Medical Microbiology Jul 2016
Topics: Anti-Bacterial Agents; Genotype; Humans; Microbial Sensitivity Tests; Multilocus Sequence Typing; Pseudomonas Infections; Pseudomonas aeruginosa; Sequence Analysis, DNA; United Kingdom; beta-Lactam Resistance; beta-Lactamases; beta-Lactams
PubMed: 27126265
DOI: 10.1099/jmm.0.000269