Academic literature on the topic 'Microbiology of Ps. aeruginosa'

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Journal articles on the topic "Microbiology of Ps. aeruginosa"

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Costello, Anne, F. Jerry Reen, Fergal O’Gara, Máire Callaghan, and Siobhán McClean. "Inhibition of co-colonizing cystic fibrosis-associated pathogens by Pseudomonas aeruginosa and Burkholderia multivorans." Microbiology 160, no. 7 (July 1, 2014): 1474–87. http://dx.doi.org/10.1099/mic.0.074203-0.

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Cystic fibrosis (CF) is a recessive genetic disease characterized by chronic respiratory infections and inflammation causing permanent lung damage. Recurrent infections are caused by Gram-negative antibiotic-resistant bacterial pathogens such as Pseudomonas aeruginosa, Burkholderia cepacia complex (Bcc) and the emerging pathogen genus Pandoraea. In this study, the interactions between co-colonizing CF pathogens were investigated. Both Pandoraea and Bcc elicited potent pro-inflammatory responses that were significantly greater than Ps. aeruginosa. The original aim was to examine whether combinations of pro-inflammatory pathogens would further exacerbate inflammation. In contrast, when these pathogens were colonized in the presence of Ps. aeruginosa the pro-inflammatory response was significantly decreased. Real-time PCR quantification of bacterial DNA from mixed cultures indicated that Ps. aeruginosa significantly inhibited the growth of Burkholderia multivorans, Burkholderia cenocepacia, Pandoraea pulmonicola and Pandoraea apista, which may be a factor in its dominance as a colonizer of CF patients. Ps. aeruginosa cell-free supernatant also suppressed growth of these pathogens, indicating that inhibition was innate rather than a response to the presence of a competitor. Screening of a Ps. aeruginosa mutant library highlighted a role for quorum sensing and pyoverdine biosynthesis genes in the inhibition of B. cenocepacia. Pyoverdine was confirmed to contribute to the inhibition of B. cenocepacia strain J2315. B. multivorans was the only species that could significantly inhibit Ps. aeruginosa growth. B. multivorans also inhibited B. cenocepacia and Pa. apista. In conclusion, both Ps. aeruginosa and B. multivorans are capable of suppressing growth and virulence of co-colonizing CF pathogens.
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Nelson, Lisa K., Genevieve H. D'Amours, Kimberley M. Sproule-Willoughby, Douglas W. Morck, and Howard Ceri. "Pseudomonas aeruginosa las and rhl quorum-sensing systems are important for infection and inflammation in a rat prostatitis model." Microbiology 155, no. 8 (August 1, 2009): 2612–19. http://dx.doi.org/10.1099/mic.0.028464-0.

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Pseudomonas aeruginosa frequently acts as an opportunistic pathogen of mucosal surfaces; yet, despite causing aggressive prostatitis in some men, its role as a pathogen in the prostate has not been investigated. Consequently, we developed a Ps. aeruginosa infection model in the rat prostate by instilling wild-type (WT) Ps. aeruginosa strain PAO1 into the rat prostate. It was found that Ps. aeruginosa produced acute and chronic infections in this mucosal tissue as determined by bacterial colonization, gross morphology, tissue damage and inflammatory markers. WT strain PAO1 and its isogenic mutant PAO-JP2, in which both the lasI and rhlI quorum-sensing signal systems have been silenced, were compared during both acute and chronic prostate infections. In acute infections, bacterial numbers and inflammatory markers were comparable between WT PA01 and PAO-JP2; however, considerably less tissue damage occurred in infections with PAO-JP2. Chronic infections with PAO-JP2 resulted in reduced bacterial colonization, tissue damage and inflammation as compared to WT PAO1 infections. Therefore, the quorum-sensing lasI and rhlI genes in Ps. aeruginosa affect acute prostate infections, but play a considerably more important role in maintaining chronic infections. We have thus developed a highly reproducible model for the study of Ps. aeruginosa virulence in the prostate.
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Irvin, Randall T., and Howard Ceri. "Immunochemical examination of the Pseudomonas aeruginosa glycocalyx: a monoclonal antibody which recognizes L-guluronic acid residues of alginic acid." Canadian Journal of Microbiology 31, no. 3 (March 1, 1985): 268–75. http://dx.doi.org/10.1139/m85-050.

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Mice immunized with Formalin-fixed mucoid Pseudomonas aeruginosa cells developed an immune response directed, in part, towards the P. aeruginosa glycocalyx. The polyclonal mouse sera produced good immunofluorescent staining of the P. aeruginosa glycocalyx and cell surface. A library of 250 hybridoma cell lines which produced monoclonal antibodies directed against P. aeruginosa was established. Twelve clones (4.8%) produced antibody which reacted with alginate in an enzyme-linked immunosorbent assay (ELISA). Clone Ps 53 was chosen for further study, cloned, and an ascites tumor established. Clone Ps 53 was chosen for further study because the antibody produced demonstrated a specificity similar to that of a recently isolated heparin – rat-lung lectin which recognizes alginates of the Homma nontypable P. aeruginosa strains. The Ps 53 clone produced an immunoglobulin M which reacted with P. aeruginosa alginate and produced good immunofluorescent staining of the P. aeruginosa glycocalyx. The Ps 53 monoclonal antibody has an apparent specificity for L-guluronic residues in ELISA. Competitive binding studies with various alginates and monosaccharides suggest that the C6 carboxyl group of uronic acids are recognized by the antibody and that the antigen-binding site is fairly large and may recognize a particular sequence or epitope of alginic acid which is rich in L-guluronic acid. The Ps 53 monoclonal antibody did not react uniformily with all P. aeruginosa alginates but did react with all of the alginates of the Homma nontypable strains tested, suggesting that acetylation or various modifications found in P. aeruginosa alginates may interfere with antibody binding and define specific epitopes. The Ps 53 antibody also reacted with purified outer membrane, indicating that some alginate or L-guluronic acid is intimately associated with outer membrane.
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Rasmussen, Thomas Bovbjerg, Mette E. Skindersoe, Thomas Bjarnsholt, Richard K. Phipps, Kathrine Bisgaard Christensen, Peter Ostrup Jensen, Jens Bo Andersen, et al. "Identity and effects of quorum-sensing inhibitors produced by Penicillium species." Microbiology 151, no. 5 (May 1, 2005): 1325–40. http://dx.doi.org/10.1099/mic.0.27715-0.

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Quorum sensing (QS) communication systems are thought to afford bacteria with a mechanism to strategically cause disease. One example is Pseudomonas aeruginosa, which infects immunocompromised individuals such as cystic fibrosis patients. The authors have previously documented that blockage of the QS systems not only attenuates Ps. aeruginosa but also renders biofilms highly susceptible to treatment with conventional antibiotics. Filamentous fungi produce a battery of secondary metabolites, some of which are already in clinical use as antimicrobial drugs. Fungi coexist with bacteria but lack active immune systems, so instead rely on chemical defence mechanisms. It was speculated that some of these secondary metabolites could interfere with bacterial QS communication. During a screening of 100 extracts from 50 Penicillium species, 33 were found to produce QS inhibitory (QSI) compounds. In two cases, patulin and penicillic acid were identified as being biologically active QSI compounds. Their effect on QS-controlled gene expression in Ps. aeruginosa was verified by DNA microarray transcriptomics. Similar to previously investigated QSI compounds, patulin was found to enhance biofilm susceptibility to tobramycin treatment. Ps. aeruginosa has developed QS-dependent mechanisms that block development of the oxidative burst in PMN neutrophils. Accordingly, when the bacteria were treated with either patulin or penicillic acid, the neutrophils became activated. In a mouse pulmonary infection model, Ps. aeruginosa was more rapidly cleared from the mice that were treated with patulin compared with the placebo group.
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Hemachandra, Sonali, Kulwant Kamboj, Janna Copfer, Gerald Pier, Larry L. Green, and John R. Schreiber. "Human Monoclonal Antibodies againstPseudomonas aeruginosa Lipopolysaccharide Derived from Transgenic Mice Containing Megabase Human Immunoglobulin Loci Are Opsonic and Protective against Fatal Pseudomonas Sepsis." Infection and Immunity 69, no. 4 (April 1, 2001): 2223–29. http://dx.doi.org/10.1128/iai.69.4.2223-2229.2001.

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ABSTRACT Pseudomonas aeruginosa is a significant human pathogen, and no vaccine is commercially available. Passive antibody prophylaxis using monoclonal antibodies (MAb) against protectiveP. aeruginosa epitopes is an alternative strategy for preventing P. aeruginosa infection, but mouse MAb are not suitable for use in humans. Polyclonal human antibodies from multiple donors have variable antibody titers, and human MAb are difficult to make. We used immunoglobulin-inactivated transgenic mice reconstituted with megabase-size human immunoglobulin loci to generate a human MAb against the polysaccharide (PS) portion of the lipopolysaccharide O side chain of a common pathogenic serogroup ofP. aeruginosa, 06ad. The anti-PS human immunoglobulin G2 MAb made from mice immunized with heat-killed P. aeruginosa was specific for serogroup 06ad pseudomonas. The MAb was highly opsonic for the uptake and killing of P. aeruginosa by human polymorphonuclear leukocytes in the presence of human complement. In addition, 25 μg of the MAb protected 100% of neutropenic mice from fatal P. aeruginosasepsis. DNA sequence analysis of the genes encoding the MAb revealed VH3 and Vκ2/A2 variable-region genes, similar to variable-region genes in humans immunized with bacterial PS and associated with high-avidity anti-PS antibodies. We conclude that human MAb to P. aeruginosa made in these transgenic mice are highly protective and that these mice mimic the antibody response seen in humans immunized with T-cell-independent antigens such as bacterial PS.
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Abdelrahman, Dina N., Aya A. Taha, Mazar M. Dafaallah, Alaa Abdelgafoor Mohammed, Abdel Rahim M. El Hussein, Ahmed I. Hashim, Yousif F. Hamedelnil, and Hisham N. Altayb. "β-lactamases (bla TEM, bla SHV, bla CTXM-1, bla VEB, bla OXA-1) and class C β-lactamases gene frequency in Pseudomonas aeruginosa isolated from various clinical specimens in Khartoum State, Sudan: a cross sectional study." F1000Research 9 (April 1, 2021): 774. http://dx.doi.org/10.12688/f1000research.24818.3.

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Background: Pseudomonas aeruginosa is a pathogenic bacterium, causing nosocomial infections with intrinsic and acquired resistance mechanisms to a large group of antibiotics, including β-lactams. This study aimed to determine the susceptibility pattern to selected antibiotics and to index the first reported β-lactamases genes frequency in Ps. aeruginosa in Khartoum State, Sudan. Methods: 121 Ps. aeruginosa clinical isolates from various clinical specimens were used in this cross sectional study conducted in Khartoum State. Eighty isolates were confirmed as Ps. aeruginosa through conventional identification methods and species specific primers. The susceptibility pattern of the confirmed isolates to selected antibiotics was done following the Kirby Bauer disk diffusion method. Multiplex PCR was used for detection of seven β-lactamase genes (blaTEM, blaSHV, blaCTXM-1, blaVEB, blaOXA-1, blaAmpC and blaDHA). Results: Of the 80 confirmed Ps. aeruginosa isolates, 8 (10%) were resistant to Imipenem while all isolates were resistant to Amoxicillin and Amoxyclav (100%). A total of 43 (54%) Ps. aeruginosa isolates were positive for blaTEM, blaSHV, blaCTXM-1, blaVEB and blaOXA-1 genes, while 27 (34%) were positive for class C β- Lactamases, and 20 (25%) were positive for both classes. Frequency of beta-lactamases genes was as follows: blaTEM, 19 (44.2%); blaSHV, 16 (37.2%); bla CTX-M1, 10 (23.3%); blaVEB, 14 (32.6%); blaOXA-1, 7 (16.3%). blaAmpC 22 (81.5%) and bla DHA 8 (29.6%). In total, 3 (11.1%) isolates were positive for both bla AmpC and blaDHA genes. Conclusion: Ps. aeruginosa isolates showed a high rate of β- lactamases production, with co-resistance to other antibiotic classes. The lowest resistance rate of Ps. aeruginosa was to Imipenem followed by Gentamicin and Ciprofloxacin. No statistically significant relationship between production of β-lactamases in Ps. aeruginosa and resistance to third generation cephalosporins was found.
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Gashaw, Getachew, Amare Fassil, and Fuad Redi. "Evaluation of the Antibacterial Activity of Pleurotus spp. Cultivated on Different Agricultural Wastes in Chiro, Ethiopia." International Journal of Microbiology 2020 (August 27, 2020): 1–9. http://dx.doi.org/10.1155/2020/9312489.

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In the present study, mushrooms, Pleurotus ostreatus and Pleurotus florida, were cultivated on different agricultural wastes namely coffee straw (CS), pea straw (PS), Sorghum Grain Residue (SGR), and Wheat Grain (WG) for the evaluation of antibacterial activity. Antimicrobial activity evaluation was carried out against human pathogenic microorganisms, namely, Escherichia coli, Bacillus subtilis, Streptococcus faecalis, Pseudomonas aeruginosa, and Salmonella typhi by using the disc diffusion method. Methanolic extracts of P. ostreatus cultivated on a Sorghum grain residue substrate were recorded for the highest antibacterial activity against E. coli (19.8 mm) and P. aeruginosa (16.4 mm), and methanolic extracts of P. florida cultivated on a wheat grain substrate were recorded for the highest antibacterial activity against E. coli (18.6 mm) and S. faecalis (14.8 mm). Therefore, results suggested that P. ostreatus and P. florida cultivated on the coffee straw and Sorghum grain substrate were found with the highest antimicrobial activity in comparison to other substrates. The results supported that the methanolic extracts of P. ostreatus and P. florida might indeed be potential sources of antibacterial agents.
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HANIS, T., P. JELEN, P. KLÍR, J. MÑUKOVÁ, B. PÉREZ, and M. PESEK. "Poultry Meat Irradiation - Effect of Temperature on Chemical Changes and Inactivation of Microorganisms." Journal of Food Protection 52, no. 1 (January 1, 1989): 26–29. http://dx.doi.org/10.4315/0362-028x-52.1.26.

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Chilled (10°C) and frozen (−15°C) broiler carcasses initially artificially contaminated either with Pseudomonas aeruginosa, Salmonella typhimurium or Serratia marcescens (106cfu/g) were irradiated (Co60) with doses of 0.5, 1.0, 2.5, 5.0 and 10.0 kGy. Ps. aeruginosa was eliminated by doses of 1.0 - 2.5 kGy, S. marcescens by doses of 2.5 - 5.0 kGy and S. typhimurium by a dose of 10 kGy. Characteristic radiation odor increasing with radiation dose and temperature was well removed by heat meat preparation. Radiation resulted in increase of acid and peroxide values and destruction of thiamine (up to 57%/10 kGy) and riboflavin (up to 27%/10 kGy), lower increase of fat indexes and lower destruction of vitamins was observed at lower irradiation temperature. Content of amino acids was not affected by the treatment.
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Satapute, Praveen, and Basappa Kaliwal. "Biodegradation of the fungicide propiconazole by Pseudomonas aeruginosa PS-4 strain isolated from a paddy soil." Annals of Microbiology 66, no. 4 (June 15, 2016): 1355–65. http://dx.doi.org/10.1007/s13213-016-1222-6.

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Kimura, Soichiro, Kazuhiro Tateda, Yoshikazu Ishii, Manabu Horikawa, Shinichi Miyairi, Naomasa Gotoh, Masaji Ishiguro, and Keizo Yamaguchi. "Pseudomonas aeruginosa Las quorum sensing autoinducer suppresses growth and biofilm production in Legionella species." Microbiology 155, no. 6 (June 1, 2009): 1934–39. http://dx.doi.org/10.1099/mic.0.026641-0.

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Bacteria commonly communicate with each other by a cell-to-cell signalling mechanism known as quorum sensing (QS). Recent studies have shown that the Las QS autoinducer N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C12-HSL) of Pseudomonas aeruginosa performs a variety of functions not only in intraspecies communication, but also in interspecies and interkingdom interactions. In this study, we report the effects of Pseudomonas 3-oxo-C12-HSL on the growth and suppression of virulence factors in other bacterial species that frequently co-exist with Ps. aeruginosa in nature. It was found that 3-oxo-C12-HSL, but not its analogues, suppressed the growth of Legionella pneumophila in a dose-dependent manner. However, 3-oxo-C12-HSL did not exhibit a growth-suppressive effect on Serratia marcescens, Proteus mirabilis, Escherichia coli, Alcaligenes faecalis and Stenotrophomonas maltophilia. A concentration of 50 μM 3-oxo-C12-HSL completely inhibited the growth of L. pneumophila. Additionally, a significant suppression of biofilm formation was demonstrated in L. pneumophila exposed to 3-oxo-C12-HSL. Our results suggest that the Pseudomonas QS autoinducer 3-oxo-C12-HSL exerts both bacteriostatic and virulence factor-suppressive activities on L. pneumophila alone.
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Dissertations / Theses on the topic "Microbiology of Ps. aeruginosa"

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Hewinson, R. G. "#BETA#-Lactamase-mediated resistance to '#beta#-lactamase-stable' cephalosporins in Pseudomonas aeruginosa." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382716.

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Silistre, Hazel. "Riboregulation in Pseudomonas aeruginosa." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/32634/.

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The opportunistic human pathogen Pseudomonas aeruginosa controls virulence, production of secondary metabolites, motility, biofilm formation, growth in anaerobic conditions, intracellular and intercellular signalling and the switch from an acute to a chronic mode of infection at the transcriptional and post-transcriptional levels by modulation of the Gac/Rsm system. Cell density-dependent signal accumulation and environmental stimulators such as pH changes and ion limitation activate the GacS/GacA two-component system which in turn triggers transcription of the small regulatory RNAs RsmY and RsmZ. These sRNAs sequester multiple copies of the RNA-binding protein RsmA, antagonising its function. The RsmA/CsrA proteins act as translational repressors by binding to the GGA-motifs in the untranslated region of target mRNAs and blocking ribosome binding. In this study, the biological function of RsmN, an RsmA homologue with a conserved RNA-binding pocket but a distinct protein folding, the predicted autoregulatory mechanism of RsmN, the nature of target transcripts of RsmN, and the cross-regulation between the two Rsm proteins were investigated. The positive control of proteolytic and elastinolytic activities and swarming motility by RsmN has been demonstrated using single and inducible double deletion mutants of rsmN. Furthermore, rsmN deletion increased microcolony formation during biofilm formation. Regulation by RsmN was most apparent in the absence of RsmA, when rsmN expression was induced via a multicopy plasmid and at temperatures lower than 37°C. The double deletion of rsmA and rsmN affected growth, diminished proteolytic and elastinolytic activities, triggered autolysis and led to the increased secretion of the type VI secretion system protein Hcp1. Moreover, the double deletion of rsmA and rsmN altered the colony morphology of P. aeruginosa. Mutagenesis of the functionally critical, conserved RNA-binding residue which is identified as Arg44 in RsmA and Arg62 in RsmN resulted in the loss of RsmN function. In a genome-wide analysis by RNASeq, target transcripts were co-purified with RsmN from 37°C and 34°C cultures of a wild-type strain expressing rsmN in multicopy numbers. RNASeq results indicated that small regulatory RNAs such as CrcZ, RsmY and RgsA are common targets of RsmN and RsmA, whereas PhrS is a target of RsmN only. Other common RsmA and RsmN targets included transcriptional regulators, heat shock proteins, proteases, starvation response proteins, components of the denitrification pathway, outer membrane proteins required for pore formation, type III and type VI secretion system proteins and RsmA. Transcripts of heat shock proteins, the tss operon genes and rsmA were enriched by RsmN at 37°C but not at 34°C whereas the lasB transcript was enriched by RsmN at 34°C but not at 37°C. Based on the list of common targets of RsmA and RsmN and the results obtained from phenotypic assays, induction of the lytic Pf4 prophage, accumulation of alkyl quinolone or c-di-GMP signalling molecules, imbalanced redox state, carbon starvation, increased membrane permeability, and aggregation of misfolded proteins are suggested as possible mechanisms triggering the excessive autolysis of the rsmNind ΔrsmA mutant under uninducing conditions. The data gathered so far suggests that rsmN is differentially expressed, with increased RsmN activity at temperatures below 37°C in comparison with RsmA, and, RsmA and RsmN collectively contribute to the regulation of secondary metabolite production, motility and microcolony formation in P. aeruginosa.
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Janssen, Kayley Hope. "Post-transcriptional regulation of virulence factors in Pseudomonas aeruginosa." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5952.

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Pseudomonas aeruginosa is a Gram-negative bacterium capable of causing infections in immunocompromised individuals. The CsrA family of RNA-binding proteins are widely distributed in bacteria and regulate gene expression at the post-transcriptional level. P. aeruginosa has a canonical CsrA family member (RsmA) and a novel, structurally distinct variant (RsmF). To better understand RsmF binding properties, we performed parallel systematic evolution of ligands by exponential enrichment (SELEX) experiments for both RsmA and RsmF. The initial target aptamer was a 57 nt RNA transcript containing a central core randomized at 15 sequential positions. Most of the selected aptamers were the expected size and shared a common consensus sequence (CAnGGAyG). Longer aptamers (80-140 nts) containing two consensus-binding sites were also identified. Representative short (single consensus site) and long (two consensus sites) aptamers were tested for RsmA and RsmF binding. Whereas RsmA bound the short aptamers with high affinity, RsmF was unable to bind the same targets. RsmA and RsmF both bound the long aptamers with high affinity. Mutation of either consensus GGA site in the long aptamers reduced or eliminated RsmF binding, suggesting a requirement for two binding sites. Based on our observations that high affinity binding by RsmF appears to require two binding sites, we used an in-silico approach to search for candidate RsmF targets in the P. aeruginosa genome. We queried a library of 5’ UTRs (untranslated regions) for potential targets of RsmF based on the number and positions of GGA motifs, and secondary structure. Experimental validation of potential targets yielded few direct targets for both RsmA and RsmF indicating that additional factors contribute to differential binding in vivo. P. aeruginosa has distinct acute and chronic virulence phenotypes. Whereas acute virulence is typically associated with expression of a type III secretion system (T3SS), chronic virulence is characterized by biofilm formation. Many of the phenotypes associated with acute and chronic virulence are inversely regulated by RsmA and RsmF. RsmA activity is controlled by two small, non-coding regulatory RNAs (RsmY and RsmZ). In addition, we recently identified a sRNA (RsmV) that also contributes to RsmA and RsmF activity. Bioinformatic analyses suggest that these sRNAs each have 3-4 putative RsmA/RsmF bindings sites. Each site contains a GGA motif presented in the loop portion of a predicted stem-loop structure. These sRNAs regulate RsmA activity, and possibly RsmF, by sequestering RsmA and/or RsmF from target mRNAs. We characterize the contribution of each GGA site in RsmV, RsmY, and RsmZ using functional assays. We provided evidence that RsmF has more restrictive binding preferences compared to RsmA. The type III secretion system (T3SS) is an important virulence factor that contributes to P. aeruginosa pathogenesis. Production of the T3SS is activated by host-associated signals and is tightly controlled at several levels. Global regulators including cAMP-Vfr signaling and Hfq contribute to tight regulation of the T3SS. Vfr (virulence factor regulator) is a transcription factor that responds to increased intracellular levels of cAMP. Vfr directly activates exsA transcription. ExsA activates transcription of the entire T3SS regulon. Hfq is an RNA chaperone that stabilizes sRNA and/or facilitates their binding to mRNA targets. Hfq is found in many bacteria and regulates stress responses, metabolism, and virulence. P. aeruginosa Hfq regulates about 5% of the genome and has a role in post-transcriptional control of T3SS in many Gram-negative bacteria. The mechanism of Hfq control of P. aeruginosa T3SS remains to be described. To better understand how Hfq regulates the T3SS we sought to identify mRNA targets of Hfq. Utilizing several reporters to genes involved in T3SS gene expression, we found that exsA transcription is decreased by Hfq activity. ExsA translation is also decreased by Hfq in conjunction with sRNA 179. Our findings show that Hfq may indirectly and directly regulate exsA translation.
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Vareechon, Chairut Charles. "Host-Pathogen Interaction in Pseudomonas aeruginosa Infection." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499427972888735.

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Nelson, Shona Margaret. "Studies on biofilm growth of Pseudomonas aeruginosa PA01." Thesis, Aston University, 1993. http://publications.aston.ac.uk/12581/.

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The development of in vitro techniques to model the surface-associated mode of growth is a prerequisite to understanding more fully the physiological changes involved in such a growth strategy. Key factors believed to influence bacterial persistence in chronic infections are those of the biofilm mode of growth and slow growth rate. Methods for controlling Pseudomonas aeruginosa biofilm population growth rates were investigated in this project. This microorganism was incompatible with the in vitro 47mm diameter membrane filter-based biofilm technique developed for the study of Escherichia coli and Staphylococcus epidermidis by Gilbert et al (Appl. Environ. Microbiol. 1989, 55, 1308-1311). Two alternative methods were designed. The first comprised a 25mm diameter cellulose acetate membrane filter supported in an integral holder. This was found to be limited to the study of low microbial population densities with low flow rates. The second, based on a cylindrical cellulose fibre depth filter, permitted rapid flow rates to be studied and allowed growth rate control of biofilm and eluted cells. Model biofilms released cells to the perfusing medium as they grew and divided. The viability of released cells was reduced during, and shortly after, inclusion of ciprofloxacin in the perfusate. Outer membrane profiles of biofilm populations exhibited at least two bands not apparent in planktonic cells grown in batch and chemostat culture, and LPS profiles of biofilm populations showed variation with growth rate. Cell surface hydrophobicity of resuspended biofilm cells varied little with growth rate, whilst it decreased markedly for cells released from the biofilms as growth rate increased. Cells released from the biofilm were more hydrophilic than their sessile counterparts. Differing growth rates, LPS profiles and hydrophobicity are proposed to have a bearing on the release of cells from the adherent population.
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Lam, Howard Andrew. "Cranberry derived materials modulate quorum sensing in Pseudomonas aeruginosa." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114290.

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Cranberry-derived materials (CDMs) have recently been shown to block the group associated swarming motility in Pseudomonas aeruginosa without blocking swimming or twitching motilities. However, their mechanism of action is as of yet unknown. We hypothesized that these CDMs interfere with communication pathways important in swarming called quorum sensing (QS) and measured the impact of the CDMs on QS at three levels: QS signalling gene transcription, QS signal production, and activity/production of QS-controlled virulence factors. Crude cranberry powder extract (CP) repressed the las and rhl systems, the two main QS systems in P. aeruginosa, – as measured by the use of a lacZ bioreporter and β-galactosidase assay. CP also reduced the accumulation of both las and rhl QS signals in the medium. Exposure to 5 mg/mL or 10 mg/mL CP stimulated cell growth but still resulted in the reduction of the growth-normalized activity of key virulence factors. Cranberry-derived proanthocyanidins (cPACs) had little direct effect on the regulatory QS gene transcription or QS signal production in P. aeruginosa but reduced the activity/production of key virulence factors. Compounds found in cranberries may be clinically useful; however, further research is required to isolate the active compound(s) from CP and overcome the associated increased cell growth.
Les matériaux dérivés des canneberges (MDC) ont été récemment démontré ayant la capacité de bloquer le mode de déplacement communautaire de type swarming au Pseudomonas aeruginosa sans bloquer les modes de déplacement individuels de type swimming et twitching. Pourtant, leur mode d'action est inconnu. Nous avons supposé que ces MDC interférent avec une voie de communication essentiel pour le mode de déplacement de type swarming appelé quorum sensing (QS), et nous avons mesuré l'impact des MDC sur QS à trois niveaux : la transcription des gènes de signalisation QS, la production des signaux QS, et l'activité/production des facteurs de virulence contrôlées par le QS.L'extrait de canneberges en poudre brut (CP) a réprimé la transcription des gènes de signalisation dans les systèmes las et rhl, les deux systèmes de QS majeurs au P. aeruginosa, utilisant un rapporteur biologique lacZ et un essai β-galactosidase. Le CP a aussi causé une réduction de l'accumulation des signaux pour les systèmes las et rhl dans le médium. L'addition du CP aux concentrations de 5 mg/mL ou 10 mg/mL a stimulé la croissance des cellules mais a aussi réduit l'activité et la production de plusieurs facteurs de virulence. Les proanthocyanidines d'origine de canneberges (cPACs) ont eu peu d'effet sur les systèmes QS de P. aeruginosa mais ont quand même réduit l'activité et la production de plusieurs facteurs de virulence, normalisée pour la croissance des cellules. Les MDC pourraient un jour être cliniquement utiles, mais des recherches supplémentaires sont nécessaires pour isoler le(s) composé(es) actif(s) du CP et de surmonter le problème de la croissance cellulaire augmenté.
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Qureshi, Asif Mahmood. "Studies of mutability in Methylophilus methylotrophus and Pseudomonas aeruginosa." Thesis, University of Kent, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328558.

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Beaudoin, Trevor Wayne. "Investigating the role of ndvB in Pseudomonas aeruginosa biofilms." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28352.

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Pseudomonas aeruginosa is an opportunistic pathogen prevalent in nosocomial infections and patients with cystic fibrosis. P. aeruginosa shows a high degree of antibiotic tolerance which in part can be attributed to the formation of biofilms. The increased antibiotic resistance seen in biofilms can be attributed to several factors including differential gene expression within biofilms that can lead to biofilm specific mechanisims of antibiotic resistance. The ndvB gene is important for biofilm specific antibiotic resistance in P. aeruginosa. It is important in signaling and regulation of gene expression in other pathogens. Microarray analysis comparing gene expression between wildtype and a ndvB deletion mutant was performed to identify genes that might be regulated by the gene product, believed to be cyclic glucans, that contribute to biofilm specific antibiotic resistance. The array analysis identified 24 genes that were differentially regulated by ndvB, including a response regulator, agmR, as well as most of the genes which it regulates. Quantitative real-time polymerase chain reactions using primers specific to agmR and its associated genes confirmed that they were expressed in a ndvB related manner. Minimal bactericidal concentration assays were performed and confirmed that these genes are important in resistance to tobramycin and ciprofloxacin.
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Fu, Yinan. "Structure and dynamics of Pseudomonas aeruginosa ICP." Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/723/.

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Pseudomonas aeruginosa inhibitor of cysteine peptidases (PA-ICP) is a potent protein inhibitor of papain-like cysteine peptidases (CPs) identified in Pseudomonas aeruginosa, an opportunistic pathogenic bacteria that can cause severe infections in human. It belongs to the newly characterized natural CP inhibitors of the I42 family, designated the ICP family. The members of this family are present in some protozoa and bacterial pathogens. They can inhibit both parasite and mammalian CPs with high affinity and specificity. Whether the main biological function of the proteins in the pathogens is to regulate the hydrolytic activity of the organisms’ endogenous CPs or exogenous CPs so as to facilitate the pathogens’ invasion or survival is still under investigation. Although Pseudomonas aeruginosa contains a CP inhibitor, no CP genes are found in its genome, suggesting that the targets of PA-ICP may be exogenous. This hypothesis is supported by the presence of a putative secretion signal peptide at the N-terminus of PA-ICP which may be involved in exporting the protein to target exogenous CPs. In order to shed light on the biological function and inhibitory specificity of PA-ICP, the structure and backbone dynamics of this protein were characterised using NMR spectroscopy. In this project, the inhibitory activity of PA-ICP to a range of mammalian model CPs was also studied. Like its previously studied homologs, PA-ICP adopts an immunoglobulin fold comprised of seven β-strands. Three highly conserved sequence motifs located in mobile loop regions form the CP binding site. The inhibitor exhibits higher affinity toward the mammalian CP cathepsin L than cathepsins H and B. Homology modelling of the PA-ICP-cathspin L interaction based on the crystal structure of the chgasin-cathpsin L complex shows that PA-ICP may inhibit the peptidases by blocking the enzyme’s active site and that the interactions between chagasin and CPs may be conserved in PA-ICP-peptidase complexes. The specificity of the inhibitors may be determined by the relative flexibility of the loops bearing the binding site motifs and the electrostatic properties of certain residues near the binding sites.
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Lindestam, Arlehamn Cecilia Sofie. "Intracellular triggering of inflammation by the extracellular bacterium Pseudomonas aeruginosa." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1401/.

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Abstract P.aeruginosa is an extracellular, Gram-negative opportunistic pathogen. One of the most important virulence factors during infection is the type III secretion system (T3SS). This system is found exclusively in Gram-negative bacteria and it forms a conduit between the bacteria and the host cell through which effector molecules can be translocated. These effectors alter the function of the host cell to promote survival of the bacterium. Infections are detected initially by the innate immune system via germ-line encoded receptors, pathogen recognition receptors (PRRs). These receptors recognise conserved microbial patterns, known as pathogen-associated molecular patterns and molecules which signal danger, danger-associated molecular patterns. PRRs are both membrane bound, such as Toll-like receptors (TLRs), and cytosolic, such as Nod-like receptors (NLRs). Some NLRs are involved in the formation of multimeric protein complexes, the Nod-signalosome and inflammasomes. These lead to the activation of NF-κB and the activation of caspase-1 and subsequent proteolytic processing of interleukin-1β (IL-1β) into its mature form. Both processes contribute to the inflammatory response following infection. In this study we sought to elucidate whether P.aeruginosa is able to trigger cytosolic PRRs and the mechanism of this activation. Initially we studied inflammasome activation by P.aeruginosa. We demonstrated that P.aeruginosa is able to activate the NLRC4/ASC-inflammasome complex. This was found to be dependent on a functional T3SS, but independent of any effectors passing through the system. The activation was discovered by detection of processed, and thus active caspase-1 fragments, as well as by secretion of mature IL-1β. The mechanism of the inflammasome activation was then investigated. We found that the NLRC4-dependent inflammasome activation is also dependent on extracellular potassium. An increase of extracellular potassium leads to a complete abrogation of inflammasome activation by P.aeruginosa and Salmonella. To further elucidate this finding, we investigated the leakiness of the pore formed by the T3SS in the host cell membrane. No flux of ions or small molecules could be detected in the host cell membrane following infection. However, host-membrane repair mechanisms were triggered, which could be detected by lysosomal-associated membrane protein (LAMP)-1-specific staining of the plasma membrane. We hypothesize a role for membrane potential in triggering of inflammasome activation by bacteria possessing a secretion system. Potassium-efflux has previously been identified as a activator of the NLRP3 inflammasome, but no changes in intracellular potassium could be found during this study. The activation of the NLRC4 inflammasome by the Pseudomonal strain PA103 was shown, in this study, to be independent of flagellin. Instead, the bacterial molecule responsible for inflammasome activation was shown to be pilin. Pilin is important for attachment to the host cell and the function of the T3SS. We showed that a strain lacking pilin were still able to translocate effectors through its T3SS. However, it was unable to activate the inflammasome complex. Transfection of purified pilin into cells was shown to trigger inflammasome activation. This was found to be dependent on caspase-1 but independent of NLRC4 and ASC, which is not in agreement with the results found for live bacteria. We hypothesised that the reason for this is the delivery method used, since a T3SS and infection delivers proteins and molecules differently compared to a transfection reagent. Finally, the role for Nod1 in infection by P.aeruginosa was explored. We could not identify Nod1-dependent NF-κB-activation using luciferase reporter gene assays. We therefore hypothesise that Nod1 does not have a role in the innate immune response to P.aeruginosa. In conclusion, we have identified NLRC4- and ASC-dependent inflammasome activation by P.aeruginosa. This activation was shown to be dependent on a functional T3SS and the surface protein pilin, as well as extracellular potassium. This describes a novel NLRC4-activation mechanism dependent on potassium and identifies pilin as a PRR-trigger for the first time.
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Books on the topic "Microbiology of Ps. aeruginosa"

1

Foote, Nicholas. Studies on the cytochrome c peroxidase of Ps. aeruginosa. Norwich: University of East Anglia, 1985.

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Wong, Chee Fah, and Hamidah Idris. Pseudomonas Aeruginosa: A Review and Directions for Research. Nova Science Publishers, Incorporated, 2019.

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Samadpour, Mansour. Molecular Typing of Pseudomonas Aeruginosa in Distribution Systems. Amer Water Works Assn, 2001.

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Govan, John, and Andrew Jones. Microbiology of CF lung disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0003.

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This chapter presents the microbiology of CF and describes the classical bacterial pathogens including Staphylococcus aureus, Haemophilus influenza, Pseudomonas aeruginosa and organisms of the Burkholderia cepacia complex. The dominant of these is P. aeruginosa. Infections with other opportunistic pathogens including non-tuberculous mycobacteria, Stenotrophomonas maltophila, and Achromobacter (Alcaligenes) xylosoxidans are also encountered. This chapter details measures to prevent the onset of chronic infection with these organisms include regular screening of respiratory tract samples for bacterial pathogens and the use of aggressive antibiotic therapy to eradicate initial infection before the pathogen can adapt to the environment of the CF lung. Patient-to-patient spread of transmissible strains of bacterial pathogens has led to the implementation of strict infection control measures at CF centres, including patient segregation. In addition to bacterial pathogens, the contribution of fungal infection in CF lung disease is increasingly recognized.
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Book chapters on the topic "Microbiology of Ps. aeruginosa"

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Anuj, Snehal, and David M. Whiley. "Pseudomonas aeruginosa." In PCR for Clinical Microbiology, 191–95. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_24.

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Gronthoud, Firza Alexander. "Pseudomonas aeruginosa." In Practical Clinical Microbiology and Infectious Diseases, 378–82. First edition. | Boca Raton : CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9781315194080-5-4.

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Coburn, J. "Pseudomonas aeruginosa Exoenzyme S." In Current Topics in Microbiology and Immunology, 133–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76966-5_7.

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Li, X., Y. Zhang, and E. Gulbins. "Lipid Rafts and Pseudomonas aeruginosa Infections." In Handbook of Hydrocarbon and Lipid Microbiology, 3179–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-77587-4_240.

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Tart, A. H., and D. J. Wozniak. "Shifting Paradigms in Pseudomonas aeruginosa Biofilm Research." In Current Topics in Microbiology and Immunology, 193–206. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-75418-3_9.

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Lory, S., and P. C. Tai. "Biochemical and Genetic Aspects of Pseudomonas Aeruginosa Virulence." In Current Topics in Microbiology and Immunology, 53–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70586-1_4.

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Wilson, B. A., and R. J. Collier. "Diphtheria Toxin and Pseudomonas aeruginosa Exotoxin A: Active-Site Structure and Enzymic Mechanism." In Current Topics in Microbiology and Immunology, 27–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76966-5_2.

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Wu, Weihui, Yongxin Jin, Fang Bai, and Shouguang Jin. "Pseudomonas aeruginosa." In Molecular Medical Microbiology, 753–67. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-397169-2.00041-x.

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SenGupta, Manideepa, and Mallika Sengupta. "Pseudomonas aeruginosa." In Practicals in Microbiology, 105. Jaypee Brothers Medical Publishers (P) Ltd., 2016. http://dx.doi.org/10.5005/jp/books/12695_25.

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Selvaraj, Logeswari. "Pseudomonas Aeruginosa." In Textbook of Microbiology for Paramedicals, 211. Jaypee Brothers Medical Publishers (P) Ltd., 2008. http://dx.doi.org/10.5005/jp/books/11041_28.

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Conference papers on the topic "Microbiology of Ps. aeruginosa"

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Yassunaka, Natália Norika, Camila Benedetti Penha, Alex Fiori da Silva, Patrícia Regina dos Santos, Katieli da Silva Souza, Camila Fabiano de Freitas, Noboru Hioka, Tania Ueda Nakamura, and Jane Martha Graton Mikcha. "Inativação Fotodinâmica de Pseudomonas Aeruginosa com Eritrosina e Seus Derivados." In XII Latin American Congress on Food Microbiology and Hygiene. São Paulo: Editora Edgard Blücher, 2014. http://dx.doi.org/10.5151/foodsci-microal-344.

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Ferenz, Mariane, Ângela De Lucca Fazzione, Karine Angélica Dalla Costa, Marina Leda Ribeiros, Sheila Mello da Silveira, and Alessandra Farias Millezi. "Ação Antimicrobiana de Óleos Essenciais Contra Staphylococcus Aureus e Pseudomonas Aeruginosa." In XII Latin American Congress on Food Microbiology and Hygiene. São Paulo: Editora Edgard Blücher, 2014. http://dx.doi.org/10.5151/foodsci-microal-284.

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Costa, Karine Angélica Dalla, Mariane Ferenz, Marina Leda Ribeiros, Sheila Melo da Silveira, and Alessandra Farias Millezi. "Determinação da Atividade Antibacteriana do Óleo Essencial de Cymbopogon Flexuosus Contra Staphylococcus Aureus e Pseudomonas Aeruginosa." In XII Latin American Congress on Food Microbiology and Hygiene. São Paulo: Editora Edgard Blücher, 2014. http://dx.doi.org/10.5151/foodsci-microal-281.

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Costa, Karine Angélica Dalla, Mariane Ferenz, Janaira Santana Nunes, Eduardo Alves, Sheila Mello da Silveira, and Alessandra Farias Millezi. "Formação de Biofilmes por Staphylococcus Aureus e Pseudomonas Aeruginosa em Diferentes Superfícies Utilizadas em Indústrias de Alimentos." In XII Latin American Congress on Food Microbiology and Hygiene. São Paulo: Editora Edgard Blücher, 2014. http://dx.doi.org/10.5151/foodsci-microal-007.

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Singh, Vaishali, Suman Ganger, and Shweta Patil. "CHARACTERIZATION OF <em>LACTOBACILLUS BREVIS</em> WITH POTENTIAL PROBIOTIC PROPERTIES AND BIOFILM INHIBITION AGAINST <em>PSEUDOMONAS AERUGINOSA</em>." In 1st International Electronic Conference on Microbiology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecm2020-07120.

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Ferreira, Jean Carlos Nunes, Marcos de Freitas, and Fernando Cavalcanti de Albuquerque. "Combined Cycle Power Plant Long Term Preservation Program: The Arauca´ria Power Station Study Case." In ASME Turbo Expo 2008: Power for Land, Sea, and Air. ASMEDC, 2008. http://dx.doi.org/10.1115/gt2008-50405.

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Arauca´ria Power Station, a 484 MW CCPP, is powered by two NG-fired Siemens 501FD2 Combustion Turbines and one Alstom DKZ2-2N34 Steam Turbine. Located in Southern Brazil, near Curitiba, the capital of the State of Parana´, Arauca´ria PS was tested and accepted in September 2002. Due to commercial issues, the plant remained shut down since its COD until 2006. Along four years, the O&M team developed and implemented a comprehensive plant preservation program aiming to keep the equipment safe from degradation. The purpose of this paper is to describe the program and the activities performed during this period. The OEM recommendations were strictly followed. All the operations, tests and inspections were performed according to the Long Term Standby Procedure. The preventive, predictive and corrective maintenance performed in conformity with the Plant Maintenance Manual. Such activities were controlled by means of the corporative Computer-based Operations Management System and the CMMS and always in compliance of the ES&H regulations. The wooden structured cooling tower was maintained wet, the circulating water system was kept in operation, the demineralised water treatment system was run monthly and water microbiology/chemistry control (including the chemicals dosing and weekly water analysis schedule) was kept in accordance with the program designed by GE Water & Process Technologies. In a totally outdoor plant, corrosion prevention is fundamental. For this reason, a painting program designed by LACTEC, a local institute of technology, was followed. By the Plant Valves Lubrication and Tests schedules, each manual and automatic valve was lubricated and tested. The two Aalborg HRSGs (including condensate and steam piping) were maintained at minimum 0.5 barg dry nitrogen atmosphere. Dehumidifiers and heaters were installed in both HRSGs gas side, so the ambient conditions between the CTGs air inlet and the HRSGs stack inlet were maintained with relative humidity below 40%. Similar system was provided for the Steam Turbine. Both systems were automatically controlled and supervised from the Plant Control Room. When Arauca´ria PS was re-commissioned in mid-2006, this strict program proved its effectiveness once no major problems were found and the plant start-up succeeded in a very short time. The plant was operated since June, 2007 through January, 2008 with an average availability in excess of 98%. The long-term preservation program is presently being reviewed and many improvements shall be implemented in order to achieve faster installation/removal of high performance preservation systems, so they shall be used for short-term shutdown periods as well.
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Reports on the topic "Microbiology of Ps. aeruginosa"

1

Avedovech, Richard. Nutritional requirements for protease production by Pseudomonas aeruginosa, Ps-1C. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.629.

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