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Articles de revues sur le sujet « Aeruginosa »

Auteur : Grafiati
Publié le 4 juin 2021
Mis à jour le 22 juin 2024

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1

Zhang, Shulin, Bo Zhang, Kezhi Xing, Xiumei Zhang, Xiuping Tian et Wei Dai. « Inhibitory effects of golden thread (Coptis chinensis) and berberine on Microcystis aeruginosa ». Water Science and Technology 61, no 3 (1 février 2010) : 763–69. http://dx.doi.org/10.2166/wst.2010.857.

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The effects of 40 Chinese herbs on Microcystis aeruginosa growth were monitored spectrophotometrically. Golden thread (Coptis chinensis) exhibited the best inhibitory effects. Cell density of M. aeruginosa decreased with the increasing concentrations of golden thread and the prolongation of exposure time. Decreases in protein content, carbohydrate content, and chlorophyll a content were observed in a golden thread concentration-dependent manner after 96 h exposure. Changes in cell density, protein content, carbohydrate content, and chlorophyll a content of M. aeruginosa exposed to berberine, the main component of golden thread, were also investigated. It was observed that berberine exhibited the same inhibitory effects on M. aeruginosa. The results suggested that golden thread could inhibit M. aeruginosas growth effectively, and berberine might be the main allelochemical implementing the inhibitory effects of golden thread.
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Gasink, Leanne B., Neil O. Fishman, Irving Nachamkin, Warren B. Bilker et Ebbing Lautenbach. « Risk Factors for and Impact of Infection or Colonization With Aztreonam-Resistant Pseudomonas aeruginosa ». Infection Control & ; Hospital Epidemiology 28, no 10 (octobre 2007) : 1175–80. http://dx.doi.org/10.1086/520740.

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Objective.To identify risk factors for infection or colonization with aztreonam-resistant Pseudomonas aeruginosa and examine the impact of this organism on mortality.Design.A case-control study was performed to identify risk factors for infection or colonization with aztreonam-resistant P. aeruginosa. A cohort study was subsequently performed to examine the impact of aztreonam resistance on outcomes.Setting.A tertiary referral center in southeastern Pennsylvania.Participants.Inpatients with a clinical culture positive for P. aeruginosa between January 1, 1999, and December 31, 2000.Results.Of 720 P. aeruginosa, isolates, 183 (25.4%) were aztreonam-resistant and 537 (74.6%) were aztreonam susceptible. In a multivariable model, prior fluoroquinolone use (adjusted odds ratio [aOR], 1.81 [95% confidence interval {CI}, 1.17-2.80]), prior use of an antianaerobic agent (aOR, 1.56 [95% CI, 1.06-2.29]), and renal insufficiency (aOR, 1.59 [95% CI, 1.10-2.29]) were associated with infection or colonization with aztreonam-resistant P. aeruginosa, while older age (aOR, 0.98 [95% CI, 0.97-0.99] per year of age) was negatively associated with infection or colonization with this organism. In-hospital mortality was higher among subjects infected or colonized with aztreonam-resistant P. aeruginosa, compared with those who were infected or colonized with aztreonam-susceptible P. aeruginos (25.7% vs 16.8%;P = .009), but in multivariable analysis, no significant association was found between infection or colonization with aztreonam-resistant P. aeruginosa and mortality.Conclusions.Curbing the use of fluoroquinolones and antimicrobials with antianaerobic activity may be an effective strategy to limit the emergence of aztreonam-resistant P. aeruginosa.
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Higgins, Gerard, Coral Fustero Torre, Jean Tyrrell, Paul McNally, Brian J. Harvey et Valerie Urbach. « Lipoxin A4prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa ». American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no 11 (1 juin 2016) : L1053—L1061. http://dx.doi.org/10.1152/ajplung.00368.2015.

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The specialized proresolution lipid mediator lipoxin A4(LXA4) is abnormally produced in cystic fibrosis (CF) airways. LXA4increases the CF airway surface liquid height and stimulates airway epithelial repair and tight junction formation. We report here a protective effect of LXA4(1 nM) against tight junction disruption caused by Pseudomonas aeruginosa bacterial challenge together with a delaying action against bacterial invasion in CF airway epithelial cells from patients with CF and immortalized cell lines. Bacterial invasion and tight junction integrity were measured by gentamicin exclusion assays and confocal fluorescence microscopy in non-CF (NuLi-1) and CF (CuFi-1) bronchial epithelial cell lines and in primary CF cultures, grown under an air/liquid interface, exposed to either a clinical or laboratory strains of P. aeruginosa. LXA4delayed P. aeruginosa invasion and transepithelial migration in CF and normal bronchial epithelial cell cultures. These protective effects of LXA4were inhibited by the ALX/FPR2 lipoxin receptor antagonist BOC-2. LXA4prevented the reduction in mRNA biosynthesis and protein abundance of the tight junction protein ZO-1 and reduced tight junction disruption induced by P. aeruginsosa inoculation. In conclusion, LXA4plays a protective role in bronchial epithelium by stimulating tight junction repair and by delaying and reducing the invasion of CF bronchial epithelial cells by P. aeruginsosa.
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Chakraborty, Tamalika, Tushar Gupta, Nayana Verma, Zarin Parwez, Kaustav Deb et Tamoghana Chakraborty. « PREVALENCE OF ANTIBIOTIC RESISTANCE IN PSEUDOMONAS AERUGINOSA ». International Journal of Advanced Research 12, no 01 (31 janvier 2024) : 1249–60. http://dx.doi.org/10.21474/ijar01/18243.

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One of the main bacteria responsible for hospital-acquired illnesses is Pseudomonas aeruginosa. Through chromosomal changes or the horizontal acquisition of resistant determinants, antibiotic resistance can be easily developed it. High-risk clones, like ST175, are spreading together with the rising frequency of extensively-drug-resistant (XDR) or multi-drug-resistant (MDR) P. aeruginosa isolates. MDR/XDR infections should be taken seriously since they can make it difficult to choose the best empirical and conclusive antimicrobial therapies. New avenues for the treatment of MDR/XDR P. aeruginosa infections have been opened by the introduction of powerful new antibiotics. Pseudomonas aeruginosa strains are known to withstand the majority of antibiotics by utilizing their high levels of intrinsic and acquired resistance mechanisms. Furthermore, recalcitrance and infection recurrence are caused by P. aeruginosas adaptive antibiotic resistance, a recently identified process that combines biofilm-mediated resistance and the development of multidrug-tolerant persister cells. There is a growing need for and interest in the research and development of alternative therapeutic approaches that offer fresh approaches to combat P. aeruginosa infections. Much recent research has documented various novel therapeutic methods that have proven pronouncedly effective in treating drug-resistant P. aeruginosa strains, but largely at the preclinical stages. This review focuses on the Prevalence of antibiotic resistance in Pseudomonas aeruginosaand also provides an overview of the characteristics of pseudomonas bacteria, various infections caused by them, the mechanism of antibiotic resistance, their clinical implications, Challenges in treatment, strategies for management and control, and future perspectives and research directions.
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Aidah Abd Al-doori, Awatef Saber Jasem et Adnan F. AL-Azzawie. « Effects of Nd:Yag Laser on some virulence factor genes of Pseudomonas aeruginosa bacteria ». Tikrit Journal of Pure Science 25, no 2 (17 mars 2020) : 86–92. http://dx.doi.org/10.25130/tjps.v25i2.240.

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The aim of this study was to assess effects of the 532nm Nd-yag laser on the genes of Tox A, Exo S, and Opr L, of Pseudomonas aeruginosa (P. aeruginosa) bacteria isolated from clinical (wounds, burns, otitis media) and environmental (water, soil) samples. Clinical samples were collected from patients coming to Saladdin General Hospital from wound, burns and middle ear infections while environmental samples were extracted from water and soil for Saladdin General Hospital . Bacterial samples irradiated by Nd-Yag laser with wavelength of 532 nm using energies (300mj,500mj) with (15 and 25 sec) and genomic DNA were extracted from all samples after the diagnosis of P. aeruginosa bacteria depending on the macroscopic and biochemical examination, then the PCR technique was performed. The results have shown an impact on P. aeruginosa bacteria of Nd-Yag laser by comparing PCR results of treated samples with control (unexposed) as loss of normal bands. This indicates that the laser had a genetic effect on the P. aeruginosa bacteria. We conclude that the laser induces genetic changes in P. aeruginosa's DNA so that lasers can be used in treatment and sterilization for clinical and environmental . The PCR technique could be used as a biomarker study to determine the biological effects of radiation on bacteria.
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Ishida, Lilian Konno, Katsuhisa Ikeda, Noriko Tanno, Tomonori Takasaka, Kiyo Nishioka et Yasuo Tanno. « Erythromycin Inhibits Adhesion of Pseudomonas Aeruginosa and Branhamella Catarrhalis to Human Nasal Epithelial Cells ». American Journal of Rhinology 9, no 1 (janvier 1995) : 53–56. http://dx.doi.org/10.2500/105065895781874097.

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Ciliated epithelial cells were obtained from nasal polyps. Bacterial adherence to these cells was compared for the ability to bind Hemophilus influenzae, Pseudomonas aeruginosa, and Branhamella catarrhalis in the presence of 10–5 M erythromycin, which was comparable with a physiologically attainable concentration in the nasal secretion and the maxillary sinus mucosa. Quantification of bacterial adherence showed the strongest ability of P. aeruginosa to the cells. Erythromycin has an inhibitory effect on adherence of P. aeruginose and B. catarrhalis to the nasal epithelial cell. Our findings suggest that the reduced adherence to the host cell is one of the underlying mechanisms to account for efficacy of erythromycin treatment in respiratory disorders.
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Al-doori1, Aidah Abd, Awatef Saber Jasem1 et Adnan F. AL-Azzawie2. « Effects of Nd:Yag Laser on some virulence factor genes of Pseudomonas aeruginosa bacteria ». Tikrit Journal of Pure Science 25, no 2 (17 mars 2020) : 86. http://dx.doi.org/10.25130/j.v25i2.962.

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The aim of this study was to assess effects of the 532nm Nd-yag laser on the genes of Tox A, Exo S, and Opr L, of Pseudomonas aeruginosa (P. aeruginosa) bacteria isolated from clinical (wounds, burns, otitis media) and environmental (water, soil) samples. Clinical samples were collected from patients coming to Saladdin General Hospital from wound, burns and middle ear infections while environmental samples were extracted from water and soil for Saladdin General Hospital . Bacterial samples irradiated by Nd-Yag laser with wavelength of 532 nm using energies (300mj,500mj) with (15 and 25 sec) and genomic DNA were extracted from all samples after the diagnosis of P. aeruginosa bacteria depending on the macroscopic and biochemical examination, then the PCR technique was performed. The results have shown an impact on P. aeruginosa bacteria of Nd-Yag laser by comparing PCR results of treated samples with control (unexposed) as loss of normal bands. This indicates that the laser had a genetic effect on the P. aeruginosa bacteria. We conclude that the laser induces genetic changes in P. aeruginosa's DNA so that lasers can be used in treatment and sterilization for clinical and environmental . The PCR technique could be used as a biomarker study to determine the biological effects of radiation on bacteria. http://dx.doi.org/10.25130/tjps.25.2020.034
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8

Young, Heather, Bryan Knepper, Whitney Hernandez, Asaf Shor, Merribeth Bruntz, Chrystal Berg et Connie S. Price. « Pseudomonas aeruginosa ». Journal of the American Podiatric Medical Association 105, no 2 (1 mars 2015) : 125–29. http://dx.doi.org/10.7547/0003-0538-105.2.125.

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Background Pseudomonas aeruginosa has traditionally been considered a common pathogen in diabetic foot infection (DFI), yet the 2012 Infectious Diseases Society of America guideline for DFI states that “empiric therapy directed at P aeruginosa is usually unnecessary.” The objective of this study was to evaluate the frequency of P aeruginosa isolated from bone or tissue cultures from patients with DFI. Methods This study is a cross-sectional survey of diabetic patients presenting with a foot infection to an urban county hospital between July 1, 2012, and December 31, 2013. All of the patients had at least one debridement procedure during which tissue or bone cultures from operative or bedside debridements were obtained. The χ2 test and the t test of means were used to determine relationships between variables and the frequency of P aeruginosa in culture. Results The median number of bacteria isolated from DFI was two. Streptococcus spp and Staphylococcus aureus were the most commonly isolated organisms; P aeruginosa was isolated in only five of 112 patients (4.5%). The presence of P aeruginosa was not associated with the patient's age, glycosylated hemoglobin level, tobacco abuse, the presence of osteomyelitis, a prescription for antibiotic drugs in the preceding 3 months, or the type of operative procedure. Conclusions Pseudomonas aeruginosa was an infrequent isolate from DFI in this urban, underserved diabetic population. The presence of P aeruginosa was not associated with any measured risk factors. By introducing a clinical practice guideline, we hope to discourage frontline providers from using routine antipseudomonal antibiotic drugs for DFI.
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Weinberg, M. « Pseudomonas aeruginosa ». Kazan medical journal 20, no 5 (11 août 2021) : 551. http://dx.doi.org/10.17816/kazmj76617.

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Pennington, James E. « Pseudomonas aeruginosa ». Infectious Disease Clinics of North America 4, no 2 (juin 1990) : 259–70. http://dx.doi.org/10.1016/s0891-5520(20)30340-8.

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Hauser, Alan R. « Pseudomonas aeruginosa ». American Journal of Respiratory and Critical Care Medicine 178, no 5 (septembre 2008) : 438–39. http://dx.doi.org/10.1164/rccm.200805-789ed.

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Wright, Gordon L. T. « Pseudomonas aeruginosa ». Medical Journal of Australia 158, no 3 (février 1993) : 214. http://dx.doi.org/10.5694/j.1326-5377.1993.tb121719.x.

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13

Chen, Xi, Benjamin S. Bleier, Daniel R. Lefebvre et Nahyoung Grace Lee. « Pseudomonas Aeruginosa ». Ophthalmic Plastic and Reconstructive Surgery 32, no 5 (2016) : 374–77. http://dx.doi.org/10.1097/iop.0000000000000558.

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SHEFF, BARBARA. « Pseudomonas aeruginosa ». Nursing 30, no 5 (mai 2000) : 79. http://dx.doi.org/10.1097/00152193-200030050-00047.

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Cornaglia, G. « Pseudomonas aeruginosa ». International Journal of Infectious Diseases 14 (mars 2010) : e24. http://dx.doi.org/10.1016/j.ijid.2010.02.1541.

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Fahmi, Aliyah, Sumaryati Syukur, Zulkarnain Chaidir et Sri Melia. « GREEN TEA ETHANOL EXTRACT EFFICACY AGAINST PSEUDOMONAS AERUGINOSA ». BIOLINK (Jurnal Biologi Lingkungan Industri Kesehatan) 9, no 1 (19 août 2022) : 26–32. http://dx.doi.org/10.31289/biolink.v9i1.7336.

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Research about green tea ethanol extract efficacy against Pseudomonas aeruginosa has been done. The green tea leaves were sourced from tea distributor in Sidamanik District, North Sumatra, Indonesia. Green tea leaves extract was obtained by maceration technique in which green tea leaves were soaked with ethanol 96% for 24 hours. After that, the filtrate was concentrated to be thick extract with no liquid content again. After that, the concentrated extract was made by 5%, 10% and 15% as extract variations. The efficacy of green tea ethanol extract against Pseudomonas aeruginosa was signed by increasing the inhibitory diameter that using disc method, in which the distilled water was used as negative blank. The results obtained for blanks, 5%, 10% and 15% extracts were 0; 1.85; 2.9 and 4.45 mm. The conclusion of this study is that the concentration of the extract is increasing proportionally to its inhibitory power, the higher of extract concentration is higher of its inhibitory activity against Pseudomonas aeruginosa. The conclusion described the green tea ethanol extract was effective to be antibacterial agent against Pseudomonas aeruginosa.
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Al-Hashimi, Omar, Ibrahim Omar Saeed et Safaa Abed Lateef Al Meani. « Evaluating the qualitative characteristics and heavy elements of hospital water and their relationship with bioresistance in P. aeruginosa. » Technium BioChemMed 8 (1 mai 2024) : 64–75. http://dx.doi.org/10.47577/biochemmed.v8i.10934.

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ABSTRACT: Bacteria use the elements present in the environment to develop their vital defenses, trying to acquire genes from other strains or absorb heavy metals in order to adapt to them and increase their tolerance against high concentrations of heavy elements. Pseudomonas aeruginosa is an opportunistic bacterial pathogen that causes infections in hospitals and communities, including in humans and animals. P. aeruginosa's adaptability and endurance in therapeutic settings are cause for concern. Emerging pathogenic strains pose a global threat and cause significant concern. Biocides are commonly used to control the spread of resistant strains of P. aeruginosa. However, tolerance to these biocides has been reported, which hinders their effectiveness in clinical settings. This study focused on the factors contributing to the persistence of hospital-acquired P. aeruginosa, including its resistance to antibiotics and biocides and the role of heavy metals in the development of increased bacterial resistance to antimicrobials.
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Oberhardt, Matthew A., Jacek Puchałka, Kimberly E. Fryer, Vítor A. P. Martins dos Santos et Jason A. Papin. « Genome-Scale Metabolic Network Analysis of the Opportunistic Pathogen Pseudomonas aeruginosa PAO1 ». Journal of Bacteriology 190, no 8 (11 janvier 2008) : 2790–803. http://dx.doi.org/10.1128/jb.01583-07.

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ABSTRACT Pseudomonas aeruginosa is a major life-threatening opportunistic pathogen that commonly infects immunocompromised patients. This bacterium owes its success as a pathogen largely to its metabolic versatility and flexibility. A thorough understanding of P. aeruginosa's metabolism is thus pivotal for the design of effective intervention strategies. Here we aim to provide, through systems analysis, a basis for the characterization of the genome-scale properties of this pathogen's versatile metabolic network. To this end, we reconstructed a genome-scale metabolic network of Pseudomonas aeruginosa PAO1. This reconstruction accounts for 1,056 genes (19% of the genome), 1,030 proteins, and 883 reactions. Flux balance analysis was used to identify key features of P. aeruginosa metabolism, such as growth yield, under defined conditions and with defined knowledge gaps within the network. BIOLOG substrate oxidation data were used in model expansion, and a genome-scale transposon knockout set was compared against in silico knockout predictions to validate the model. Ultimately, this genome-scale model provides a basic modeling framework with which to explore the metabolism of P. aeruginosa in the context of its environmental and genetic constraints, thereby contributing to a more thorough understanding of the genotype-phenotype relationships in this resourceful and dangerous pathogen.
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Davane, Milind. « Pseudomonas aeruginosa from hospital environment ». Journal of Microbiology and Infectious Diseases 4, no 1 (1 mars 2014) : 42–43. http://dx.doi.org/10.5799/ahinjs.02.2014.01.0124.

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Balko, O. I., O. B. Balko et L. V. Avdeeva. « Thermoactivation of Pseudomonas aeruginosa Pyocins ». Mikrobiolohichnyi Zhurnal 81, no 5 (30 septembre 2019) : 85–97. http://dx.doi.org/10.15407/microbiolj81.05.085.

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De Muynck, Benedicte, Anke Van Herck, Annelore Sacreas, Tobias Heigl, Janne Kaes, Arno Vanstapel, Stijn E. Verleden et al. « Successful Pseudomonas aeruginosa eradication improves outcomes after lung transplantation : a retrospective cohort analysis ». European Respiratory Journal 56, no 4 (29 mai 2020) : 2001720. http://dx.doi.org/10.1183/13993003.01720-2020.

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Long-term survival after lung transplantation (LTx) is hampered by development of chronic lung allograft dysfunction (CLAD). Pseudomonas aeruginosa is an established risk factor for CLAD. Therefore, we investigated the effect of P. aeruginosa eradication on CLAD-free and graft survival.Patients who underwent first LTx between July, 1991, and February, 2016, and were free from CLAD, were retrospectively classified according to P. aeruginosa presence in respiratory samples between September, 2011, and September, 2016. P. aeruginosa-positive patients were subsequently stratified according to success of P. aeruginosa eradication following targeted antibiotic treatment. CLAD-free and graft survival were compared between P. aeruginosa-positive and P. aeruginosa-negative patients; and between patients with or without successful P. aeruginosa eradication. In addition, pulmonary function was assessed during the first year following P. aeruginosa isolation in both groups.CLAD-free survival of P. aeruginosa-negative patients (n=443) was longer compared with P. aeruginosa-positive patients (n=95) (p=0.045). Graft survival of P. aeruginosa-negative patients (n=443, 82%) was better compared with P. aeruginosa-positive patients (n=95, 18%) (p<0.0001). Similarly, P. aeruginosa-eradicated patients demonstrated longer CLAD-free and graft survival compared with patients with persistent P. aeruginosa. Pulmonary function was higher in successfully P. aeruginosa-eradicated patients compared with unsuccessfully eradicated patients (p=0.035).P. aeruginosa eradication after LTx improves CLAD-free and graft survival and maintains pulmonary function. Therefore, early P. aeruginosa detection and eradication should be pursued.
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Harrigan, James, Ebbing Lautenbach, Emily Reesey, Magda Wernovsky, Pam Tolomeo, Zygmunt Morawski, Jerry Jacob, Michael Grippi et Brendan Kelly. « Impact of Diagnosed and Undiagnosed Respiratory Pseudomonas on VAP and VAE During Long-Term Acute Care ». Infection Control & ; Hospital Epidemiology 41, S1 (octobre 2020) : s258—s259. http://dx.doi.org/10.1017/ice.2020.823.

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Background: Clinically diagnosed ventilator-associated pneumonia (VAP) is common in the long-term acute-care hospital (LTACH) setting and may contribute to adverse ventilator-associated events (VAEs). Pseudomonas aeruginosa is a common causative organism of VAP. We evaluated the impact of respiratory P. aeruginosa colonization and bacterial community dominance, both diagnosed and undiagnosed, on subsequent P. aeruginosa VAP and VAE events during long-term acute care. Methods: We enrolled 83 patients on LTACH admission for ventilator weaning, performed longitudinal sampling of endotracheal aspirates followed by 16S rRNA gene sequencing (Illumina HiSeq), and bacterial community profiling (QIIME2). Statistical analysis was performed with R and Stan; mixed-effects models were fit to relate the abundance of respiratory Psa on admission to clinically diagnosed VAP and VAE events. Results: Of the 83 patients included, 12 were diagnosed with P. aeruginosa pneumonia during the 14 days prior to LTACH admission (known P. aeruginosa), and 22 additional patients received anti–P. aeruginosa antibiotics within 48 hours of admission (suspected P. aeruginosa); 49 patients had no known or suspected P. aeruginosa (unknown P. aeruginosa). Among the known P. aeruginosa group, all 12 patients had P. aeruginosa detectable by 16S sequencing, with elevated admission P. aeruginosa proportional abundance (median, 0.97; IQR, 0.33–1). Among the suspected P. aeruginosa group, all 22 patients had P. aeruginosa detectable by 16S sequencing, with a wide range of admission P. aeruginosa proportional abundance (median, 0.0088; IQR, 0.00012–0.31). Of the 49 patients in the unknown group, 47 also had detectable respiratory Psa, and many had high P. aeruginosa proportional abundance at admission (median, 0.014; IQR, 0.00025–0.52). Incident P. aeruginosa VAP was observed within 30 days in 4 of the known P. aeruginosa patients (33.3%), 5 of the suspected P. aeruginosa patients (22.7%), and 8 of the unknown P. aeruginosa patients (16.3%). VAE was observed within 30 days in 1 of the known P. aeruginosa patients (8.3%), 2 of the suspected P. aeruginosa patients (9.1%), and 1 of the unknown P. aeruginosa patients (2%). Admission P. aeruginosa abundance was positively associated with VAP and VAE risk in all groups, but the association only achieved statistical significance in the unknown group (type S error <0.002 for 30-day VAP and <0.011 for 30-day VAE). Conclusions: We identified a high prevalence of unrecognized respiratory P. aeruginosa colonization among patients admitted to LTACH for weaning from mechanical ventilation. The admission P. aeruginosa proportional abundance was strongly associated with increased risk of incident P. aeruginosa VAP among these patients.Funding: NoneDisclosures: None
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Worgall, Stefan, Toshiaki Kikuchi, Ravi Singh, Katherine Martushova, Leah Lande et Ronald G. Crystal. « Protection against Pulmonary Infection with Pseudomonas aeruginosa following Immunization with P. aeruginosa-Pulsed Dendritic Cells ». Infection and Immunity 69, no 7 (1 juillet 2001) : 4521–27. http://dx.doi.org/10.1128/iai.69.7.4521-4527.2001.

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ABSTRACT To develop a Pseudomonas aeruginosa vaccine that allows the host immune system to select the antigens, we hypothesized that dendritic cells (DC) pulsed with P. aeruginosa would induce protective immunity against pulmonary infections with P. aeruginosa. Incubation of murine bone marrow-derived DC with P. aeruginosa in vitro led to uptake of P. aeruginosa and activation of the DC. Spleen-derived CD4+ cells from mice immunized withP. aeruginosa-pulsed DC showed increased proliferation, demonstrating that DC pulsed with P. aeruginosa were capable of eliciting a P. aeruginosa-specific immune response. To evaluate if P. aeruginosa-pulsed DC can induce protective immunity against P. aeruginosapulmonary infection, DC incubated with P. aeruginosa in vitro were administered systemically to syngeneic mice, and the mice were then challenged by intrapulmonary infection with P. aeruginosa (5 × 104 CFU/mouse) 13 days later. Unimmunized control mice and mice who had previously received naive DC or DC stimulated with lipopolysaccharide or Escherichia coli died within 72 h. In contrast, 45% of mice receivingP. aeruginosa-pulsed DC demonstrated prolonged survival (>14 days). Finally, DC-pulsed with heat-inactivated P. aeruginosa protected CD8−/− but not CD4−/− mice, demonstrating that CD4+ T cells were required for the DC pulsed with P. aeruginosa to induce protective immunity.
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Fujita, Jiro. « 3. Pseudomonas Aeruginosa ». Nihon Naika Gakkai Zasshi 97, no 11 (2008) : 2678–86. http://dx.doi.org/10.2169/naika.97.2678.

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Moore, Nicholas M., et Maribeth L. Flaws. « Introduction : Pseudomonas aeruginosa ». American Society for Clinical Laboratory Science 24, no 1 (janvier 2011) : 41–42. http://dx.doi.org/10.29074/ascls.24.1.41.

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Thi, Minh Tam Tran, David Wibowo et Bernd H. A. Rehm. « Pseudomonas aeruginosa Biofilms ». International Journal of Molecular Sciences 21, no 22 (17 novembre 2020) : 8671. http://dx.doi.org/10.3390/ijms21228671.

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Pseudomonas aeruginosa is an opportunistic human pathogen causing devastating acute and chronic infections in individuals with compromised immune systems. Its highly notorious persistence in clinical settings is attributed to its ability to form antibiotic-resistant biofilms. Biofilm is an architecture built mostly by autogenic extracellular polymeric substances which function as a scaffold to encase the bacteria together on surfaces, and to protect them from environmental stresses, impedes phagocytosis and thereby conferring the capacity for colonization and long-term persistence. Here we review the current knowledge on P. aeruginosa biofilms, its development stages, and molecular mechanisms of invasion and persistence conferred by biofilms. Explosive cell lysis within bacterial biofilm to produce essential communal materials, and interspecies biofilms of P. aeruginosa and commensal Streptococcus which impedes P. aeruginosa virulence and possibly improves disease conditions will also be discussed. Recent research on diagnostics of P. aeruginosa infections will be investigated. Finally, therapeutic strategies for the treatment of P. aeruginosa biofilms along with their advantages and limitations will be compiled.
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Stratton, Charles W. « Pseudomonas aeruginosa Revisited ». Infection Control and Hospital Epidemiology 11, no 2 (février 1990) : 101–4. http://dx.doi.org/10.2307/30144269.

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Akhabue, Ehimare, Marie Synnestvedt, Mark G. Weiner, Warren B. Bilker et Ebbing Lautenbach. « Cefepime-ResistantPseudomonas aeruginosa ». Emerging Infectious Diseases 17, no 6 (juin 2011) : 1037–43. http://dx.doi.org/10.3201/eid1706.100358.

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Garau, Javier, et Lucia Gomez. « Pseudomonas aeruginosa pneumonia ». Current Opinion in Infectious Diseases 16, no 2 (avril 2003) : 135–43. http://dx.doi.org/10.1097/00001432-200304000-00010.

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Sirat, Hasnah, Shajarhtunnur Jamil et Ahmad Rahman. « Sesquiterpenes fromCurcuma aeruginosa ». Planta Medica 64, no 06 (août 1998) : 584–85. http://dx.doi.org/10.1055/s-2006-957525.

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Chen, Sharon C. A., Richard H. Lawrence, Karen Byth et Tania C. Sorrell. « Pseudomonas aeruginosa bacteraemia ». Medical Journal of Australia 159, no 9 (novembre 1993) : 592–97. http://dx.doi.org/10.5694/j.1326-5377.1993.tb138046.x.

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Stratton, Charles W. « Pseudomonas aeruginosa Revisited ». Infection Control and Hospital Epidemiology 11, no 2 (février 1990) : 101–4. http://dx.doi.org/10.1086/646129.

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Barbier, François, et Michel Wolff. « Multirésistance chezPseudomonas aeruginosa ». médecine/sciences 26, no 11 (novembre 2010) : 960–68. http://dx.doi.org/10.1051/medsci/20102611960.

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Lin, Ming-Feng, et Yung-Liang Chen. « Pseudomonas aeruginosa Bacteremia ». Infectious Diseases in Clinical Practice 14, no 3 (mai 2006) : 150–53. http://dx.doi.org/10.1097/01.idc.0000202257.34917.a2.

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Akhabue, Ehimare, Marie Synnestvedt, Mark G. Weiner, Warren B. Bilker et Ebbing Lautenbach. « Cefepime-ResistantPseudomonas aeruginosa ». Emerging Infectious Diseases 17, no 6 (juin 2011) : 1037–43. http://dx.doi.org/10.3201/eid/1706.100358.

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Kipnis, Eric, et Karine Faure. « Pseudomonas aeruginosa bacteremia ». Critical Care Medicine 40, no 4 (avril 2012) : 1354–55. http://dx.doi.org/10.1097/ccm.0b013e31823c8b55.

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Pennington, J. E. « Pseudomonas aeruginosa immunotherapy ». European Journal of Clinical Microbiology & ; Infectious Diseases 9, no 6 (juin 1990) : 377–80. http://dx.doi.org/10.1007/bf01979465.

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Sheppard, M. « Pseudomonas aeruginosa endocarditis ». Journal of Hospital Infection 19, no 4 (décembre 1991) : 283. http://dx.doi.org/10.1016/0195-6701(91)90246-5.

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Buchanan, E. B., et S. D. Kominos. « Pseudomonas aeruginosa mastitis ». Clinical Microbiology Newsletter 12, no 8 (avril 1990) : 63–64. http://dx.doi.org/10.1016/0196-4399(90)90011-y.

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Kaye, Keith S., Zeina A. Kanafani, Ashley E. Dodds, John J. Engemann, Stephen G. Weber et Yehuda Carmeli. « Differential Effects of Levofloxacin and Ciprofloxacin on the Risk for Isolation of Quinolone-Resistant Pseudomonas aeruginosa ». Antimicrobial Agents and Chemotherapy 50, no 6 (juin 2006) : 2192–96. http://dx.doi.org/10.1128/aac.00060-06.

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ABSTRACT Due to the greater in vitro activity of ciprofloxacin than that of levofloxacin against Pseudomonas aeruginosa, the likelihood of isolating a clinical strain of quinolone-resistant (QR) P. aeruginosa might be greater after exposure to levofloxacin than ciprofloxacin. We examined the risk of isolating QR P. aeruginosa in association with prior levofloxacin or ciprofloxacin exposure. A case-case-control study was conducted. Two groups of cases, one with nosocomial QR P. aeruginosa infections and one with nosocomial quinolone-susceptible (QS) P. aeruginosa infections, were compared to a control group of hospitalized patients without P. aeruginosa infections. Bivariable and multivariable analyses were used to determine risk factors for isolation of QR P. aeruginosa and QS P. aeruginosa. One hundred seventeen QR P. aeruginosa and 255 QS P. aeruginosa cases were identified, and 739 controls were selected. Exposures to ciprofloxacin were similar among all three groups (8% for controls, 9.4% for QR P. aeruginosa cases, and 7.5% for QS P. aeruginosa cases; P ≥ 0.6). Levofloxacin use was more frequent in the QR P. aeruginosa cases than in the controls (35.9% and 22.1%, respectively; odds ratio [OR] = 2.0; 95% confidence interval [CI] = 1.3 to 3.0) and less frequent in QS P. aeruginosa cases (14.1% of QS P. aeruginosa cases; OR = 0.6; 95% CI = 0.4 to 0.9). In multivariable analysis, levofloxacin, but not ciprofloxacin, was a significant risk factor for isolation of QR P. aeruginosa (OR for levofloxacin = 1.7 [95% CI = 1.0 to 2.9]; OR for ciprofloxacin = 1.2 [95% CI = 0.6 to 2.5]). Levofloxacin was associated with a reduced risk of isolation of QS P. aeruginosa (OR = 0.6; 95% CI = 0.4 to 0.9), whereas ciprofloxacin had no significant effect (OR = 1.0; 95% CI = 0.6 to 1.8). In conclusion, the use of levofloxacin, but not ciprofloxacin, was associated with isolation of QR P. aeruginosa.
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Daróczy, Judit. « Erosio interdigitalis caused by Pseudomonas aeruginosa ». Bőrgyógyászati és Venerológiai Szemle 95, no 5 (5 novembre 2019) : 232–35. http://dx.doi.org/10.7188/bvsz.2019.95.5.6.

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Mikucionyte, Greta, Asta Dambrauskiene, Erika Skrodeniene et Astra Vitkauskiene. « Biofilm formation and serum susceptibility in Pseudomonas aeruginosa ». Open Medicine 9, no 2 (1 avril 2014) : 187–92. http://dx.doi.org/10.2478/s11536-013-0241-y.

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AbstractPseudomonas aeruginosa (P. aeruginosa) is one of the most important opportunistic pathogens. The pathogenicity of P. aeruginosa has been associated with multiple bacterial virulence factors. The aim of this study was to evaluate the association between P. aeruginosa strains obtained from various clinical samples and resistance to antibiotics and pathogenicity factors, such as resistance to serum bactericidal activity and biofilm formation. This study included 121 P. aeruginosa strains isolated from clinical samples; 65 of the isolated P. aeruginosa strains were carbapenem-resistant, and 56 were carbapenem-sensitive. Carbapenem-resistant P. aeruginosa strains were more often resistant to the majority of tested antibiotics, compared to carbapenem-sensitive strains. We did not find any statistically significant difference between resistance to carbapenems and serum resistance and ability of tested P. aeruginosa strains to produce biofilms. Carbapenem-resistant P. aeruginosa strains were recovered from the urinary tract significantly more often (75.0%) than carbapenem-sensitive P. aeruginosa strains (25.0%). Carbapenem-sensitive P. aeruginosa strains were recovered significantly more often from the respiratory tract than carbapenem-resistant strains, 60.0% and 40.0%, respectively. All the P. aeruginosa strains recovered from blood were serum-resistant. P. aeruginosa strains recovered from the respiratory tract and wounds were significantly frequently serum sensitive, 95.6% and 56.6%, respectively. We did not find any differences in biofilm production among the P. aeruginosa strains recovered from different sources.
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Pan, Chieh-Yu, Jian-Chyi Chen, Jenn-Feng Sheen, Tai-Lang Lin et Jyh-Yih Chen. « Epinecidin-1 Has Immunomodulatory Effects, Facilitating Its Therapeutic Use in a Mouse Model of Pseudomonas aeruginosa Sepsis ». Antimicrobial Agents and Chemotherapy 58, no 8 (12 mai 2014) : 4264–74. http://dx.doi.org/10.1128/aac.02958-14.

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ABSTRACTAntimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against a multidrug-resistant clinical isolate ofP. aeruginosa(P. aeruginosaR) and aP. aeruginosastrain from ATCC (P. aeruginosaATCC 19660)in vivo. The MICs of epinecidin-1 againstP. aeruginosaR andP. aeruginosaATCC 19660 were determined and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused byP. aeruginosaR orP. aeruginosaATCC 19660 in mouse models, without inducing adverse behavioral effects or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the rate of survival of mice infected with the bacterial pathogenP. aeruginosathrough both antimicrobial and immunomodulatory effects.
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Paliy, G. K., О. А. Nazarchuk, V. І. Nagaychuk, І. М. Vovk et G. G. Nazarchuk. « ОБГРУНТУВАННЯ ДОЦІЛЬНОСТІ ЗАСТОСУВАННЯ ДЕКАМЕТОКСИНУ ПРИ АНТИБІОТИКО– ТА ФАГОРЕЗИСТЕНТНОСТІ ПСЕВДОМОНАДНОЇ ХІРУРГІЧНОЇ ІНФЕКЦІЇ ». Klinicheskaia khirurgiia, no 9 (29 juillet 2017) : 64. http://dx.doi.org/10.26779/2522-1396.2017.09.64.

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Вступ. Pseudomonas aeruginosa (P. aeruginosa) є провідним збудником інфекційних ускладнень у пацієнтів комбустіологічних віддалень. Мета. Обгрунтувати доцільність використання декаметоксину (ДМ) при резистентності P. aeruginosa до цефалоспоринів. Матеріали і методи. Вивчено ефективність використання ДМ в подоланні резистентності P. aeruginosa до цефалоспоринів,псевдомонадного бактеріофагу на 50 клінічних штамах, виділених у постраждалих з опіками. Результати. Встановлено, що штами P. aeruginosa, що спричиняли інфекційні ускладнення у постраждалих з опіками, мали виражену резистентність до цефтазидиму (у 80% спостережень), цефепіму (у 80%), цефоперазону/сульбактаму (у 68%). Визначено ефективну бактерицидну дію ДМ на 66% штамів P. aeruginosa , мінімальна бактерицидна концентрація (МБцК) становила у середньому (106,1 ± 5,6) мкг/мл. Обговорення. Чутливість P. aeruginosa до бактеріофагу та цефалоспоринів підвищувалася в присутності ДМ у суббактеріостатичній концентрації (СК). Висновки. Резистентні до цефалоспоринів штами P. aeruginosa не мали перехресної стійкості до ДМ, бактеріофагу. Застосування антисептика ДМ у СК підвищувало чутливість P. aeruginosa до цефалоспоринів в 7 – 8,5 разу; покращувало чутливість помірно стійких фаголізабельних культур P. aeruginosa до бактеріофагу.
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Murad, Khairiyah, Sharaniza Ab-Rahim et Hassanain Al-Talib. « Antimicrobial effect of Tetraspanin CD9 Peptides on Pseudomonas aeruginosa ». Journal of Pure and Applied Microbiology 17, no 3 (1 septembre 2023) : 1764–75. http://dx.doi.org/10.22207/jpam.17.3.41.

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It is critical to find an alternative therapeutic approach to combat Pseudomonas aeruginosa (P. aeruginosa) that can simultaneously reduce the occurrence of bacterial resistance. The tetraspanin CD9, a highly expressed membrane protein in melanocytes was chosen for this study because it is highly expressed in keratinocytes and has been implicated in the pathogenesis of bacterial infections in a previous study. The antimicrobial activity of CD9 peptides against the standard strain P. aeruginosa (ATCC 27853) and a clinical multidrug-resistant P. aeruginosa (MDR- P. aeruginosa) was studied using the disc diffusion method. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of CD9 peptides were determined by broth microdilution assays with concentrations ranging from 1 mg/mL to 4.88×10-4 mg/mL. The antibiofilm activity of the CD9 peptides was also determined. CD9 peptides showed an 11.75 ± 2.36 mm inhibition zone against the standard P. aeruginosa strain but none against the MDR- P. aeruginosa. Both isolates had the same MIC value, 0.25 mg/mL. The MBC for the standard strain P. aeruginosa was 0.5 mg/mL, while for the MDR- P. aeruginosa strain, it was 1 mg/mL. CD9 peptides significantly inhibited up to 70% biofilm against both P. aeruginosa isolates. CD9 peptides showed a modest inhibitory effect against the standard strain P. aeruginosa but not against MDR- P. aeruginosa. Interestingly, CD9 peptides were found to be a good anti-biofilm treatment against both P. aeruginosa isolates. This study demonstrated that CD9 peptides have the potential to be an alternative antimicrobial treatment against P. aeruginosa.
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Chaudhary, Jitendra Kumar. « A Clinical-Bacteriological Profile of Multidrug Resistant Pseudomonas aeruginosa at Tertiary Care Hospital Shahjahanpur, Uttar Pradesh ». International Journal of Current Microbiology and Applied Sciences 10, no 9 (10 septembre 2021) : 301–13. http://dx.doi.org/10.20546/ijcmas.2021.1009.035.

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The Pseudomonas aeruginosa is predominant agent causing nosocomial infections. In recent time, it develops resistance continuously to the antibiotics becomes Multidrug-resistant P. aeruginosa. So, in cystic fibrosis patents it difficult to eradicate P. aeruginosa infections with antimicrobial treatment. Therefore, focus on alternative mechanisms for treating P. aeruginosa infections. On the basis of growth, morphological and biochemical characteristics, P. aeruginosa strains were isolated from the clinical samples in this work. After that the antibiotic sensitivity was performed and the Multidrug resistant Pseudomonas aeruginosa was identified according to CLSI standard guideline chart by measuring the zone of inhibition for P. aeruginosa. The isolated strains showed resistance against three or more antibiotics, considered as MDR Pseudomonas aeruginosa. By antibiogram pattern 51 showed Multi drug resistant strains out of 102 isolated strains. As P. aeruginosa abide to develop resistance to the antibiotics, the quorum sensing increased transcriptional regulator QscR might performs another target. Thus the prevalence of MDR strains of Pseudomonas aeruginosa was investigated on current study. The antibiogram pattern revealed 51 MDR strains of P. aeruginosa. In which the majority of strains exhibited resistance towards Piperacillin (98%), Ciprofloxacin (90%), Ofloxacin (90%), Levofloxacin (80%) and Tobramycin (60%).
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Ikarashi, Kei, Ryo Kutsuna, Junko Tomida, Yoshiaki Kawamura et Yuji Morita. « Overexpression of the MexXY Multidrug Efflux System Correlates with Deficient Pyoverdine Production in Pseudomonas aeruginosa ». Antibiotics 10, no 6 (31 mai 2021) : 658. http://dx.doi.org/10.3390/antibiotics10060658.

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Multidrug-resistant Pseudomonas aeruginosa poses a serious problem due to hospital- and healthcare-associated infections. A major drug resistance mechanism of P. aeruginosa involves active efflux via resistance nodulation cell division (RND)-type multidrug efflux pumps of which MexXY is increasingly recognized as a primary determinant of aminoglycoside resistance in P. aeruginosa. MexXY overexpression is often observed in drug-resistant P. aeruginosa clinical isolates. MexXY deficiency increased pyoverdine production in all four P. aeruginosa strains we tested. MexXY-overproducing multidrug-resistant P. aeruginosa PA7 exhibited the greatest effect among the strains. Complementation with a MexXY-expressing plasmid restored low-level pyoverdine production in a MexXY-deficient P. aeruginosa mutant from PA7, indicating that MexXY expression decreases pyoverdine production. Because P. aeruginosa produces pyoverdine to acquire iron, MexXY-deficient mutants might be more susceptible to iron deficiency than MexXY-producing strains or might require extra iron. High-risk clones of multidrug-resistant P. aeruginosa reportedly tend to be MexXY overproducers but defective pyoverdine producers. This study suggests that P. aeruginosa reduces production of a virulence factor after acquiring a drug resistance factor.
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Balko, O. B. « Low Molecular Weight Pseudomonas aeruginosa Bacteriocins ». Mikrobiolohichnyi Zhurnal 81, no 6 (30 novembre 2019) : 97–109. http://dx.doi.org/10.15407/microbiolj81.06.097.

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Gonzaga, Zennia Jean C., Christina Merakou, Antonio DiGiandomenico, Gregory P. Priebe et Bernd H. A. Rehm. « A Pseudomonas aeruginosa-Derived Particulate Vaccine Protects against P. aeruginosa Infection ». Vaccines 9, no 7 (20 juillet 2021) : 803. http://dx.doi.org/10.3390/vaccines9070803.

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Despite numerous efforts to develop an effective vaccine against Pseudomonas aeruginosa, no vaccine has yet been approved for human use. This study investigates the utility of the P. aeruginosa inherently produced polyhydroxyalkanaote (PHA) inclusions and associated host–cell proteins (HCP) as a particulate vaccine platform. We further engineered PHA inclusions to display epitopes derived from the outer membrane proteins OprF/OprI/AlgE (Ag) or the type III secretion system translocator PopB. PHA and engineered PHA beads induced antigen-specific humoral, cell-mediated immune responses, anti-HCP and anti-polysaccharide Psl responses in mice. Antibodies mediated opsonophagocytic killing and serotype-independent protective immunity as shown by 100% survival upon challenge with P. aeruginosa in an acute pneumonia murine model. Vaccines were stable at 4 °C for at least one year. Overall, our data suggest that vaccination with subcellular empty PHA beads was sufficient to elicit multiple immune effectors that can prevent P. aeruginosa infection.
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Zhou, Su, Hua Yin, Shaoyu Tang, Hui Peng, Donggao Yin, Yixuan Yang, Zehua Liu et Zhi Dang. « Physiological responses of Microcystis aeruginosa against the algicidal bacterium Pseudomonas aeruginosa ». Ecotoxicology and Environmental Safety 127 (mai 2016) : 214–21. http://dx.doi.org/10.1016/j.ecoenv.2016.02.001.

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