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Tracheal and Bronchial Developmental Abnormalities, and Inflammatory Diseases including Bronchiectasis, Cystic Fibrosis and Bronchiolitis.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Impairment is also seen with chronic bronchitis, mucus plugs, bronchiectasis, CF, chronic pneumonia, etc. Pyocyanin (the green pigment produced in pseudomonas infection) causes ciliary paralysis (see also under cystic fibrosis ps. 3.22 - 3.24).
Chromonychia
Published in Archana Singal, Shekhar Neema, Piyush Kumar, Nail Disorders, 2019
Michela Starace, Aurora Alessandrini, Bianca Maria Piraccini
The differential diagnosis includes chemical exposure to solutions containing pyocyanin or pyoverdine.5 After clipping away of the detached nail plate, a pale green-yellow pigmentation is evident on the bottom of the nail plate and on the nail bed: the clinical history and examination may also suggest the presence of paronychia and onycholysis.
P
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Pseudomonas pyocyanea [Greek:pseudes, false + monos, alone] (Syn: P. aeruginosa) A blue pigment was obtained from organic material, and named ‘pyocyanine’ by M. Fordos of France in 1860. The bacterial source of the pigment was discovered by French physician, Carle Gessard (b 1850), in 1882. The bacillus was first called‘le microbe pyocynique’ by Gessard. The term ‘aeroginosa’ was first used by J. Schroeter in 1875.
Subtle relationships between Pseudomonas aeruginosa and fungi in patients with cystic fibrosis
Published in Acta Clinica Belgica, 2022
Kaicheng Yan, Hong Yin, Jin Wang, Yun Cai
Phenazines are the metabolite of many microorganisms, many of which have antibiotic activity [28]. It has been reported that PA can produce phenazine, which is a heterocyclic compound with redox activity and naturally occurs in the form of soluble reduction. The aromatic ring is replaced by different functional groups to obtain derivatives of various colors. These natural pigments make pyocyanin green, yellow for phenazine-1-carboxylic acid (PCA) and phenazine-1-carboxylamide, and orange for orange 1-hydroxyphenazine (1-HP) [29,30]. The pigments pyocyanin and 1-HP produced by PA inhibit the germination of AF spores, and 1-HP is the most toxic one of these pigments [31]. Pyocyanin is a well-known virulence factor notably during CF lung infections. Pyocyanin also has antibiotic activity against a wide range of bacteria, and it causes an alteration in functions of neutrophils and lymphocytes, reduction in mucociliary clearance, and inhibition of endothelial–NO interactions. It is toxic to both eukaryotic and bacterial cells, and many mechanisms have been speculated, including induction of oxidative stress and redox activity [32,33]. Other than PCA and pyocyanin, Xu et al. have reported that PA produces small-molecule antimicrobials, including PA06ER10, PA06ER16, PA06ER23, and PA06ER31. They have speculated that these small molecular components may be phenazine analogs because of their similar functions and heavier molecular weights [34].
Synthesis and biological evaluation of thiazolidinedione derivatives with high ligand efficiency to P. aeruginosa PhzS
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Thamires Quadros Froes, Bianca Trindade Chaves, Marina Sena Mendes, Rafael Matos Ximenes, Ivanildo Mangueira da Silva, Priscila Brandão Gomes da Silva, Julianna Ferreira Cavalcanti de Albuquerque, Marcelo Santos Castilho
One approach to overcome the dilemma relies on bacterial virulence modulation. Although pyocyanin is a virulence factor from Pseudomonas aeruginosa employed as an end-point in most anti-virulence drug development projects, the enzymes responsible for its biosynthesis remain largely unexplored as potential therapeutic targets. The results described here show that unsubstituted N1 at the thiazolidine-2,4-dione ring is essential for PaPhzS inhibition and that molecular simplification of (E)-5–(4-((4-oxo-3-phenyl-3,4-dihydroquinazolin-2-yl)methoxy)benzylidene)thiazolidine-2,4-dione affords improved lead compounds that retain the original mode of inhibition (competitive to NAD+). Moreover, steric clashes due to simultaneous substitution at both meta positions are detrimental to 5-arylidene-thiazolidine-2,4-dione derivatives affinity. However, there seems to be some plasticity within PaPhzS binding site, since the replacement of benzyl ring by indole substituted ring does not abolish the affinity. Taken together, this information paves the way to develop the third round of PaPhzS inhibitors with improved potency.
Recent advances in antibacterial applications of metal nanoparticles (MNPs) and metal nanocomposites (MNCs) against multidrug-resistant (MDR) bacteria
Published in Expert Review of Anti-infective Therapy, 2019
Major infections of P. aeruginosa can be categorized in five groups: (1) skin and soft tissues, (2) lungs (pneumonia), (3) gastrointestinal, (4) urinary tract, and (5) septic shock (blood) infections. In patients with cystic fibrosis disease, resulted pneumonia from P. aeruginosa colonization in lung epithelial cells as well as production of pyocyanin virulence factor may be difficult to treat. Nosocomial infections caused by P. aeruginosa are most frequent in hospital devices such as catheter, implants, and other prosthesis. These infections are caused by biofilm formation and resistance to wide range of antibiotics. Moreover, wound and burn infections caused by this bacterium is yet main problem in health-care-associated parts [20]. P. aeruginosa is resistant to antibiotic by using various mechanisms. Enzyme of Verona Integron-encoded Metallo β-lactamase (VIM) is responsible for destruction of β-lactams antibiotics such as carbapenemase. Resistance to cephalosporins and β-lactams is resulted from expression of chromosomal or plasmid (infrequent)-mediated AmpC genes [1]. In addition, OXA-11 strain of P. aeruginosa can destruct third-generation cephalosporins. Alterations of target-binding site as well as reduction of internal antibiotic concentrations by lack of porins and application of efflux pumps are other important mechanisms of antibiotic resistance in this bacterium [21].