Correlation between serogroup,<i>in vitro</i>biofilm formation and elaboration of virulence factors by uropathogenic<i>Pseudomonas aeruginosa</i>

Mittal, Rahul; Sharma, Shaveta; Chhibber, Sanjay; Aggarwal, Sudhir; Gupta, Varsha; Harjai, Kusum

doi:10.1111/j.1574-695x.2009.00627.x

Cited by 22 publications

(13 citation statements)

References 45 publications

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“…aeruginosa can form bacterial biofilm that protects the organism from defenses and antimicrobial therapy [14]. P. aeruginosa biofilm is difficult to eradicate, and it causes bacterial persistence, leading to infection chronicity and morbidity [15].…”

Section: Introductionmentioning

confidence: 99%

Biofilm formation and serum susceptibility in Pseudomonas aeruginosa

et al. 2014

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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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Section: Introductionmentioning

confidence: 99%

Biofilm formation and serum susceptibility in Pseudomonas aeruginosa

et al. 2014

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“…The presence of hemolysin has been reported previously for Pseudomonas aeruginosa and its activity is considered an important virulence factor in infection [19].…”

Section: Discussionmentioning

confidence: 72%

Draft genome sequence of the strain 16-537536, isolated from a patient with bronchiectasis and its relationship to the Pseudomonas koreensis group of the Pseudomonas fluorescens complex

et al. 2020

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Objective: The Pseudomonas koreensis group bacteria are usually found in soil and are associated with plants. Currently they are poorly described. Here we report on the whole genome sequence of a bacterial isolate from a patient with bronchiectasis that was first identified as P. koreensis, and on its position in the P. koreensis group. Results: Strain 16-537536 was isolated from a patient with bronchiectasis from Spain and initially identified by MALDI-TOF as P. koreensis, a member of the Pseudomonas fluorescens complex. However, the average nucleotide identity analysis (ANIb) and whole genome alignments of the draft genome sequence of this strain showed it to be a member of the P. koreensis group of the P. fluorescens complex, but belonging to an undescribed species. In addition, based on ANIb analysis, the P. koreensis group contains several other unnamed species. Several genes for putative virulence factors were identified. The only antibiotic resistance gene present in strain 16-537536 was a class C β-lactamase. The correct identification of bacterial species from patients is of utmost importance in order to understand their pathogenesis and to track the potential spread of pathogens between patients. Whole genome sequence data should be included for the description of new species.

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“…[3–4] The financial and societal burdens incurred by biofilm-associated bacterial infections alone are enormous. [5–6] As just one example, biofilms formed by the Gram-negative bacterium Pseudomonas aeruginosa – a species identified as the primary cause of infection in cystic fibrosis patients, [7–10] a leading source of infection in burn victims, [10] and one of the most common bacteria found on the surfaces of indwelling medical devices [11–13] – can increase treatment costs substantially and impact the quality of life in a broad spectrum of patients. [14] Biofouling and other issues associated with the formation of biofilms on the surfaces of pipes, ship hulls, and other objects also present substantial challenges in many other contexts.…”

Section: Introductionmentioning

confidence: 99%

Surface‐Mediated Release of a Small‐Molecule Modulator of Bacterial Biofilm Formation: A Non‐Bactericidal Approach to Inhibiting Biofilm Formation in Pseudomonas aeruginosa

Broderick

Breitbach

Frei

et al. 2013

Adv Healthcare Materials

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We report an approach to preventing bacterial biofilm formation that is based on the surface-mediated release of 5,6-dimethyl-2-aminobenzimidazole (DMABI), a potent and non-bactericidal small-molecule inhibitor of bacterial biofilm growth. Our results demonstrate that DMABI can be encapsulated in thin films of a model biocompatible polymer [poly(lactide-co-glycolide), PLG] and be released in quantities that inhibit the formation of Pseudomonas aeruginosa biofilms by up to 75–90% on surfaces that otherwise support robust biofilm growth. This approach enables the release of this new anti-biofilm agent for over one month, and it can be used to inhibit biofilm growth on both film-coated surfaces and other adjacent surfaces (e.g., on other uncoated surfaces and at air/water interfaces). Our results demonstrate a non-bactericidal approach to the prevention of biofilm growth and provide proof of concept using a clinically relevant human pathogen. In contrast to coatings designed to kill bacteria on contact, this release-based approach should also permit the design of strategically placed depots that disseminate DMABI more broadly and exert inhibitory effects over larger areas, which could prove useful in applications where the design or function of a surface prohibits the application of a uniform coating. This approach could also be used to design new polymer-coated surfaces useful for fundamental studies of bacterial biofilm growth. In a broader context, the non-bactericidal nature of DMABI could also provide opportunities to address concerns related to evolved resistance that currently face approaches based on the release of traditional microbicidal agents (e.g., antibiotics). Finally, the results of initial in vitro mammalian cell culture studies indicate that DMABI is not toxic to cells at concentrations required for strong anti-biofilm activity, suggesting that this new agent is well suited for further investigation in biomedical and personal care contexts. The surface-mediated approach reported here provides new tools useful for fundamental studies of biofilm formation and could, with further development, prove useful in a range of other industrial and commercial contexts in which bacterial biofilm growth is endemic.

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Correlation between serogroup,in vitrobiofilm formation and elaboration of virulence factors by uropathogenicPseudomonas aeruginosa

Cited by 22 publications

References 45 publications

Biofilm formation and serum susceptibility in Pseudomonas aeruginosa

Biofilm formation and serum susceptibility in Pseudomonas aeruginosa

Draft genome sequence of the strain 16-537536, isolated from a patient with bronchiectasis and its relationship to the Pseudomonas koreensis group of the Pseudomonas fluorescens complex

Surface‐Mediated Release of a Small‐Molecule Modulator of Bacterial Biofilm Formation: A Non‐Bactericidal Approach to Inhibiting Biofilm Formation in Pseudomonas aeruginosa

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