Data-Density-Analysis-Classify-Microorganisms-Biofilm-Developers-Biofilm-Developers-Biofilm-Developers-Developers-v — различия между версиями

Текущая версия на 11:35, 21 февраля 2024

The results were expressed in two ways, using in both cases the same statistical method: without standardization, where controls were different depending on the day optic density measurements were performed, and standardized using a correction factor, using the same control for every strain of all our bacterium species in our study, which allows result homogenization. The obtained results in our study after data analysis and standardization show that over the 153 Gram negative strains in our study, 105 of them were no biofilm developers, representing 635% of all the studied bacterium genera. We consider that standardization and quantification of biofilm development in Gram negative bacteria can be useful in clinical practice, because biofilm development ability can lead or focus the gold treatment of pathologies produced by these microorganisms. Optimization of an automatic counting system for the quantification of Staphylococcus epidermidis cells in biofilms. Campus de Gualtar, Braga, Portugal; ICBAS-UP - Instituto de Ciências Biomédicas Biofilm formation is recognized as the main virulence factor in a variety of chronic infections. In vitro evaluation of biofilm formation is often achieved by quantification of viable or total cells.

However, these methods depend on biofilm disruption, which is often achieved by vortexing or sonication. In this study, we investigated the effects of sonication on the elimination of Staphylococcus epidermidis cell clusters from biofilms grown over time, and quantification was performed by three distinct analytical techniques. Even when a higher number of sonication cycles was used, some stable cell clusters remained in the samples obtained from 48- and 72-h-old biofilms, interfering with the quantification of sessile bacteria by plate counting. On Colanic acid compound , the fluorescence microscopy automatic counting system allowed proper quantification of biofilm samples that had undergone any of the described sonication cycles, suggesting that this is a more accurate method for assessing the cell concentration in S. epidermidis biofilms, especially in mature Heteroresistance to colistin in Klebsiella pneumoniae is triggered by small colony variants sub-populations within biofilms. The emergence of Klebsiella pneumoniae multidrug-resistant strains paves the way to the re-introduction of colistin as a salvage therapy. However, recent planktonic studies have reported several cases of heteroresistance to this antimicrobial agent.

The aim of this present work was to gain better understanding about the response of K. pneumoniae biofilms to colistin antibiotherapy and inspect the occurrence of heteroresistance in biofilm-derived cells. Biofilm formation and its susceptibility to colistin were evaluated through the determination of biofilm-cells viability. The profiling of planktonic and biofilm cell populations was conducted to assess the occurrence of heteroresistance. Colony morphology was further characterized in order to inspect the potential role of colistin in K. pneumoniae phenotypic differentiation. https://notes.io/wp3Yc show that K.

pneumoniae was susceptible to colistin in its planktonic form, but biofilms presented enhanced resistance. Population analysis profiles pointed out that K. pneumoniae manifest heteroresistance to colistin only when grown in biofilm arrangements, and it was possible to identify a resistant sub-population presenting a small colony morphology linking heteroresistance to biofilm formation and a morphological distinctive sub-population. Moreover, this is the first evidence that biofilm formation can trigger the emergence of heteroresistance in an apparently susceptible strain. Pseudomonas aeruginosa aggregates in cystic fibrosis sputum produce exopolysaccharides that likely impede current therapies. In cystic fibrosis (CF) airways, Pseudomonas aeruginosa forms cellular aggregates called biofilms that are thought to contribute to chronic infection. own pathogenic implications.

However, how they form in vivo is controversial and unclear. One mechanism involves a bacterially produced extracellular matrix that holds the aggregates together. Pel and Psl exopolysaccharides are structural and protective components of this matrix. We develop an immunohistochemical method to visualize Pel and Psl in CF sputum. We demonstrate that both exopolysaccharides are expressed in the CF airways and that the morphology of aggregates is consistent with an exopolysaccharide-dependent aggregation mechanism. We reason that the cationic exopolysaccharide Pel may interact with some of the abundant anionic host polymers in sputum.