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opencc-by-4.0Feb 2020View details →

Global trends of Pseudomonas aeruginosa biofilm research in the past two decades: A bibliometric study

This dataset was used to conduct bibliometric and visualised analyses on research relating to Pseudomonas aeruginosa biofilms over the past two decades.

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Data from: Top-down effects of a lytic bacteriophage and protozoa on bacteria in aqueous and biofilm phases

Lytic bacteriophages and protozoan predators are the major causes of bacterial mortality in natural microbial communities, which also makes them potential candidates for biological control of bacterial pathogens. However, little is known about the relative impact of bacteriophages and protozoa on the dynamics of bacterial biomass in aqueous and biofilm phases. Here, we studied the temporal and spatial dynamics of bacterial biomass in a microcosm experiment where opportunistic pathogenic bacteria Serratia marcescens was exposed to particle-feeding ciliates, surface-feeding amoebas, and lytic bacteriophages for 8 weeks, ca. 1300 generations. We found that ciliates were the most efficient enemy type in reducing bacterial biomass in the open water, but least efficient in reducing the biofilm biomass. Biofilm was rather resistant against bacterivores, but amoebae had a significant long-term negative effect on bacterial biomass both in the open-water phase and biofilm. Bacteriophages had only a minor long-term effect on bacterial biomass in open-water and biofilm phases. However, separate short-term experiments with the ancestral bacteriophages and bacteria revealed that bacteriophages crash the bacterial biomass dramatically in the open-water phase within the first 24 h. Thereafter, the bacteria evolve phage-resistance that largely prevents top-down effects. The combination of all three enemy types was most effective in reducing biofilm biomass, whereas in the open-water phase the ciliates dominated the trophic effects. Our results highlight the importance of enemy feeding mode on determining the spatial distribution and abundance of bacterial biomass. Moreover, the enemy type can be crucially important predictor of whether the rapid defense evolution can significantly affect top-down regulation of bacteria.

opencc-zeroDec 2013View details →

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Data from: Biofilm-associated multidrug-resistant and methicillin-resistant staphylococcus aureus infections in children

Introduction: The ability of Staphylococcus aureus to form biofilms—architectural complexes that cause chronic and recalcitrant infections—along with its notorious variant, methicillin-resistant S. aureus (MRSA), leads to multidrug-resistant (MDR) infections that are challenging to treat with antibiotics. This cross-sectional study investigated the prevalence of S. aureus infections in children (<17 years) and characterized the antibiograms of MDR, MRSA, and biofilm-forming strains, along with their coexistence. Methods: S. aureus strains were isolated and identified from clinical samples and tested for antibiograms following standard microbiology guidelines. MDR strains were non-susceptible to at least one agent in three antimicrobial categories, whereas MRSA strains were cefoxitin-resistant. The gold-standard microtiter plate method was used to detect biofilms. Statistical analyses were performed using SPSS version 17.0. Results: S. aureus was detected in 9.02% of 543 samples, primarily from pus (79.59%, 39/49). Children aged 1 to <3 years most commonly contracted infections (30.61%, 15/49), and males (67.35%, 33/49) had twice as many infections as females (32.65%, 16/49). As high as 84.69% (83/98) of strains were penicillin-resistant, while 18.37% (27/147) were aminoglycoside-resistant. MDR accounted for 79.59% (39/49) of all S. aureus infections, while MRSA and biofilm-formers accounted for 67.35% (33/49) and 24.49% (12/49), respectively. Fluoroquinolone resistance in non-(MDR-MRSA-biofilm-formers), MDR-MRSA, MDR-biofilm-formers, and MRSA-biofilm-formers was 31.25%, 46.77%, 58.33%, and 60%, respectively, while aminoglycoside resistance was 0%, 32.26%, 50.0%, and 45.0%, and penicillin resistance was 87.50%, 85.48%, 100.0%, and 100.0%. Conclusion: S. aureus, mostly MDR and MRSA, caused four-fifths of infections in children. Compared to MDR-MRSA and non-(MDR-MRSA-biofilm-formers), MDR-biofilm-formers and MRSA-biofilm-formers triggered higher levels of antimicrobial resistance.

opencc-zeroDec 2023View details →

Figure 6 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 6 The absorbance of MST assay.

Figure 2 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 2 Diameter zones inhibition of S. mutans, S. aureus, P. gingivalis.

Figure 4 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 4 Inhibition of S. aureus.

Figure 1 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 1 Toothpaste appearance.

Figure 5 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 5 Inhibition of P. gingivalis.

Figure 3 from: Suryono S, Setiawan PB, Aji NRAS, Vega CAW, Rodestawati B, Lukitaningsih E, Rahman FA, Devina S, Tsabita SS, Datau SI, Alhasyimi AA (2024) Potential of 10% propolis-based toothpaste on the inhibition of biofilm-forming bacteria growth in vitro. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e118072

Figure 3 Inhibition of S. mutans.

opencc-zeroMar 2024View details →

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Determination of fluoroquinolones concentration among biofilm-forming and non-forming uropathogenic Acinetobacter Calcoaceticus-Baumannii complex and their correlation to fluoroquinolone-resistant genes

Acinetobacter spp., the predominant cause of urinary tract infection (UTI), is increasingly resistant to fluoroquinolones. Resistance to fluoroquinolones poses a serious health problem in the treatment of urinary tract infections, which are mostly associated with chromosomal mutations encoded by topoisomerase IV. The objective of the study was to detect the blaOXA-23, qnrB, and acc(6l)-lb-cr genes in fluoroquinolone-resistant biofilm-producing ACB complex isolated from UTI-suspected patients. A hospital-based cross-sectional study was carried out at the Nepal Police Hospital, Kathmandu, from April 2019 to January 2021. A total of 598 urine specimens were processed, and 78 ACB complex were isolated from a total of 366 positive cultures, which were identified based on colony morphology, Gram's staining reaction, and various biochemical tests. The antimicrobial susceptibility pattern was determined by the modified Kirby-Bauer disk diffusion method, and the result was interpreted according to CLSI guidelines. The minimum inhibitory concentration (MIC) values of levofloxacin and ciprofloxacin for fluoroquinolone-resistant ACB were determined by the broth dilution method. The fluoroquinolone-resistant ACB was selected for blaOXA-23, qnrB, and acc(6l)-lb-cr gene detection by polymerase chain reaction. ACB complex was isolated more in females 26 (55.31%); outpatients 42 (53.84); and in the age group of 21–40 years 27 (34.61%). The majority of ACB complex isolates were sensitive to Ciprofloxacin 5 (6.41%) and Levofloxacin 10 (12.82%). However, most of them were resistant to Ciprofloxacin 64 (82.05%) and Levofloxacin 60 (76.92%). A total of 78 (21.31%) ACB complex isolates were found to be multidrug resistant. The MICs of Ciprofloxacin and Levofloxacin ranged from 4 to 256 μl/ml. Among 78 (82.05%) fluoroquinolone-resistant ACB isolates, the blaOXA-23 gene was found on 32 (41.02%) isolates, the acc(6l)-Ib-cr gene on 3 (3.84%) isolates, and the qnrB gene on 1 (1.28%) isolates. The presence of blaOXA-23, acc(6l)-Ib-cr, and qnrB genes and biofilm formation lead to the emergence of fluoroquinolone-resistant strains of the ACB complex. So, the identification of responsible genes is required for AMR surveillance and guidelines for empirical therapy, which aid in preventing the emergence of antibiotic-resistant isolates.

opencc-by-4.0Sep 2018View details →

Enhanced biofilm formation aids adaptation to extreme warming and environmental instability in the diatom Thalassiosira pseudonana and its associated bacteria

These files contain all data necessary to create the figures published in "Enhanced biofilm formation aids adaptation to extreme warming and environmental instability in the diatom Thalassiosira pseudonana and its associated bacteria". In most cases, these are also the data that were used for analysis. Raw data and R code are available from the author upon request. Sequencing data will be available From GenBank in due course (accession numbers will be added to the zenodo file descriptor).   1. File "20180930_biofilm_trajectories" contains the evolutionary trajectories of biofilm forming cells. The column names are as follows: 'count' for number of cells, 'size' is a unites ImageJ estimate, '%area' gives the area of the cover slip that had biofilm growth, 'date' is the date of the measurement and was used for internal purposes only, 'temp' is the selection temperature  , 'nutrient' gives the nutrient status with n+ for nutrient replete and n- for lower nutrient status, 'week' for week of the experiment. Evoplas indicates whether the measurement was for the evolved samples in their selection environment ('evo', assay temperature is the same as selection temperature) or whether it was an assay for plasticity ('plas' , assay at a temperature other than the selection temperature). assay details the assay temperature. These data can be used to re-create and analyse Figure 3. (Figures 1 and 2 are conceptual figures; i.e there are no data associated) 2. File "20180930Ability_to_form_biofilms" contains data for analysing whether a naive planktonic sample presented with a coverslip grows in a biofilm as well as a sample selected to form biofilms. Column names are the same as above, apart from the 'ability [...]' column, which is the ratio of biofilm growth of a biofilm-selected sample compared to a naive sample. Values >1 indicate that the biofilm selected samples grew larger biofilms faster than a planktonic samples subjected to the same conditions. These data are for Figure 6.   3. File "20183009_biofilm_characterise" contains the data for Figure 4, i.e. information on cell size, chlorophyll a content, and bacterial load. The column names are as follows: trait is for either cell diameter in µm ('size'), chlorophyll a content ('chlorophyll'), or bacterial load. Selection temp is the selection temperature and nutr, the nutrient regime with full for full f/2 media and deplete for 1/3 of f/2 media. in 'sampletype' p is for planktonic cells, bf for the biofilm cells, and pbf for planktonic cells sloughed off the biofilm. Traitvalue is for the trait values. Size in µm, chlorophyll in pg per cell, and bacterial load in % of total biomass.

opencc-by-4.0Jan 2023View details →

Effect of quorum sensing molecule farnesol on mixed biofilms of Candida albicans and Staphylococcus aureus

In the present work, the effect of farnesol either alone or in combination with oxacillin on mixed biofilms formed by clinically relevant pathogens, Candida albicans and Staphylococcus aureus was studied.

opencc-by-4.0Aug 2023View details →

Additional information for Biofilm colonization and succession in a full-scale partial nitritation-anammox moving bed biofilm reactor

Here we include additional files for Suarez et al. Biofilm colonization and succession in a full-scale partial nitritation-anammox moving bed biofilm reactor Files included here: <ul> <li>MAG_annotations_EUK.tsv. Genome annotation of eukaryotic MAGs made with eggnog-mapper v2.1.9.  </li> <li>MAG_annotations_PROK.tsv. Genome annotation of bacterial and Archaeal MAGs made with eggNOG-mapper v2.1.9</li> </ul> Metagenome reads and MAGs have been deposited at the European Nucleotide Archive (ENA) under accession PRJEB58181.

closedIPD-NOFeb 2026View details →

Safety and Tolerability of Single and Multiple Doses of SoftOx Biofilm Eradicator (SBE) in Chronic Leg Wounds

ClinicalTrials.gov study NCT05710094. IPD Sharing: NO. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →

Characterisation of Biofilm Growth on Coated vs. Uncoated Urinary Catheter Surfaces in Normal Clinical Use

ClinicalTrials.gov study NCT05513677. IPD Sharing: NO. Countries: 1. Publications: 0.

Treatment of Chronic Wound Biofilms

ClinicalTrials.gov study NCT01646502. IPD Sharing: Not stated. Countries: 1. Publications: 0.

The Impact of Different Citrate Concentrations as Locking Solutions on Development of Biofilm and Function of Hemodialysis Catheters

ClinicalTrials.gov study NCT03683563. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.

Immunological Interaction Between the Host and Candida Albicans Biofilm

ClinicalTrials.gov study NCT01919931. IPD Sharing: Not stated. Countries: 1. Publications: 0.

Investigation of Biofilm Formation on Temporary push-on Rings of Implant Crowns

ClinicalTrials.gov study NCT05122897. IPD Sharing: Not stated. Countries: 1. Publications: 0.