Disease relevance of Biofilms

• Effect of vancomycin and rifampicin on meticillin-resistant Staphylococcus aureus biofilms [1].
• Inorganic polyphosphate in Bacillus cereus: motility, biofilm formation, and sporulation [2].
• srf-3, a mutant of Caenorhabditis elegans, resistant to bacterial infection and to biofilm binding, is deficient in glycoconjugates [3].
• Expression of the Pho regulon negatively regulates biofilm formation by Pseudomonas aureofaciens PA147-2 [4].
• The results indicated that the bacterial biofilm on the urinary catheter could be eliminated by fleroxacin at 30 mg/kg q8h i.v. and 20 mg/kg q8h i.v. Fleroxacin concentrations in urine exceeded the levels necessary to destroy E. coli [5].

High impact information on Biofilms

• Biofilm formation is associated with elevated synthesis of short-chain (C56-C68) fatty acids, and strains with altered mycolate profiles--including an InhA mutant resistant to the antituberculosis drug isoniazid and a strain overexpressing KasA--are defective in biofilm formation [6].
• By chelating iron, lactoferrin stimulates twitching, a specialized form of surface motility, causing the bacteria to wander across the surface instead of forming cell clusters and biofilms [7].
• We found that antibiotic-resistant phenotypic variants of P. aeruginosa with enhanced ability to form biofilms arise at high frequency both in vitro and in the lungs of CF patients [8].
• We propose that this response is critical for the development of biofilm resistance to tobramycin [9].
• Formation of sphalerite (ZnS) deposits in natural biofilms of sulfate-reducing bacteria [10].

Chemical compound and disease context of Biofilms

• Bile acid induction of biofilms was found to be dependent on the vps genes (Vibrio polysaccharide synthesis) and their transcriptional activator VpsR, but VpsT is not required [11].
• The Gram-negative periodontal pathogen Actinobacillus actinomycetemcomitans forms an extremely tenacious biofilm on solid surfaces such as glass, plastic and hydroxyapatite [12].
• CONCLUSIONS: A wide range of different branches and groups of bacteria participate in the development of biofilms on the surfaces of foreign bodies, such as biliary stents, mixed gall stones, or calcific pancreatic ducts, but not on the surface of pure cholesterol gall stones [13].
• Effects of glucose on fsr-mediated biofilm formation in Enterococcus faecalis [14].
• Here we describe the isolation and characterization of transposon (Tn917) mutants of Staphylococcus epidermidis O-47 which were biofilm negative in the polystyrene microtiter plate assay [15].

Biological context of Biofilms

• Because bacterial motility is often crucial for their survival in a natural environment and for systemic infection inside a host, the dependence for motility on PPK reveals important roles for poly P in diverse processes such as biofilm formation, symbiosis, and virulence [16].
• Interestingly, rpfF mutants can still form in planta biofilms, which differ architecturally from biofilms in insects, suggesting that biofilm architecture, rather than a passive response to the environment, is actively determined by X. fastidiosa gene expression [17].
• In this work, we demonstrate a role for the O-antigen polysaccharide of V. cholerae in Ca2+-dependent biofilm development in model and true sea water [18].
• We report the isolation of insertional mutations to the pstC and pstA genes of the phosphate-specific transport (pst) operon that results in loss of biofilm formation by Pseudomonas aureofaciens PA147-2 [4].
• Recent findings indicate that sigmaB also plays an important role in antibiotic resistance, pathogenesis and cellular differentiation processes such as biofilm formation and sporulation [19].

Anatomical context of Biofilms

• Human leukocytes, in the presence of recombinant human IFN-gamma, killed biofilm bacteria lacking alginate after a 4-h challenge at 37 degrees C. Bacterial killing was dependent on the presence of IFN-gamma [20].
• These data suggest that fleroxacin may be useful for treating catheter-related infections because these therapeutic dosages limited ascending infections of the urethra and bladder, eliminated catheter-associated biofilms, and killed planktonic bacteria in urine [5].
• Mannose-resistant Proteus-like fimbriae are produced by most Proteus mirabilis strains infecting the urinary tract, dictate the in vivo localization of bacteria, and contribute to biofilm formation [21].
• The effect of the beta-lactam antibiotic, amdinocillin, on the bacterial biofilm adherent to the Foley catheter surface, the bacterial microcolonies attached to the urinary bladder mucosa, and on planktonic bacteria in the urine was studied in a rabbit model of the closed urinary catheter drainage system [22].
• With viability assays, biofilm formation assessment, and ethidium bromide uptake testing, farnesol was shown to inhibit biofilm formation and compromise cell membrane integrity [23].

Associations of Biofilms with chemical compounds

• A specific signaling mutant, a lasI mutant, forms flat, undifferentiated biofilms that unlike wild-type biofilms are sensitive to the biocide sodium dodecyl sulfate [24].
• Abundant, micrometer-scale, spherical aggregates of 2- to 5-nanometer-diameter sphalerite (ZnS) particles formed within natural biofilms dominated by relatively aerotolerant sulfate-reducing bacteria of the family Desulfobacteriaceae [10].
• Late-onset infections of synthetic vascular grafts (LO-SVGIs) are generally caused by staphylococci that produce a slime polysaccharide and grow as a biofilm on the graft surface [25].
• Biofilm formation on polystyrene and medical-grade silicone was examined [26].
• Triclosan became impregnated throughout the silicone catheter material and completely inhibited the formation of crystalline biofilm, whereas catheters inflated with water became blocked in 24 h [27].

Gene context of Biofilms

• Together, these experiments suggest that mucin, which may serve as an attachment surface in CF airways, impacts P. aeruginosa biofilm development and function [28].
• The data obtained in these analyses suggested that in approximately 30% of the variants the missing biofilm formation was due to the inactivation of either the icaA or the icaC gene by the insertion of the insertion sequence element IS256 [29].
• Biofilm formation is not regulated by csrA, csrB or uvrY in a DeltapgaC mutant, which cannot synthesize PGA [30].
• Study of the isolated mutant strains allowed the identification of four genes involved in biofilm formation (RIF1, SIR4, EPA6 and YAK1) [31].
• This result suggests that gene(s) within the Pho regulon act to regulate biofilm formation negatively in low-P(i) environments, and that phoR mutations uncouple PA147-2 from such regulatory constraints [4].

Analytical, diagnostic and therapeutic context of Biofilms

• Scanning electron microscopy of biofilms formed by PA14 gacA(-) revealed diffuse clusters of cells that failed to aggregate into microcolonies, implying a deficit in biofilm development or surface translocation [32].
• Site-directed mutagenesis of the catalytic Ser of TEM-1, but not Oxa-3, abolished the biofilm defect, while disruption of either TEM-1 or Oxa-3 expression restored wild-type levels of biofilm formation [33].
• Confocal scanning laser microscopy was used to visualize and confirm normal and farnesol-inhibited biofilms [34].
• Under these growth conditions, N. gonorrhoeae formed a biofilm with or without the addition of 10 microM sodium nitrite to the perfusion medium [35].
• Northern blot analyses revealed that Candida biofilms expressed CDR and MDR1 genes in all the developmental phases, while planktonic cells expressed these genes only at the 12- and 48-h time points [36].

References