How to build a biofilm: a fungal perspective. Curr Opin Microbiol 9:588-594

Department of Microbiology, Hammer Health Sciences Center, Room 906, 701 W 168th Street, New York, NY 10032, USA.
Current Opinion in Microbiology (Impact Factor: 5.9). 01/2007; 9(6):588-94. DOI: 10.1016/j.mib.2006.10.003
Source: PubMed


Biofilms are differentiated masses of microbes that form on surfaces and are surrounded by an extracellular matrix. Fungal biofilms, especially those of the pathogen Candida albicans, are a cause of infections associated with medical devices. Such infections are particularly serious because biofilm cells are relatively resistant to many common antifungal agents. Several in vitro models have been used to elucidate the developmental stages and processes required for C. albicans biofilm formation, and recent studies have begun to define biofilm genetic control. It is clear that cell-substrate and cell-cell interactions, hyphal differentiation and extracellular matrix production are key steps in biofilm development. Drug resistance is acquired early in biofilm formation, and appears to be governed by different mechanisms in early and late biofilms. Quorum sensing might be an important factor in dispersal of biofilm cells. The past two years have seen the emergence of several genomic strategies to uncover global events in biofilm formation and directed studies to understand more specific events, such as hyphal formation, in the biofilm setting.

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    • "In recent years, emerging cases of C. albicans drug resistance have been primarily attributed to the formation of biofilms, with resistance increasing in conjunction with the maturation of the biofilm (8). Mature Candida biofilms consist of a complex three-dimensional structure of layers of yeast cells, hyphae and an abundant exopolysaccharide matrix (9,10). As natural resistance barriers of antifungal drugs, biofilms play a significant role in the invasion and dissemination of C. albicans. "
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    ABSTRACT: With the increasing usage of indwelling medical devices in clinical practice, the frequency of fungal infections has increased, such as that of Candida albicans (C. albicans). Biofilms, a protected niche for microorganisms, are resistant to a range of current antifungal agents. Chitosan is a polyatomic biopolymer with advantageous biocompatibility, biodegradation, nontoxicity and antibacterial properties. To investigate the inhibitory effect of chitosan on biofilms formed by C. albicans, cell viability, 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-caboxanilide reduction, and morphological assays, including fluorescence microscopy and scanning electron microscopy (SEM), were employed. As assessed by cell viability assay, chitosan showed significant inhibitory effects on the planktonic cells and the biofilm of C. albicans in a dose-dependent manner. Fluorescence microscopy and SEM assays confirmed that the chitosan-treated group showed delayed C. albicans biofilm formation with defect morphological features, due to the inhibitory effects of the vast majority of fungal cell growth. In conclusion, C. albicans biofilms were compromised by the treatment with chitosan, providing an alternative therapeutic strategy against the fungal biofilms in the medical devices.
    Experimental and therapeutic medicine 09/2014; 8(3):929-934. DOI:10.3892/etm.2014.1839 · 1.27 Impact Factor
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    • "The presence of medical devices such as central venous catheters (CVC’s) are known to be important risk factors [14] suggesting that biofilm formation is a key feature in the pathogenesis of candidaemia. The past decade has seen a significant leap in our knowledge and understanding of the biology of C. albicans biofilms, particularly with respect to the molecular basis of their development and homeostasis [15]. However, in the clinical setting it is generally assumed that all C. albicans isolates have the capacity to form biofilms, but often with little regard to individual differences within the species when managing the infection. "
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    ABSTRACT: Background Candida albicans infections have become increasingly recognised as being biofilm related. Recent studies have shown that there is a relationship between biofilm formation and poor clinical outcomes in patients infected with biofilm proficient strains. Here we have investigated a panel of clinical isolates in an attempt to evaluate their phenotypic and transcriptional properties in an attempt to differentiate and define levels of biofilm formation. Results Biofilm formation was shown to be heterogeneous; with isolates being defined as either high or low biofilm formers (LBF and HBF) based on different biomass quantification. These categories could also be differentiated using a cell surface hydrophobicity assay with 24 h biofilms. HBF isolates were more resistance to amphotericin B (AMB) treatment than LBF, but not voriconazole (VRZ). In a Galleria mellonella model of infection HBF mortality was significantly increased in comparison to LBF. Histological analysis of the HBF showed hyphal elements intertwined indicative of the biofilm phenotype. Transcriptional analysis of 23 genes implicated in biofilm formation showed no significant differential expression profiles between LBF and HBF, except for Cdr1 at 4 and 24 h. Cluster analysis showed similar patterns of expression for different functional classes of genes, though correlation analysis of the 4 h biofilms with overall biomass at 24 h showed that 7 genes were correlated with high levels of biofilm, including Als3, Eap1, Cph1, Sap5, Plb1, Cdr1 and Zap1. Conclusions Our findings show that biofilm formation is variable amongst C. albicans isolates, and categorising isolates depending on this can be used to predict how pathogenic the isolate will behave clinically. We have shown that looking at individual genes in less informative than looking at multiple genes when trying to categorise isolates at LBF or HBF. These findings are important when developing biofilm-specific diagnostics as these could be used to predict how best to treat patients infected with C. albicans. Further studies are required to evaluate this clinically.
    BMC Microbiology 07/2014; 14(1):182. DOI:10.1186/1471-2180-14-182 · 2.73 Impact Factor
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    • "A. colubrina also demonstrated a fungistatic nature, with a high MFC (1 to 2 mg/mL), which suggests the inhibition of the growth of the microorganism without causing its death C. albicans biofilm consists of a mixture of yeast, hyphae and pseudohyphae [25]. In the maturation phase occur an increase in the growth of the hyphae and a reduction in the yeast [25] [26] [27]. In the SEM analysis, the A. colubrina demonstrated the capacity to inhibit the formation of hyphae, with a predominance of blastospores, demonstrating the susceptibility of the C. albicans biofilm to this plant. "
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    ABSTRACT: The aim of the present study was to perform an in vitro analysis of the antimicrobial and antiproliferative potential of an extract from Anadenanthera colubrina (Vell.) Brenan (angico) and chemically characterize the crude extract. Antimicrobial action was evaluated based on the minimum inhibitory concentration (MIC), minimum bactericidal/fungicidal concentration, and the inhibition of formation to oral biofilm. Cell morphology was determined through scanning electron microscopy (SEM). Six strains of tumor cells were used for the determination of antiproliferative potential. The extract demonstrated strong antifungal activity against Candida albicans ATCC 18804 (MIC = 0.031 mg/mL), with similar activity found regarding the ethyl acetate fraction. The extract and active fraction also demonstrated the capacity to inhibit the formation of Candida albicans to oral biofilm after 48 hours, with median values equal to or greater than the control group, but the difference did not achieve statistical significance (P > 0.05). SEM revealed alterations in the cell morphology of the yeast. Regarding antiproliferative activity, the extract demonstrated cytostatic potential in all strains tested. The present findings suggest strong antifungal potential for Anadenanthera colubrina (Vell.) Brenan as well as a tendency toward diminishing the growth of human tumor cells.
    Evidence-based Complementary and Alternative Medicine 06/2014; 2014(1):802696. DOI:10.1155/2014/802696 · 1.88 Impact Factor
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