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  Table of Contents    
LETTER TO EDITOR  
Year : 2019  |  Volume : 62  |  Issue : 3  |  Page : 514-515
Biofilms: Fungal perspective


Department of Microbiology, Government Medical College Hospital, Chandigarh, India

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Date of Web Publication26-Jul-2019
 

How to cite this article:
Singla N, Gulati N, Chander J. Biofilms: Fungal perspective. Indian J Pathol Microbiol 2019;62:514-5

How to cite this URL:
Singla N, Gulati N, Chander J. Biofilms: Fungal perspective. Indian J Pathol Microbiol [serial online] 2019 [cited 2019 Aug 21];62:514-5. Available from: http://www.ijpmonline.org/text.asp?2019/62/3/514/263470




Editor,

Conventionally, fungi are considered to be planktonic organisms. However, many fungi, namely, Saccharomyces cerevisiae, Candida, Malassezia, Trichosporon, Cryptococcus, Aspergillus, Fusarium, and even Mucorales and dermatophytes have been proven to form biofilms. Fungal biofilms are mostly polymicrobial in nature.

Biofilm formation is a fungal adaptation strategy for survival against environmental pressures. Fungi form biofilms for metabolic cooperation, acquisition of new genetic traits, and increased stress resistance. We are concerned about the increasing fungal infections. The modern medicine has provided fungi with many niche such as catheters, shunts, tubings, implants, contact lenses, dentures, and prosthetic devices. The devices become colonized by the fungi and form biofilms over the abiotic surfaces. Biofilms are the known causes of chronic recalcitrant infections.[1]

The term biofilm was introduced by Costerton in 1985. Biofilms by definition are “a microbially derived sessile community characterized by cells that are irreversibly attached to a substratum or to each other, in a matrix of extracellular polymeric substance and exhibit an altered phenotype with respect to growth rate and gene transcription.”[2] Formation occurs in a sequential manner: (a) adherence and adsorption, (b) intermediate stage: it is of maximum metabolic activity. Extracellular matrix (ECM) is enhanced which is the nutrient source and protects biofilm community from desiccation, ultraviolet radiations, immune cells and the antimicrobial agents, and (c) maturation stage: a stage of release and dissemination when newer sites are colonized. Biofilm formation is not a classical virulence factor. However, biofilms do lead to increased pathogenicity as the community of cells gets too big to be phagocytozed. The fungi in biofilms are more tolerant to defensins, oxidative stress, and ECM impairs the recognition of fungal surface epitopes by immune cells, leading to immune escape. In a study done on clinical isolates of Candida, there was a direct correlation between clinical outcomes and mortality in high-biofilm formers than low-biofilm formers.[3]

Persister cells in biofilms form at least 1% population. These are dormant cells which ensure the survival even after an extensive and long-term course of antifungal therapy, leading to recurrence and relapse.[4] They are highly tolerant to antifungal agents as they do not divide.

Antifungals also fail to act effectively as there is an environmental gradient (heterogenicity) within biofilms. These biofilms being mushroom-like structure lead to concentration gradient in the form of oxygen, chemical, pH, or nutrient gradient. Different antibiotic concentrations reach different individual cells in different layers of biofilms. This suboptimal concentration acts as a stimulus for further biofilm formation and also leads to the development of drug resistance. Organisms in biofilm community have minimum inhibitory concentration (MIC) as high as 10–1000-fold greater than that for planktonic organisms.

Other mechanisms involved in drug resistance are increased cell density, alteration in drug targets, and upregulation of efflux pumps as the biofilms mature. ECM acts as a physical barrier to the entry of antifungals. There is an increased concentration of substances such as beta-glucans and mannans in ECM which act as “drug sponges” sequestering the azoles, pyrimidines, or polyenes.[5] ECM has extracellular DNA. If DNase is added to the biofilm models, the MIC of antifungals decreases significantly.[6]

There is very limited armamentarium of antifungals and it has been observed that among them only amphotericin B and echinocandins can retain their activity against biofilm forms of fungi. Hence, there is a need of more agents, which can inhibit biofilm adherence (the very first step of formation of biofilm) or can eliminate biofilm or can disrupt the already formed biofilm. Antifungal lock therapy has been proposed just like antibiotic lock solutions used in bacterial biofilm infections.[7] Several new targets in the form of components of ECM have been identified. Many natural plants or substances are under trial. Silver ion coating, silver nanoparticles, nitric oxide, chitosan, etc., have been tried for catheters and intravascular devices to prevent biofilm formation on the surfaces. Hence, to conclude, it is time that we wake up to the perspective of fungal biofilms. They might be more commonly associated with human diseases than we give them credit for. With many fungal infections, namely, aspergillomas, dermatophytomas, and mycetoma being speculated as a form of biofilms by fungi, there is a need that we strategically control the biofilms before they become a menace.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest to declare.



 
   References Top

1.
Jabra-Rizk MA, Falkler WA, Meiller TF. Fungal biofilms and drug resistance. Emerg Infect Dis 2004;10:14-9.  Back to cited text no. 1
    
2.
Donlan RM, Costerton JW. Biofilms: Survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002;15:167-93.  Back to cited text no. 2
    
3.
Rajendran R, May A, Sherry L, Kean R, Williams C, Jones BL, et al. Integrating Candida albicans metabolism with biofilm heterogeneity by transcriptome mapping. Sci Rep 2016;6:35436.  Back to cited text no. 3
    
4.
Lewis K. Persister cells. Annu Rev Microbiol 2010;64:357-72.  Back to cited text no. 4
    
5.
Nett JE, Crawford K, Marchillo K, Andes DR. Role of fks1p and matrix glucan in Candida albicans biofilm resistance to an echinocandin, pyrimidine, and polyene. Antimicrob Agents Chemother 2010;54:3505-8.  Back to cited text no. 5
    
6.
Martins M, Uppuluri P, Thomas DP, Cleary IA, Henriques M, Lopez-Ribot JL, et al. Presence of extracellular DNA in the Candida albicans biofilm matrix and its contribution to biofilms. Mycopathologia 2010;169:323-31.  Back to cited text no. 6
    
7.
Bink A, Pellens K, Cammue BP, Thevissen K. Anti-biofilm strategies: How to eradicate Candida biofilms? Open Mycol J 2011;5:29-38.  Back to cited text no. 7
    

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Correspondence Address:
Nidhi Singla
Associate Professor, Department of Microbiology, Government Medical College Hospital, Sector 32-B, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_20_18

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