<i>Candida</i>
            Biofilms: Development, Architecture, and Resistance

Chandra, Jyotsna; Mukherjee, Pranab K.

doi:10.1128/microbiolspec.mb-0020-2015

Cited by 132 publications

(104 citation statements)

References 154 publications

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“…Fungal cells encased within the biofilm are resistant to most clinically used antifungals, including azole drugs, ultimately resulting in treatment failure (Chandra et al, 2001; Mathé and Van Dijck, 2013; Chandra and Mukherjee, 2015). Biofilm-related C. albicans infections thus pose a major threat to the public (Mathé and Van Dijck, 2013).…”

Section: Discussionmentioning

confidence: 99%

Repurposing Approach Identifies Auranofin with Broad Spectrum Antifungal Activity That Targets Mia40-Erv1 Pathway

Thangamani

Maland

Mohammad

et al. 2017

Front. Cell. Infect. Microbiol.

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Current antifungal therapies have limited effectiveness in treating invasive fungal infections. Furthermore, the development of new antifungal is currently unable to keep pace with the urgent demand for safe and effective new drugs. Auranofin, an FDA-approved drug for the treatment of rheumatoid arthritis, inhibits growth of a diverse array of clinical isolates of fungi and represents a new antifungal agent with a previously unexploited mechanism of action. In addition to auranofin's potent antifungal activity against planktonic fungi, this drug significantly reduces the metabolic activity of Candida cells encased in a biofilm. Unbiased chemogenomic profiling, using heterozygous S. cerevisiae deletion strains, combined with growth assays revealed three probable targets for auranofin's antifungal activity—mia40, acn9, and coa4. Mia40 is of particular interest given its essential role in oxidation of cysteine rich proteins imported into the mitochondria. Biochemical analysis confirmed auranofin targets the Mia40-Erv1 pathway as the drug inhibited Mia40 from interacting with its substrate, Cmc1, in a dose-dependent manner similar to the control, MB-7. Furthermore, yeast mitochondria overexpressing Erv1 were shown to exhibit resistance to auranofin as an increase in Cmc1 import was observed compared to wild-type yeast. Further in vivo antifungal activity of auranofin was examined in a Caenorhabditis elegans animal model of Cryptococcus neoformans infection. Auranofin significantly reduced the fungal load in infected C. elegans. Collectively, the present study provides valuable evidence that auranofin has significant promise to be repurposed as a novel antifungal agent and may offer a safe, effective, and quick supplement to current approaches for treating fungal infections.

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Section: Discussionmentioning

confidence: 99%

Repurposing Approach Identifies Auranofin with Broad Spectrum Antifungal Activity That Targets Mia40-Erv1 Pathway

Thangamani

Maland

Mohammad

et al. 2017

Front. Cell. Infect. Microbiol.

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“…Other pathogenic Candida species include C. tropicalis , C. glabrata , C . parapsilosis , and C. krusei accounting for 25%, 8%, 7%, and 4% of candidiasis, respectively [4]. Pathogenesis of candidiasis depends on the expression of virulence factors like germ tube formation, adhesions, phenotypic switching, biofilm formation, and the production of hydrolytic enzymes [5].…”

Section: Introductionmentioning

confidence: 99%

Antifungal Susceptibility and Biofilm Production of Candida spp. Isolated from Clinical Samples

Marak

Dhanashree

2018

International Journal of Microbiology

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Objective The study aims to speciate clinical Candida isolates and detect their biofilm-forming ability and antifungal resistance. Methods All the Candida spp. isolated from different clinical samples like pus, urine, blood, and body fluid were included in the study. Biofilm production was tested by the microtiter plate method. Antifungal susceptibility was studied by the disk diffusion method. Patient's demographic details such as age, sex, and clinical information were collected. Presence of other risk factors such as diabetes mellitus, history of antibiotic use, and any urinary tract instrumentations was also recorded. Results Among 90 Candida species isolated, most predominant species was found to be C. albicans (45.5%) followed by C. tropicalis (28.88%), C. krusei (20%), C. glabrata (3.33%), and C. parapsilosis (2.22%). Candida spp. were isolated from urine (43%), BAL/sputum (18.88%), high vaginal swab (8.88%), suction tips (7.77%), blood and wound swabs (6.66%), pus (3.33%), bile aspirate (2.22%), and deep tissue (1.11%). A larger number of females were affected than males, and the age group of 51 to 60 years was more susceptible to candidiasis. A higher number of C. albicans isolates produced biofilm followed by C. parapsilosis, C. tropicalis, and C. krusei. However, C. glabrata showed no biofilm production in our study. All Candida isolates were 100% sensitive to amphotericin B. Voriconazole was the next effective drug with 81.11% susceptibility. 24.44% of strains were resistant to fluconazole. Conclusion Speciation of Candida isolates, detection of ability to form the biofilm, and monitoring of antifungal susceptibility testing are necessary for appropriate treatment.

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“…This review does not cover in detail the literature on the signal transduction pathways that regulate gene expression during biofilm formation, the genes that are differentially regulated, or the molecular mechanisms regulating matrix formation or drug resistance, unless that information pertains to the specific aim set forth. The reader is directed to a number of excellent reviews on these subjects, published in the past several years (47)(48)(49)(50)(51)(52)(53)(54)(55).…”

mentioning

confidence: 99%

Plasticity of Candida albicans Biofilms

Soll

Daniels

2016

Microbiol Mol Biol Rev

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SUMMARYCandida albicans, the most pervasive fungal pathogen that colonizes humans, forms biofilms that are architecturally complex. They consist of a basal yeast cell polylayer and an upper region of hyphae encapsulated in extracellular matrix. However, biofilms formedin vitrovary as a result of the different conditions employed in models, the methods used to assess biofilm formation, strain differences, and, in a most dramatic fashion, the configuration of the mating type locus (MTL). Therefore, integrating data from different studies can lead to problems of interpretation if such variability is not taken into account. Here we review the conditions and factors that cause biofilm variation, with the goal of engendering awareness that more attention must be paid to the strains employed, the methods used to assess biofilm development, every aspect of the model employed, and the configuration of theMTLlocus. We end by posing a set of questions that may be asked in comparing the results of different studies and developing protocols for new ones. This review should engender the notion that not all biofilms are created equal.

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Candida Biofilms: Development, Architecture, and Resistance

Cited by 132 publications

References 154 publications

Repurposing Approach Identifies Auranofin with Broad Spectrum Antifungal Activity That Targets Mia40-Erv1 Pathway

Repurposing Approach Identifies Auranofin with Broad Spectrum Antifungal Activity That Targets Mia40-Erv1 Pathway

Antifungal Susceptibility and Biofilm Production of Candida spp. Isolated from Clinical Samples

Plasticity of Candida albicans Biofilms

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