Latest News on Candida Albicans Research: Jan – 2020

Virulence factors of Candida albicans

Candidiasis may be a common infection of the skin, mouth and esophagus, alimentary canal , vagina and system of humans. Although most infections occur in patients who are immunocompromised or debilitated in another way, the organism most frequently liable for disease, Candida albicans , expresses several virulence factors that contribute to pathogenesis. These factors include host recognition biomolecules (adhesins), morphogenesis (the reversible transition between unicellular yeast cells and filamentous, growth forms), secreted aspartyl proteases and phospholipases. Additionally, ‘phenotypic switching’ is amid changes in antigen expression, colony morphology and tissue affinities in C. albicans and a number of other other Candida spp. [1]

Candida albicans pathogenicity mechanisms

The polymorphic fungus Candida albicans may be a member of the traditional human microbiome. In most people , C. albicans resides as a lifelong, harmless commensal. Under certain circumstances, however, C. albicans can cause infections that range from superficial infections of the skin to life-threatening systemic infections. Several factors and activities are identified which contribute to the pathogenic potential of this fungus. Among them are molecules which mediate adhesion to and invasion into host cells, the secretion of hydrolases, the yeast-to-hypha transition, contact sensing and thigmotropism, biofilm formation, phenotypic switching and a variety of fitness attributes. Our understanding of when and the way these mechanisms and factors contribute to infection has significantly increased during the last years. [2]

Isogenic strain construction and gene mapping in Candida albicans.

Genetic manipulation of Candida albicans is constrained by its diploid genome and asexual life cycle. Recessive mutations aren’t expressed when heterozygous and undesired mutations introduced within the course of random mutagenesis can’t be removed by genetic back-crossing. to bypass these problems, we developed a genotypic screen that permitted identification of a heterozygous recessive mutation at the URA3 locus. The mutation was introduced by targeted mutagenesis, homologous integration of remodeling DNA, to avoid introduction of extraneous mutations. The ura3 mutation was rendered homozygous by a second round of transformation leading to a Ura- strain otherwise isogenic with the parental clinical isolate. [3]

Identification of a Phenylthiazole Small Molecule with Dual Antifungal and Antibiofilm Activity Against Candida albicans and Candida auris

Candida species are a number one source of healthcare infections globally. The limited number of antifungal drugs combined with the isolation of Candida species, namely C. albicans and C. auris, exhibiting resistance to current antifungals necessitates the event of latest therapeutics. this study tested 85 synthetic phenylthiazole small molecules for antifungal activity against drug-resistant C. albicans. Compound 1 emerged because the most potent molecule, inhibiting growth of C. albicans and C. auris strains at concentrations starting from 0.25–2 µg/mL. Additionally, compound 1 inhibited growth of other clinically-relevant yeast (Cryptococcus) and molds (Aspergillus) at a degree as low as 0.50 µg/mL. Compound 1 exhibited rapid fungicidal activity, reducing the burden of C. albicans and C. [4]

Viability Kinetic Profile, Morphological Structure, and Physicochemical Characterization of Candida albicans Biofilm on Latex Silicone Surfaces

Biofilm formed by Candida albicans on latex silicone surfaces was characterized by instrumental techniques like microscopy , scanning microscopy , and Fourier transform infrared spectroscopy. the expansion and viability of C. albicans on the biofilm formed were described using different kinetic rate equations. C. albicans biofilm features a complex and heterogenous structure with hyphal elements and yeast cells entrenched within a polysaccharide matrix. Spectroscopic studies revealed specific stretching frequencies of O-H, C-O, and C=O which may be attributed to the presence of some functionalities within the biofilm formed by C. albicans. Viability of C. albicans behaved in accordance with the primary -order kinetic equation on the first 48 h, then shifted to a second-order kinetic equation until the 72 h, and had a doubling time of 70 h. [5]

Reference

[1] Calderone, R.A. and Fonzi, W.A., 2001. Virulence factors of Candida albicans. Trends in microbiology, 9(7), (Web Link)

[2] Mayer, F.L., Wilson, D. and Hube, B., 2013. Candida albicans pathogenicity mechanisms. Virulence, 4(2), (Web Link)

[3] Fonzi, W.A. and Irwin, M.Y., 1993. Isogenic strain construction and gene mapping in Candida albicans. Genetics, 134(3), (Web Link)

[4] Identification of a Phenylthiazole Small Molecule with Dual Antifungal and Antibiofilm Activity Against Candida albicans and Candida auris
Haroon Mohammad, Hassan E. Eldesouky, Tony Hazbun, Abdelrahman S. Mayhoub & Mohamed N. Seleem
Scientific Reports volume 9, (Web Link)

[5] Erl P. Sumalapao, D., C. Cabrera, E., C. Flores, M. J., M. Amalin, D., R. Villarante, N., T. Altura, M. and G. Gloriani, N. (2018) “Viability Kinetic Profile, Morphological Structure, and Physicochemical Characterization of Candida albicans Biofilm on Latex Silicone Surfaces”, Annual Research & Review in Biology, 24(3), (Web Link)

Leave a Reply

Your email address will not be published. Required fields are marked *