As a leading company in the field of biological research and drug discovery, Creative Biolabs has gained a wealth of good reputation for successfully completed numerous challenges in antifungal drug discovery. Based on our advanced technology platform and experienced scientists, we are able to provide a series of antifungal drug discovery services against various fungal diseases and related fungi. Here, we describe a pathogenic fungus Malassezia furfur that can cause tinea versicolor.

Introduction

Malassezia furfur (M. furfur), named as Pityrosporum ovale previously, is a yeast-like fungus causing various human skin manifestations including tinea versicolor, seborrhoeic dermatitis, dandruff, etc. It is a fungus belonging to genus Malassezia, family Malasseziaceae, order Malasseziales, class Exobasidiomycetes, division Basidiomycota.

Malassezia species, known as Pityriasis previously, are basidiomycetous yeasts and are only species as a part of the normal skin flora of humans and animals. M. furfur is a lipophilic yeast that requires an abundant environment in fats and lipid for growth and grows best around 35 °C. The fungus is found worldwide but is more prevalent in tropical or subtropical climate regions, which is more suited for its growth.

Mycology of M. furfur

M. furfur is a polymorphic anthropophilic microorganism characterized by a thick, multilayered cell wall. It is spherical-shaped and has a distinguishing bottleneck at one end.

  • Macroscopically, M. furfur must be cultured in the medium supplemented with fatty acids. Colonies are usually smooth, shiny, and white to cream later becoming dull and beige.
  • Microscopically, M. furfur is usually found in single-cell but can form hyphae when they become pathogenic. Each produces a single phialoconidium followed by successive budding at a single location. Hyphae, rarely produced in culture, are septate and hyaline without a branch. Conidia resemble budding yeast cells and are approximately 3 micrometers in diameter. M. furfur cells contain a plasma membrane, a thick and multilaminar cell wall, mitochondria, a nucleus, and other vital organelles.

Macroscopic and microscopic phenotypes of M. furfur. Fig.1 Macroscopic and microscopic phenotypes of M. furfur.

Pathogenesis of M. furfur

Studies indicated that M. furfur can produce several important molecules, such as tryptophan aminotransferase, β-glucosidase, various cytokine, chemokine, and adhesion molecules. This allows M. furfur to prevent infection by breaking down the cell walls of other microorganisms on our skin cells which kills the organism. M. furfur is the primary causative agent of tinea versicolor when the fungus population levels grow out of control.

Drugs like indoles impede neutrophils that would normally kill the excess M. furfur and start inflammation. Meanwhile, indirubin and indolo[3,2-b]carbazole prevent the dendritic cells from maturing properly. Moreover, it is hypothesized that Melassazin has been linked to apoptosis regulation of melanocytes. All of these cause the characteristic discoloration of the skin. Therefore, treatment of tinea versicolor should diminish the fungal levels back to a healthy range rather than eradicate the fungus.

If you are interested in the fungal disease-related services, please contact us for more detailed information.

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