Malassezia furfur

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Classification

Eukarya/Eukaryota/Fungi; Basidiomycota; Exobasidiomycetes; Malasseziales; Malassaziaceae [1]

Malassezia furfur

Description and Significance

Malassezia furfur is a fungus, specifically a yeast, that is approximately 1.5-4.5 μm wide and 2-6 μm long [2]. It is spherical (coccal) in shape and has a distinguishing bottleneck at one end. Interestingly, Malassezia are essentially the only species of fungi that are part of the flora on humans (and other animals). This makes them important in studying how fungi interact with our epithelial cells.Malassezia furfur is believed to be the causative agent in various dermatological disorders including Pityriasis versicolor, Seborrheic dermatitis, and dandruff. Malassezia furfur is usually found in single-cell individuals but unlike most other Malassezia species, Malassezia furfur forms filaments when it becomes its pathogenic form [3]. Like most of its genus, Malassezia furfur is a lipophilic yeast meaning it requires an environment high in fats and oils to flourish, and grows best around 35 °C. If grown in culture, cultures are usually smooth and cream to tan in color [4].

Structure, Metabolism, and Life Cycle

Malassezia fufur is coccal, and their cells contain a plasma membrane, a thick and multilaminar cell wall composed of chitin with an invagination characteristic of Malassezia [4], mitochondria, a nucleus, and all of the other vital organelles [5]. However, their cells contain a collarette at the end, giving them a unique bottle-necked shape [2]. In addition, they are usually single-celled but can form hyphae when they become pathogenic. M. furfur requires fatty acids from human skin to survive and it is also their carbon source. These fatty acids must be medium-length or long-chain fatty acids.Specifically, they like oleic, arachidic, stearic, and palmitic acids as well as several Tween compounds [5]. As such, they must produce an enzyme capable of using these fatty acids. Unfortunatley, we do not yet know what this enzyme is as scientists still don't know a whole lot about Malassezia. An important molecule produced by Malassezia furfur is tryptophan aminotransferase, which converts L-tryptophan to indolepyruvate [3] by transferring an amino group. Also produced is Β-Glucosidase, which allows Malassezia furfur to free up glucose by breaking down cellulose, the primary carbohydarate in plant and prokaryote cell walls. This allows M. furfur to break down the cell walls of other microorganisms on our skin cells which kills the organism. This can help prevent infection. Finally, M. furfur produces various cytokine, chemokine, and adhesion molecules. The cytokines help to regulate the inflamation response of the host, the chemokines help direct cell movement, and the adhesion molecules help Malassezia furfur stick to the epithelial layer.

Malassezia furfur reproduces asexually. It buds off in a monopolar fashion, leaving the distinctive collarette from which future Malassezia furfur can bud off [4]. However, M. furfur does not undergo telophase unlike most other organisms. M. furfur will also undergo unipolar budding rarely to produce the pathogenic hyphae (filamentous, branched yeast). Eventually, the mother cell undergoes too many buddings and the mother cell dies [5]. All of this occurs on human skin.


Ecology and Pathogenesis

Malassezia furfur lives on the epithelial cells of humans where it consumes the natural oils and fats we excrete. It can be found mostly on the chest, shoulders, and arms, and is more prevalent on people of Caucasian descent and adults over the age of 12 [4]. Malassezia furfur is the primary causative agent of Pityriasis versicolor, a skin disease in humans that causes either hyperpigmentation or hypopigmentation of the skin, scaly, slow-growing skin, and itchiness [6]. It's caused when Malassezia furfur population levels grow out of control. First, indoles like pityriarubins impede neutrophils (white-blood cells)that would normally kill the excess Malassezia furfur and start inflammation [3]. Meanwhile, indirubin and indolo[3,2-b]carbazole prevent the dendritic cells from maturing properly causing the characteristic discoloration of the skin. Also, Melassazin has been linked to apoptosis regulation of melanocytes, melanin-producing cells, and it is hypothesized that pityriacitrin has UV-absorbent properties that help to protect the fungus from UV radiation, though this has never been proven. Treatment centers not around eradicating the fungus, but instead diminishing poplulation levels back to a healthy range. Usually, a fungicidal shampoo or topical ointment is used.

Malassezia furfur has also been linked to Seborrheic dermatitis, a disease that causes skin lesions, large plaques,greasy, oily skin, dandruff, itching, redness, and hair-loss [7]. Malassezia furfur causes Seborrheic dermatitis when the skin, and consequently the fungus, are exposed to stress like UV radiation or other microorganisms. While nothing is known about the definitive pathogenesis, one proposed theory is aryl hydrocarbon receptor (AhR) ligands and its interaction with epidermal growth factor receptor (EGFR)may play a part [3]. It is also hypothesized that the increased production of inflammatory mediators (interleukin-1α [IL-1α], IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, gamma interferon [IFN-γ], and tumor necrosis factor alpha [TNF-α]) in infected skin cells caused by Melassezia furfur, and the Malassezia genus in general, may play a role. However, this has not been proven experimentally yet as their levels have been shown to vary between afflicted individuals and healthy individuals, but not between infected skin and healthy skin from the same patient. This suggests there may be a genetic component involved.

Finally, Malassezia furfur has been documented to be a cause for Onychomycosis [8], an infection of the nail bed that causes nail discolorattion and nail toughness. It can also cause, in rare cases, the nail to become brittle and pain in the skin under the nail. Onychomycosis occurs when trauma is inflicted upon the nail, giving the fungus a chance to infect the nail bed. However, other species of fungus, including Candida albicans, are much more likely to cause Onychomycosis. Malassezia furfur may also cause allergic reactions. Allergens produced include Mala f 2 (peroxisomal membrane protein), Mala f 3 (peroxisomal membrane protein), and Mala f 4(mitochondrial malate dehydrogenase) [3].

References

[1] "Malassezia furfur. National Center for Biotechnology Information. http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=55194

[2] "Malassezia furfur". Wikipedia http://it.wikipedia.org/wiki/Malassezia_furfur

[3] Gaitanis, G., Magiatis, P., Hantschke, M., Bassukas, I.D., Velegraki, A. 2012. "The Malassezia Genus in Skin and Systemic Diseases". Clinical Microbiology Reviews. 1: 106-141. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255962/

[4] Marcon, M.J., Powell, D.A. 1992. "Human Infections Due to Malassezia spp". Clinical Microbiology Reviews. 5.2: 101-119. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC358230/pdf/cmr00039-0009.pdf

[5] Slonczewski, J.L., Foster, J.W. 2011. "Microbiology: An Evolving Science 2 ed.". Norton. 761-769;A-21-A-22

[6] Mayo Clinic Staff. 2010. "Tinea versicolor: Symptoms". Mayo Clinic. http://www.mayoclinic.com/health/tinea-versicolor/DS00635/DSECTION=symptoms

[7] 2011. "Seborrheic dermatitis: Dandruff; Seborrheic eczema; Cradle cap". A.D.A.M. Medical Encyclopedia. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001959/

[8] Chowdhary, A., Randhawa, HS., Sharma, S., Brandt, M.E., Kumar, S. 2005. "Malassezia furfur in a case of onychomycosis: colonizer or etiologic agent?". Medical Mycology. 43: 87–90. http://www.ncbi.nlm.nih.gov/pubmed/15712613


Author

Page authored by Shayne Haag, student of Mandy Brosnahan, Instructor at the University of Minnesota-Twin Cities, MICB 3301/3303: Biology of Microorganisms.