Malassezia sympodialis
1. Classification
a. Higher order taxa
Eukaryota; Opisthokonta; Fungi; Dikarya; Basidiomycota; Ustilaginomycotina; Malasseziomycetes; Malasseziales; Malasseziaceae; Malassezia; sympodialis (Schoch NCBI:txid76777).
Malassezia sympodialis belongs to the domain Eukarya, clade Opisthokonta, kingdom Fungi, subkingdom Dikarya, phylum Basidiomycota, subphylum Ustilaginomycotina; class Malasseziomycetes, order Malasseziales, family Malasseziaceae and genus Malassezia. Its species is sympodialis (Schoch NCBI:txid76777).
2. Description and significance
Malassezia sympodialis is an oval-shaped yeast fungus most commonly found on human skin. It was first recognized in Germany through the work of Karl Ferdinand Eichstedt in 1846 with patients presenting with pityriasis versicolor (Gueho et al 1996). Early studies on this microbe were difficult to conduct until their lipid-dependent nature was elucidated in 1927 (Acton & Panja 1927). This microbe grows best in the presence of a high concentration of fatty acids. The role of M. sympodialis in the skin microbiome is controversial because it is present on both healthy and diseased human skin. M. sympodialis causes certain skin infections such as atopic dermatitis and cephalic pustulosis. Advancements in research of this microbe are focused on more efficient drug discovery campaigns for better fungicides and antifungal agents. Additionally, it can benefit the medical community in the sense that understanding its pathogenicity allows for better diagnoses in how to treat its corresponding ailments. While studied in 1996 by Gueho and colleagues, their optimal growing conditions are at 37oC (with an upper limit of 40-41oC) in slightly acidic environments at about a pH of 6.0 (Gueho et al 1996). Morphologically, their yellowish colonies have an average diameter of 5 mm, with individual oval-shaped cells approximately 2 x 4 micrometers in size. This species is dimorphic, meaning it can take either the form of yeast or hyphae, yet the mechanism behind their morphological conversions remains poorly understood. Their method of reproduction is asexual in nature, occurring either through repetitive or sympodial budding. Their growth is heavily dependent on oxygen, suggesting this microbe is a facultative anaerobe (Madeleine & Mathias 2020).
3. Genome structure
The genome of M. sympodialis is 7.67 million base pairs long, yet members of this genus have relatively small genomes compared to other fungi (Gioti et al. 2013). It is hypothesized that their smaller genome structure is related to their reliance on animals. M. sympodialis has 3,517 protein coding genes in its genome, many of which code for enzymes that break down lipids. The mitochondrial genome of M. sympodialis is 38,622 base pairs long and contains 15 protein-coding genes, 2 ribosomal RNA genes, and 25 transcriptional RNA genes for all 20 amino acids, some of which have multiple tRNAs. Its mitochondrial genome contains a large inverted repeat of the ATP9 gene and inverted genes for methionine, leucine, and arginine transcriptional RNAs. This is uncommon for fungal mitochondrial DNA, and its role in M. sympodialis is unknown.
4. Cell structure
Malassezia sp. all share distinctive morphological features, including a thick, multi-layered cell wall and production of blastoconidia. Blastoconidia are produced through repetitive monopolar or symbodial budding which leaves a prominent scar on mother cells (Gueho et al 1996). M. sympodialis has ovoid cells with it’s base narrower than the mother cell but equal in width to the bud (Gueho et al 1996). Colonies of M. sympodialis are smooth and flat except for a small amount of central elevation (Gueho et al 1996). M. sympodialis appears to lack (1-->3)-beta-D-glucan in it’s cell wall. Instead, the M. sympodialis cell wall is mainly composed of (1-->6)-beta-D-glucan (Kruppa et al 2009).
5. Metabolic processes
Metabolically, the Malassezia species depends on lipids as a carbon source and uses fatty acids (FAs) to conduct a range of biological processes. Since FA synthase and other lipid-metabolism enzymes are absent in Malassezia sympodialis, it cannot make its own FAs (Lorch et al., 2018). Instead it acquires them from sebum produced by the sebaceous glands of human skin (Ro and Dawson, 2005). Sebum consists of nonpolar lipids like triglycerides, esters, squalene, fatty acids and smaller amounts of cholesterol, esters and diglycerides (Pappas, 2009). The organism uses a number of lipid-hydrolyzing enzymes to convert the lipids to FAs, including lipases, phospholipases C, and acid sphingomyelinases (Gioti et al., 2013). These FAs are then metabolized or modified for functions such as membrane biogenesis, energy homeostasis, and energy storage (Celis Ramirez et al., 2017). For a source of sulfur, Malassezia typically uses methionine but can use cystine or cysteine as well (Ashbee, 2002). The bacteria can obtain nitrogen from many amino acids and ammonium salts. It does not need any trace elements, vitamins, or electrolytes (Mayser et al., 1998).
6. Ecology
M. sympodialis lives on the epidermis of many organisms. The Malassezia sp. consists of lipid-dependent basidiomycetous yeast that live on the epidermis of humans and other warm blooded animals (Theelan et al. 2018). M. sympodialis is mainly found on human, horse, pig and sheep epidermis (Theelan et al. 2018). It was previously thought that Malassezia sp. were only found on the epidermis of their mammalian hosts, but new evidence suggests that they are found in a much broader amount of ecosystems such as in marine ecosystems and bilateral nematodes (Theelan et al. 2018).
7. Pathology
Malassezia yeasts are a significant aspect of the human skin microbiome of a healthy adult (Wu et al., 2015), and colonize an individual's skin shortly after birth (Nagata et al., 2012). However, multiple species of Malassezia are linked to human dermatological conditions ranging from mild diseases like seborrheic dermatitis (dandruff), atopic dermatitis, and eczema to more severe illnesses including serious infections and pancreatic cancer (Grice and Dawson, 2017). The primary factors of pathogenesis of eczema could be a mix of a disturbed skin barrier, genetic, and environmental factors like lifestyle, stress, allergens, and various microbes (Akdis et al., 2006). If a condition is left untreated, M. sympodialis can continue to induce recurrent and chronic skin infections, increasing the risk of complications with the serious diseases (Cattana et al., 2014). M. sympodialis is also one of the three Malassezia species found to be the cause of bloodstream infections (Ilahi et al., 2017). This can be attributed to its thick cell walls and biofilm formation (Celis et al., 2017).
8. Current Research
Much of the current research on M. sympodialis focuses on its interactions with humans, specifically its ability to cause skin diseases. Current research agrees that many of these diseases are caused or made worse by an allergic response to this yeast. M. sympodialis produces thioredoxin(Asgari et al 2019), an allergen produced by some fungi. It has been found that genes encoding TRX are expressed at a much higher rate when the microbe is inhabiting the skin of a person with pityriasis versicolor, a skin disease that leads to discoloration (Asgari et al 2019). Extracellular vesicles of M. sympodialis have also been found to carry allergens that contribute to eczema. These vesicles are able to increase the expression of a particular ligand, ICAM-1, on human skin cells that creates an allergic response by recruiting immune cells(Johansson et al 2020). Considering both TRX and the extracellular vesicles is important in understanding M. sympodialis as a cause of disease.
Another important area of study has been its interaction with antifungal agents. It has been found that the most effective against M. sympodialis are ketoconazole and itraconazole, while the least effective are fluconazole and amphotericin B (Cheng et al 2020). This discovery provides an argument for eventual discontinuation of fluconazole and amphotericin for conditions thought to involve the Malassezia species. However, the exact reason as to why ketoconazole and itraconazole are more effective remains unknown. Another finding reveals that UV radiation helps M. sympodialis to build up a greater tolerance to anti-fungal agents (Gharehbolagh et al 2019). Understanding how this fungus behaves under different conditions is crucial in the development of more effective treatments against fungal skin diseases.
9. References
Acton, H. W., and Panja, G. 1927. Seborrheic dermatitis or pityriasis capitis: a lesion caused by the Malassezia ovale. Indian Med. Gaz. 62:603-614.
Akdis, C. A., et al. 2006. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus report. J. Allergy Clin. Immunol. 118:152–169.
Asgari Y, et al. 2019. Thioredoxin is a potential pathogenesis attribute of Malassezia globosa and Malassezia sympodialis in pityriasis versicolor. Gene Reports 17:1004684.
Ashbee, H Ruth, and E Glyn V Evans. 2002. “Immunology of diseases associated with Malassezia species.” Clin. Microbiol. Rev. 15:1 21-57. doi:10.1128/CMR.15.1.21-57.2002.
Cattana, M. E., et al. 2014. Antifungal susceptibility of Malassezia furfur, Malassezia sympodialis, and Malassezia globosa to azole drugs and amphotericin B evaluated using a broth microdilution method. Medical Mycology 52:641–646.
Celis Ramirez, A. M., Wösten, H. A. B., Triana, S., Restrepo, S., and de Cock, J. J. P. A. 2017. Malassezia spp. beyond the mycobiota. SM Dermatol. J. 3:1019.
Cheng, L., et al. 2020. Susceptibilities of Malassezia strains from pityriasis versicolor, Malassezia folliculitis and seborrheic dermatitis to antifungal drugs. Heliyon 6:e04203.
Garehbolagh S et al. 2019. Effect of various ultraviolet radiation on antifungal susceptibility pattern and related genes expression in Malassezia sympodialis. Gene Reports 17:100506.
Gioti, A., Nystedt, B., Li, W., Xu, J., Andersson, A., Averette, A. F., et al. 2013. Genomic insights into the atopic eczema-associated skin commensal yeast Malassezia sympodialis. MBio 4:e00572-12.
Grice, E. A., and Dawson, T. L. 2017. Host-microbe interactions: malassezia and human skin. Curr. Opin. Microbiol. 40, 81–87. doi: 10.1016/j.mib.2017.10.024.
Guého, E., Midgley, G. and Guillot, J. 1996. The genus Malassezia with description of four new species. Antonie van Leeuwenhoek. 69, 337–355.
Ilahi, A., Hadrich, I., Goudjil, S., Kongolo, G., Chazal, C., Léké, A., et al. 2017. Molecular epidemiology of a Malassezia pachydermatis neonatal unit outbreak. Med. Mycol. 56: 69–77.
Johansson, C., et al. 2020. Extracellular vesicles released from the skin commensal yeast Malassezia sympodialis activate human primary keratinocytes. Frontiers in Cellular and Infection Microbiology 10:6.
Kruppa, Michael D., et al. 2009. Identification of (1→ 6)-β-d-glucan as the major carbohydrate component of the Malassezia sympodialis cell wall. Carbohydrate research 344.18: 2474-2479.
Lorch, J. M., Palmer, J. M., Vanderwolf, K. J., Schmidt, K. Z., Verant, M. L., Weller, T. J., et al. 2018. Malassezia vespertilionis sp. nov.: a new cold-tolerant species of yeast isolated from bats. Persoonia Mol. Phylogeny Evolut. Fungi 41: 56–70. doi: 10.3767/persoonia.2018.41.04.
Madeleine, S., and Mathias, R. 2020. Overview of the Potential Role of Malassezia in Gut Health and Disease. Front. Cell. Infect. Microbiol. 10, 201 .
Mayser, P., A. Imkampe, M. Winkeler, and C. Papvassilis. 1998. Growth requirements and nitrogen metabolism of Malassezia furfur. Arch. Dermatol. Res. 290:277–282.
Nagata, R. et al. 2012. Transmission of the major skin microbiota, Malassezia, from mother to neonate. Pediatr. Int. 54:350–355.
Pappas, A. 2009. “Epidermal surface lipids.” Dermatoendocrinol. 1:72-6. doi:10.4161/derm.1.2.7811.
Schoch, C. L., et al. 2020. NCBI Taxonomy: a comprehensive update on curation, resources and tools. Database (Oxford). baaa062. PubMed: 32761142 PMC: PMC7408187.
Theelen, B., et al. 2018. Malassezia ecology, pathophysiology, and treatment." Medical mycology 56.suppl_1: S10-S25.
Wu, G., Zhao, H., Li, C., Rajapakse, M. P., Wong, W. C., Xu, J., et al. 2015. Genus-wide comparative genomics of Malassezia delineates its phylogeny, physiology, and niche adaptation on human skin. PLoS Genet. 11:e1005614. doi: 10.1371/journal.pgen.1005614.
10. Authorship Statement
Rhianna Murphy completed the classification section of Malassezia sympodialis. Anthony Avila completed the introduction section of this wikipedia article. Annabel Mears completed the current research of this wikipedia article. Serena Yu, Rhianna Murphy and Douglas Alvarado contributed portions to Section 3: “Organisms-Key Points”. Everyone who used articles in their respective sections cited the articles correctly in the Works Cited section. Douglas Alvarado completed Section 5 Authorship Statement.
Edited by Rhianna Murphy, student of Jennifer Bhatnagar for BI 311 General Microbiology, 2021, Boston University.
