Malassezia sympodialis

Malassezia sympodialis is a species in the genus Malassezia.[2] It is characterized by a pronounced lipophily, unilateral, percurrent or sympodial budding and an irregular, corrugated cell wall ultrastructure.[3][4] It is one of the most common species found on the skin of healthy and diseased individuals.[5] It is considered to be part of the skin's normal human microbiota[2][6] and begins to colonize the skin of humans shortly after birth.[7] Malassezia sympodialis, often has a symbiotic or commensal relationship with its host, but it can act as a pathogen causing a number of different skin diseases,[8] such as atopic dermatitis.[8][9]

Malassezia sympodialis
Scientific classification
Kingdom:
Fungi
Division:
Basidiomycota
Class:
Exobasidiomycetes
Order:
Malasseziales
Family:
Malasseziaceae
Genus:
Malassezia
Species:
M. sympodialis
Binomial name
Malassezia sympodialis
Simmons & Gueho, 1990[1]

History

In 1846, Karl Ferdinand Eichstedt was the first to identify the association of fungi with pityriasis versicolor, a common infection associated with the genus Malassezia.[8] The name applied to the fungal agent responsible shifted multiple times over the next 150 years until the genus Pityrosporum was settled upon for the teleomorph, and Malassezia for the anamorph.[8][9] Through the use of genetic sequencing, a number of new species have since been identified.[2][8][10]

Description

Malassezia sympodialis exhibits unipolar budding,[3][5] similar to a number of other Malassezia species including M. pachydermatis.[5] The colonies achieve a size of 5 mm in diameter after a week of growth, and develop a soft texture and a round, smooth shape.[11] The individual cells are oval in shape[4][10][11] and 2.5-7.5 × 2.0-8.0 μm in size and acquire a yellowish appearance en masse when grown in culture at 37 °C (99 °F).[10] The optimal growth of this species occurs at 34 °C (93 °F).[10] A range of specialized growth media such as Cremophor EL and Leeming-Notman agar that incorporate fatty acids support the growth of M. sympodialis.[3][12] However, non-specialized growth media overlaid with sterile olive oil also support the growth of this species in culture.[10] Malassezia sympodialis can be identified in the laboratory by the presence of β-glucosidase activity which causes darkening of the growth medium.[3]

Pathogenicity in humans and animals

The innate and adaptive immune systems are both important for the health of the skin.[5] There are several different types of cells, such as neutrophils, that search their environment for antigens by using pattern recognition receptors and are essential in the innate immune response.[13] Malassezia sympodialis causes atopic eczema in susceptible individuals.[2] Many of the skin diseases caused by this species occur when the barrier of the skin is breached, allowing the organism to access the damaged integument,[5] such as occurs in individuals infected with atopic eczema.[14] The M. sympodialis peptide LL-37 is found in monocyte-derived dendritic cells where it is involved in initiating a Th-2 like response.[13] The Th-2 like response is involved in the creation of IgE and is therefore important for individuals with atopic eczema.[13] There are several factors that contribute to the development of atopic eczema, including the environment and genetics.[14]

Human diseases

Malassezia sympodialis has been identified conjunction with a number of human skin disorders include pityriasis versicolor, seborrheic dermatitis and dandruff and atopic dermatitis.[5] There have also been reports of M. sympodialis in patients with granulomatous dermatitis.[15]

Pityriasis versicolor

Pityriasis versicolor is a skin disorder that leads to the formation of patches on the skin that are either hypo- or hyperpigemented.[5] It may be found on oilier areas of the body including the neck and trunk.[5] Besides M. sympodialis, several species of Malassezia have been identified on individuals with the disorder including, M. globosa, M. slooffiae and several others.[5] Some believe that M. globosa is responsible for the disease as it has been found in higher numbers, but this has not yet been confirmed.[5] Confirmation of the agent of disease involves microscopic examination of skin scrapings from the infected individuals for the presence of thick-walled yeast cells intermixed with broad hyphae.[5] Ointments containing fungicidal ingredients such as selenium can be applied to the affected area.[5] Oral medications are also used in some cases.[5]

Seborrhoeic dermatitis and dandruff

Seborrheic dermatitis is a skin disorder where inflammation and desquamation occurs in areas of the body with a high density of sebaceous glands, particularly the face and trunk.[5] The dandruff form does not result in inflammation and is restricted to the scalp.[5] Although 'M. sympodialis has been reported as an agent of seborrhoeic dermatitis and dandruff, other species including M. furfur and M. globosa are more commonly associated with the disorder.[5]

Atopic dermatitis

Atopic dermatitis occurs in individuals that have an abnormal immune reaction to allergens resulting in inflammation on the affected area of the skin.[5] This disorder is associated with M. furfur, M. restricta, M. sympodialis and a number of other species.[5]

Animal diseases

Malassezia sympodialis has been identified in high frequency on dogs that have some form of dermatitis and is found in association with other species of Malassezia.[16] This species has also been associated with otitis in cattle, cats and other animals.[5]

gollark: I've gotten 6 coppers so far. 6 have been male. Why must you do this, RNG?
gollark: The AP has almost hit ER times.
gollark: BSA idea: recover an egg you AP'd as long as it's actually in the AP still.
gollark: I think a lot of people actually just hit up against the weekly limit though.
gollark: Ah.

References
  1. Simmons, Robert B.; Gueho, Eveline (December 1990). "A new species of Malassezia". Mycological Research. 94 (8): 1146–1149. doi:10.1016/S0953-7562(09)81349-X.
  2. Gaitanis, G.; Magiatis, P.; Hantschke, M.; Bassukas, I. D.; Velegraki, A. (9 January 2012). "The Malassezia Genus in Skin and Systemic Diseases". Clinical Microbiology Reviews. 25 (1): 106–141. doi:10.1128/CMR.00021-11. PMC 3255962. PMID 22232373.
  3. Howard, Dexter H. (2007). Pathogenic fungi in humans and animals (2nd ed.). New York, NY: Dekker. ISBN 978-0824706838.
  4. de Hoog, G. S. (2000). Atlas of clinical fungi (2. ed.). Utrecht: Centraalbureau voor Schimmelcultures [u.a.] ISBN 9070351439.
  5. Chen, Tai-an; Hill, Peter B. (February 2005). "The biology of Malassezia organisms and their ability to induce immune responses and skin disease". Veterinary Dermatology. 16 (1): 4–26. doi:10.1111/j.1365-3164.2005.00424.x. PMID 15725101.
  6. Gehrmann, Ulf; Qazi, Khaleda Rahman; Johansson, Catharina; Hultenby, Kjell; Karlsson, Maria; Lundeberg, Lena; Gabrielsson, Susanne; Scheynius, Annika; Zimmer, Jacques (22 July 2011). "Nanovesicles from Malassezia sympodialis and Host Exosomes Induce Cytokine Responses – Novel Mechanisms for Host-Microbe Interactions in Atopic Eczema". PLoS ONE. 6 (7): e21480. doi:10.1371/journal.pone.0021480. PMC 3142114. PMID 21799736.
  7. Cabanes, F.J. (2014). "Malassezia Yeasts: How Many Species Infect Humans and Animals?". PLoS Pathogens. 10 (2): e1003892. doi:10.1371/journal.ppat.1003892. PMC 3937305. PMID 24586146.
  8. Gaitanis, Georgios; Velegraki, Aristea; Mayser, Peter; Bassukas, Loannis D. (July 2013). "Skin diseases associated with Malassezia yeasts: Facts and controversies". Clinics in Dermatology. 31 (4): 455–463. doi:10.1016/j.clindermatol.2013.01.012. PMID 23806162.
  9. Scheynius, A; Johansson, C; Buentke, E; Zargari, A; Linder, MT (March 2002). "Atopic eczema/dermatitis syndrome and Malassezia". International Archives of Allergy and Immunology. 127 (3): 161–9. doi:10.1159/000053860. PMID 11979041.
  10. Kurtzman, Cletus P.; Fell, Jack W. (1998). The yeasts : a taxonomic study (4th ed.). Amsterdam: Elsevier. pp. 783–784. ISBN 0444813128.
  11. Guého, E.; Midgley, G.; Guillot, J. (May 1996). "The genus Malassezia with description of four new species". Antonie van Leeuwenhoek. 69 (4): 337–355. doi:10.1007/BF00399623. PMID 8836432.
  12. Kaneko, T.; Makimura, K.; Abe, M.; Shiota, R.; Nakamura, Y.; Kano, R.; Hasegawa, A.; Sugita, T.; Shibuya, S.; Watanabe, S.; Yamaguchi, H.; Abe, S.; Okamura, N. (19 September 2007). "Revised Culture-Based System for Identification of Malassezia Species". Journal of Clinical Microbiology. 45 (11): 3737–3742. doi:10.1128/JCM.01243-07. PMC 2168522. PMID 17881545.
  13. Agerberth, B.; Buentke, E.; Bergman, P.; Eshaghi, H.; Gabrielsson, S.; Gudmundsson, G. H.; Scheynius, A. (April 2006). "Malassezia sympodialis differently affects the expression of LL-37 in dendritic cells from atopic eczema patients and healthy individuals". Allergy. 61 (4): 422–430. doi:10.1111/j.1398-9995.2005.00952.x. PMID 16512803.
  14. Schmid-Grendelmeier, Peter; Scheynius, Annika; Crameri, Reto (2006). "The role of Sensitization to Malassezia sympodialis in Atopic Eczema". Chemical Immunology and Allergy. 91: 98–109. doi:10.1159/000090246. ISBN 3-8055-8000-2. PMID 16354952.
  15. Desai, H.B.; Perkins, P.L.; Procop, G.W. (2011). "Granulomatous dermatitis due to malassezia sympodialis". Archives of Pathology & Laboratory Medicine. 135 (9): 1085–1087. doi:10.5858/2010-0588-crr.1. PMID 21877990. ProQuest 887762913.
  16. Nardoni, S.; Mancianti, F.; Corazza, M.; Rum, A. (May 2004). "Occurrence of Malassezia species in healthy and dermatologically diseased dogs". Mycopathologia. 157 (4): 383–388. doi:10.1023/B:MYCO.0000030416.36743.dd. PMID 15281400.
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