Malassezia

Ashbee, H. R.; Scheynius, Annika

doi:10.1007/978-3-642-03150-2_10

Cited by 9 publications

(17 citation statements)

References 144 publications

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“…Malassezia is a monophyletic genus of fungi found on the skin of seven billion humans and associated with a variety of conditions, including dandruff, seborrheic dermatitis, atopic eczema/dermatitis, pityriasis versicolor, and folliculitis [8]. Recently, this genus represents a hot topic of basic research on taxonomy, physiology, biochemistry, ecology, immunology, and metabolomics [2].…”

Section: Etiology Of Seborrheic Dermatitismentioning

confidence: 99%

New Insights into the Etiopathogenesis of Seborrheic Dermatitis

Argirov¹,

Bakardzhiev²

2017

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Seborrheic dermatitis represents a chronic, widespread skin disease that is considered a multifactorial disorder influenced, in part, by Malassezia spp.opportunistic activities as well as by various endogenous and exogenous factors. This review systematizes the recent scientific achievements in the field of insufficiently elucidated etiology and pathogenesis of seborrheic dermatitis. IntroductionSeborrheic dermatitis is initially described by P. G. Unna in 1887 and the association with Malassezia yeasts is accepted up to the middle of the 20th century, when the observed increased epidermal cell turnover gradually prompts researchers to characterize this condition as being intrinsic to the skin[1, 2].Seborrheic dermatitis is common dermatological problem that affects the seborrheic areas of the body. It is considered the same basic condition like dandruff sharing many features and responding to similar treatments, differing only in locality and severity. Current use of varying terms for seborrheic dermatitis such as sebopsoriasis, seborrheic eczema, dandruff, and pityriasis capitis reflects the complex nature of this common skin pathology [3]. Much controversy remains regarding the pathogenesis of seborrheic dermatitis and its classification in the spectrum of cutaneous diseases as a form of dermatitis, a fungal disease, or an inflammatory disease, closely related with psoriasis.The prevalence of seborrheic dermatitis peaks when sebaceous gland activity is high, during the first three months of life (infantile seborrheic dermatitis), during puberty and when sebum excretion is reduced after the age of 50 years [2]. Because of smaller sebum production, seborrheic dermatitis flares occur more often in spring than in summer. Disease flare could be associated with altered population dynamics affected not only by variations in sebaceous gland activity but also by modifications in other nutrients supplied by sweat, such as essential amino acids like glycine and tryptophan.Glycine stimulates the fast growth of M. furfur and after its exhaustion yeast cells employ tryptophan as a nitrogen source, increasing the production of indolic metabolites [4]. Such cycles of population growth, bioactive indole production, and subsequent deprivation of nutrients result in insufficiently masked antigens and ligands on the surface of the yeast cells leading to immune system activation.Seborrheic dermatitis occurs on the scalp as well as on face, retroauricular area, and the upper chest, causing flaking, scaling, inflammation, pruritus, and, sometimes, marked erythema [5]. Flaking is usually white-to-yellowish, and may be oily or dry. Various intrinsic and environmental factors, such as sebaceous secretions, skin surface fungal colonization, individual susceptibility, and interactions between these factors play a pathogenetic role in seborrheic dermatitis. Etiology of Seborrheic DermatitisThere are three principal factors that play a role in the etiology of seborrheic dermatitis [6]: sebaceous gland secretion, alteration in col...

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Section: Etiology Of Seborrheic Dermatitismentioning

confidence: 99%

New Insights into the Etiopathogenesis of Seborrheic Dermatitis

Argirov¹,

Bakardzhiev²

2017

CRDOA

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“…With a plethora of lipase genes, M. globosa likely satisfies its lipid requirement by hydrolysis of sebum triglycerides. Within the genus, only Malassezia pachydermatis , isolated from dogs and other non-human animals [5], is known to grow in the absence of exogenous lipid [1]. It will be interesting to learn whether this atypical species contains a fatty acid synthase gene similar to that found in the close relative Ustilago maydis and whether the habitat requirements of M. pachydermatis are, as a consequence, less stringent by relieving the requirement for exogenous lipids.…”

Section: What Is Known About the Gene Content Of Malassezia?mentioning

confidence: 99%

“…IgG and IgM specific to Malassezia can be detected in healthy individuals [1]. The defective skin barrier in AE patients, both in lesional and non-lesional skin, fails to provide sufficient protection against microbes and allergens, facilitating interactions with Malassezia and the host immune system.…”

Section: How Does Malassezia Interact With the Host?mentioning

confidence: 99%

“…Restoring the epidermal-barrier function and avoiding IgE sensitization are major targets for the prevention and treatment of AE [1]. It is important to stress that while there is some evidence that anti-fungal therapies may be of clinical benefit in patients with eczema associated with M. sympodialis , the vast majority of patients are treated with topical steroids or other immunosuppressive agents.…”

Section: How Do People Treat or Eradicate Malassezia From Their Skin?mentioning

confidence: 99%

“…Malassezia is a monophyletic genus of fungi found on the skin of 7 billion humans and associated with a variety of conditions, including dandruff, atopic eczema (AE)/dermatitis, pityriasis versicolor, seborrheic dermatitis, and folliculitis ([1], [2]; Figure 1). In immunocompromised hosts Malassezia can also cause systemic infections.…”

Section: Introductionmentioning

confidence: 99%

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Malassezia Fungi Are Specialized to Live on Skin and Associated with Dandruff, Eczema, and Other Skin Diseases

2012

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Resistance to antifungals that target CYP51

et al. 2014

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Fungal diseases are an increasing global burden. Fungi are now recognised to kill more people annually than malaria, whilst in agriculture, fungi threaten crop yields and food security. Azole resistance, mediated by several mechanisms including point mutations in the target enzyme (CYP51), is increasing through selection pressure as a result of widespread use of triazole fungicides in agriculture and triazole antifungal drugs in the clinic. Mutations similar to those seen in clinical isolates as long ago as the 1990s in Candida albicans and later in Aspergillus fumigatus have been identified in agriculturally important fungal species and also wider combinations of point mutations. Recently, evidence that mutations originate in the field and now appear in clinical infections has been suggested. This situation is likely to increase in prevalence as triazole fungicide use continues to rise. Here, we review the progress made in understanding azole resistance found amongst clinically and agriculturally important fungal species focussing on resistance mechanisms associated with CYP51. Biochemical characterisation of wild-type and mutant CYP51 enzymes through ligand binding studies and azole IC50 determinations is an important tool for understanding azole susceptibility and can be used in conjunction with microbiological methods (MIC50 values), molecular biological studies (site-directed mutagenesis) and protein modelling studies to inform future antifungal development with increased specificity for the target enzyme over the host homologue.

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Malassezia

Cited by 9 publications

References 144 publications

New Insights into the Etiopathogenesis of Seborrheic Dermatitis

New Insights into the Etiopathogenesis of Seborrheic Dermatitis

Malassezia Fungi Are Specialized to Live on Skin and Associated with Dandruff, Eczema, and Other Skin Diseases

Resistance to antifungals that target CYP51

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