Susceptibilities of Malassezia strains from pityriasis versicolor, Malassezia folliculitis and seborrheic dermatitis to antifungal drugs

The incidence and prevalence of recalcitrant cutaneous fungal infections is on the rise. Terbinafine‐resistant Trichophyton has not only been widespread in India, but has also been reported in countries spread throughout the globe. Strains of yeasts such as Malassezia and Candida, which exist both as commensals and as pathogens to the human skin, have also been found to develop resistance to antifungals. Non‐dermatophyte moulds which can colonize and infect damaged nails are especially difficult to treat, not only due to resistance, but also because of poor drug penetration of hard keratin. Psychosocial factors such as the indiscriminate broad‐spectrum antifungal use in agriculture and in medicine, and poor adherence to hygienic measures to break the chain of infection contribute to the development of antifungal resistance. Such environments encourage fungi to develop various resistance mechanisms to withstand antifungal treatment. These include: (a) alteration of the drug target, (b) increasing efflux of drug/metabolites, (c) inactivation of drug, (d) bypass mechanisms or substitution of the pathway affected by the drug, (e) stress adaptation mechanisms and (f) biofilm formation. Understanding of such mechanisms and how they arise are crucial for development of new ways to prevent or overcome resistance. Novel antifungal treatments have recently been approved in the United States of America for treatment of vulvovaginal candidiasis. Ibrexafungerp (enfumafungin derivative) and oteseconazole (tetrazole) differ from their respective related drug classes of echinocandins and triazoles by having different structures, which lend these medicines advantage compared to traditional treatment by having a different binding site and more selectivity for fungi respectively. Other drugs designed to circumvent the known mechanisms of antifungal resistance are also at various phases of development. Concurrent measures at an institutional and individual level to address and limit inappropriate antifungal use to reduce development of antifungal resistance should be undertaken in a concerted effort to address this epidemic.

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“…remain sensitive. 2,8 Multidrug resistance in Candida spp. is mostly reported in the context of invasive candidiasis in the existing literature.…”

Section: Epidemiology Of Antifungal Resistance In Cutaneous Mycosesmentioning

confidence: 99%

Recalcitrant cutaneous fungal infections—A growing problem

Koh

Pan

2023

Aust J Dermatology

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“…Tinea versicolor is caused by dimorphic lipophilic and lipid-dependent yeasts in the genus Malassezia (formerly known as Pityrosporum) species, notably Malassezia globosa (M. globose), M. furfur and M. sympodialis. [2][3][4][5][6][7][8][9][10][11][12] Other species that have been implicated include M. restricta, M. obtuse, M. slooffiae, M. pachydermatis and M. japonica. [13][14][15][16] These yeasts are normal commensals on the skin surface.…”

Section: Review Aetiopathogenesismentioning

confidence: 99%

“…globose ), M. furfur and M. sympodialis . 2 – 12 Other species that have been implicated include M. restricta , M. obtuse , M. slooffiae , M. pachydermatis and M. japonica . 13 – 16 These yeasts are normal commensals on the skin surface.…”

Section: Reviewmentioning

confidence: 99%

Tinea versicolor: an updated review

Leung¹,

Barankin²,

Lam³

et al. 2022

DIC

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A search was conducted in July 2022 in PubMed Clinical Queries using the key terms "tinea versicolor" OR "pityriasis versicolor". The search strategy included all clinical trials (including open trials, non-randomized controlled trials and randomized controlled trials), observational studies and reviews (including narrative reviews and meta-analyses) published within the past 10 years. Only papers published in the English literature were included in this review. The information retrieved from the search was used in the compilation of this article. Review AetiopathogenesisTinea versicolor is caused by dimorphic lipophilic and lipid-dependent yeasts in the genus Malassezia (formerly known as Pityrosporum) species, notably Malassezia globosa (M. globose), M. furfur and M. sympodialis. [2][3][4][5][6][7][8][9][10][11][12] Other species that have been implicated include M. restricta, M. obtuse, M. slooffiae, M. pachydermatis and M. japonica. [13][14][15][16] These yeasts are normal commensals on the skin surface. 17,18 Skin colonization increases with age; 25% of children and almost 100% of adults are affected. 19 Tinea versicolor occurs when the saprophytic yeast or budding form of the organism converts to the pathogenic hyphal or mycelial form. The fungal infection is localized to the stratum corneum. Predisposing factors for the conversion include a hot and humid environment, hyperhidrosis, application of oily lotion or cream to the skin, wearing of masks, excessive lipid-containing sebaceous secretions, malnutrition, poor general health, use of oral contraceptives, pregnancy, diabetes mellitus, use of topical or systemic corticosteroids, Cushing disease, Helicobacter pylori infection, immunodeficiency and genetic predisposition. [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] A recent study showed oxidative stress has no role in the pathogenesis of tinea versicolor. 29

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“…6 Multiple Malassezia species, including the SD-associated species M. restricta and M. globosa, have been found to be susceptible to ketoconazole. 7 Topical ketoconazole is consistently effective across randomized controlled trials, with an efficiency of 63%-90% in SD treatment. 8 At present, there are limited data focusing on the effects of ketoconazole on shaping the skin microbiome in patients with SD.…”

Section: Introductionmentioning

confidence: 99%

“…Ketoconazole is a broad‐spectrum azole antifungal that is considered a level A recommendation for the treatment of SD 6 . Multiple Malassezia species, including the SD‐associated species M. restricta and M. globosa , have been found to be susceptible to ketoconazole 7 . Topical ketoconazole is consistently effective across randomized controlled trials, with an efficiency of 63%–90% in SD treatment 8 …”

Section: Introductionmentioning

confidence: 99%

Ketoconazole 2% cream alters the skin fungal microbiome in seborrhoeic dermatitis: a cohort study

Tao

Wang

Wan

et al. 2022

Clinical and Experimental Dermatology

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Summary Background Seborrhoeic dermatitis (SD) is a common chronic inflammatory dermatosis. Current theories on the pathogenesis of SD highlight the role of microbes on the skin surface. Ketoconazole is commonly used for the treatment of SD; however, there are limited data focusing on the effects of ketoconazole in shaping the skin microbiome in patients with SD. Aim In this prospective cohort study, we used a high‐throughput DNA sequencing method to characterize the cutaneous microbial communities of patients with SD before and after topical ketoconazole treatment. Methods In total, 30 patients with facial SD and 15 age‐ and sex‐matched healthy controls (HCs) were enrolled in this study. Skin swabs were collected from SD lesional sites of the cheek at baseline, after ketoconazole treatment and 2 weeks post‐treatment. DNA was extracted from skin samples. The bacterial 16S V3V4 rRNA and fungal internal transcribed spacer 1–5F regions were sequenced, and the microbial community compositions were analysed. Results Significantly lower bacterial and fungal diversities were detected at the lesional sites of facial SD compared with HCs. A decreased relative abundance of Cutibacterium and increased abundances of Malassezia and Staphylococcus were found in facial SD. Disease diversity was positively correlated with the relative abundances of Malassezia, Staphylococcus and Corynebacterium, while transepidermal water loss was negatively associated with the relative abundance of Cutibacterium. After ketoconazole treatment, fungal Shannon diversity and the relative abundances of Candida and Aspergillus were significantly increased at the lesional sites, and the relative abundance of Malassezia showed a decreasing trend. These changing trends were maintained until 2 weeks post‐treatment. Conclusion Facial SD showed lower fungal diversity accompanied by increased relative abundances of Malassezia and Staphylococcus and decreased relative abundance of Cutibacterium. Ketoconazole treatment reduced Malassezia and increased fungal diversity to restore skin microbial communities.

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Susceptibilities of Malassezia strains from pityriasis versicolor, Malassezia folliculitis and seborrheic dermatitis to antifungal drugs

Cited by 18 publications

References 36 publications

Recalcitrant cutaneous fungal infections—A growing problem

Recalcitrant cutaneous fungal infections—A growing problem

Tinea versicolor: an updated review

Ketoconazole 2% cream alters the skin fungal microbiome in seborrhoeic dermatitis: a cohort study

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