What does the commensal fungus Malassezia have to do with atopic dermatitis? What’s new in dermatophytes? Is there a risk of fungal transmission when coming into contact with hedgehogs? How is tinea corporis treated correctly? Experts provided answers to these questions at the Zurich Dermatology Training Days 2018.
In addition to bacteria, fungi are also part of the normal skin microbiome. Malassezia is the dominant fungus in most skin areas of the body. There are currently 17 known species of this lipophilic yeast fungus, which is also found in dogs and many other mammals as well as birds. Malassezia species are not only normally occurring commensals in humans, but are also associated with diseases of the skin. Dr. Martin Glatz, Allergy Ward, Dermatology Clinic, University Hospital Zurich, spoke about this.
Commensal fungus associated with skin diseases
Skin diseases associated with Malassezia include: Pityriasis versicolor, seborrheic eczema, head dandruff (pityriasis simplex capillitii), atopic dermatitis, and Malassezia folliculitis (especially in immunosuppressed and HIV patients). M. furfur, the best known Malassezia species, can cause systemic infections in immunocompromised individuals in rare cases. Research is currently underway to determine which factors are responsible for Malassezia being a commensal that leaves the skin unaffected on the one hand and can contribute to skin diseases on the other. A review article recently summarized the current state of research on mammalian skin responses to Malassezia [1].
Malassezia and atopic dermatitis
Numerous immunogenic proteins produced by Malassezia can lead to the release of proinflammatory cytokines and, as allergens, to the production of specific IgE antibodies [2]. While healthy individuals are practically never sensitized to Malassezia, sensitization is common in patients with atopic dermatitis (detection of specific IgE antibodies directed against Malassezia in serum, positive skin prick test). In vitro, Malassezia produces much greater amounts of allergens (e.g., proinflammatory protein Mala s 12) at a pH of 6.1 (as in atopic dermatitis skin) than at a more acidic pH of 5.0 (as in healthy skin). Thus, the elevated skin pH in patients with atopic dermatitis may contribute to increased release of proinflammatory proteins acting as allergens. The impaired skin barrier function facilitates penetration of allergens into the skin, which may result in the release of proinflammatory cytokines and, in sensitized patients, activation of mast cells by cross-linking specific IgE antibodies. Thus, Malassezia may increase skin inflammation in atopic dermatitis [2].
Resistant Malassezia strains not uncommon
Topical azoles are usually used to treat pityriasis versicolor, such as topical ketoconazole once daily until healing. Resistance of the fungus to certain antifungal agents (including ketoconazole) is not uncommon and may be responsible for frequent recurrences or chronic courses with poor healing. However, Malassezia resistance testing is not routine in the laboratory. The “antiseborrheic” substance selenium disulfide (e.g., Selsun®) is well effective for pityriasis versicolor. In patients prone to frequent recurrences, application once a month may be useful (hair washing and application to the upper body).
Filamentous fungi as the most frequent cause of dermatomycoses
Dermatomycoses occur in 20-25% of the population worldwide. Dermatophytes (filamentous fungi) are most frequently responsible for fungal infections of the skin and appendages (tinea = dermatophyte infection). Three genera of dermatophytes are distinguished:
- Trichophyton (16 species)
- Epidermophyton (only one species: E. floccosum)
- Microsporum (3 species)
In Europe, T. rubrum and T. interdigitale form the cause of infection in 90%. As a result of migration from Africa, M. audouinii, T. violaceum and T. soudanense are also playing an increasing role as pathogens of tinea corporis, reported Prof. Dr. Stephan Lautenschlager, Chief Physician at the Dermatological Outpatient Clinic, Stadtspital Triemli, Zurich. The lifetime risk of contracting tinea pedis is very high at 70%, especially in men. The risk of fungal infection is significantly increased in professional football players, especially on the feet [3]. It is likely that shear forces, microtrauma, and hyperhidrosis promote infection. In a recent German study, 84 professional football players were found to have tinea pedis in 36.9% and onychomycosis in 60.7%, compared with only 3.3% and 3.2%, respectively, in 8186 control subjects (men aged 17 to 35 years) [3].
Multiple clinical pictures in tinea corporis
In the case of tinea corporis, transmission usually occurs from animal to human or from human to human, rarely via objects (e.g., clothing). The incubation period is one to three weeks. The spectrum of clinical pictures is broad and depends on the pathogen species (with different proteases), the size of the inoculum, the localization and the immune response (or immunosuppression). The common, classic clinical picture consists of round lesions with scaly, erythematous margins, centrifugal spread, and central healing. In cases of severe inflammatory dermatosis, zoophilic pathogens should be considered, e.g., transmitted by contact with guinea pigs or hedgehogs. One study detected T. benhamiae in 93% of guinea pigs for sale by polymerase chain reaction (PCR) in 15 pet shops in Berlin [4]. Only 9% of the animals showed tinea symptoms, the rest were asymptomatic carriers in which the fungal infection was not detectable. The study authors therefore recommend that guinea pigs should first be examined by a veterinarian for skin fungi after purchase, as they are very likely to be carriers of pathogens that can be transmitted to humans (especially children) through body contact. A study conducted in French-speaking Switzerland found fungal infections in 30% of the guinea pigs examined, the speaker reported. A review with case reports from Germany recently indicated that T. erinacei should be newly expected as an “emerging pathogen” in hedgehog contact [5]. For example, a female animal caregiver with hedgehog contact developed marginal, papular, vesicular, and erosive-crusted skin lesions on her index finger. Culturally, T. erinacei was detectable. With ciclopiroxolamine cream and terbinafine perorally for 14 days, the tinea healed.
Treatment of tinea corporis
No current guideline is available for the therapy of tinea corporis, but a useful review article is available [6]. Localized tinea corporis can be treated topically. Systemic treatment is indicated in cases of “extensive infestation” (without precise definition) or if topical therapy has not been successful or if follicles are also affected. If azoles are chosen for topical therapy, they should be applied twice daily for four to six weeks (e.g., clotrimazole, econazole, miconazole). When terbinafine or ciclopiroxolamine is used topically, two weeks of treatment (once daily) is sufficient. In the case of systemic treatment, the duration of therapy is two to four weeks (e.g. B. Fluconazole 150 mg once a week, Itraconazole 100 mg once a day, Terbinafine 250 mg once a day).
Source: Lectures by Martin Glatz “Malassezia-associated skin manifestations” and by Stephan Lautenschlager “Common and rare infections caused by dermatophytes” in the context of the update course 1 “News on skin infections – mycology”, 8th Zurich Dermatological Training Days, Zurich, June 20, 2018.
Literature:
- Sparber F, et al: Host responses to Malassezia spp. in the mammalian skin. Front Immunol 2017; 8: 1614.
- Glatz M, et al: The role of Malassezia spp. in atopic dermatitis. J Clin Med 2015; 4: 1217-1228.
- Buder V, et al: Prevalence of dermatomycoses in professional football players. Dermatologist 2018; 69: 401-407.
- Kupsch C, et al: Dermatophytes and guinea pigs – An underestimated danger? Dermatologist 2017; 68: 827-830.
- Kargl A, et al: Hedgehog fungi in a Munich dermatology practice. Dermatologist 2018; 69: 576-585.
- Sahoo AK, et al: Management of tinea corporis, tinea cruris and tinea pedis: A comprehensive review. Indian Dermatol Online J 2016; 7: 77-86.
DERMATOLOGIE PRAXIS 2018; 28(4): 34-36
