General Characteristics and Epidemiology
General features of Malassezia
- Formerly known as Pityrosporum
- Family: Malasseziaceae
- Genus: Malassezia
- Yeast: spherical or oval
- Mycelial form: short hyphae
- Colonies are cream or yellowish in color.
- Most species are lipid-dependent.
- Not a dermatophyte
- Reproduce by unipolar budding
Clinically relevant species
There are a number of recognized species:
- M. furfur (most common)
- M. globosa (common)
- M. caprae
- M. cuniculi
- M. dermatis
- M. equina
- M. japonica
- M. nana
- M. obtusa
- M. pachydermatis
- M. psittaci
- M. restricta
- M. slooffiae
- M. sympodialis
- M. yamatoensis
- Tinea (pityriasis) versicolor
- Seborrheic dermatitis
- Malassezia folliculitis
- Catheter-associated fungemia
- Septic arthritis
- Urinary tract infections
- Highest incidence in tropical climates and summer months
- More common in adults (ages 20–50 years)
- Common in hot, humid environments
- More common in adolescents and young adults (ages 13–45 years)
Malassezia are part of the normal skin flora in humans and animals.
Host risk factors
Predisposing risk factors for disease include:
- Genetic predisposition
- Warm, humid environments
- Steroid use
- Hematologic malignancy
- Organ transplantation
- Excessive sebum production
- Neonates (catheter-associated infections)
- Malassezia conversion to pathogenic mycelial form → overgrowth in stratum corneum → degradation of lipids → azelaic acid production → inhibition of tyrosinase and melanocyte damage → hypopigmentation and scaling
- Inflammatory response → hyperpigmentation and/or pink discoloration
- Exact pathophysiologic mechanism remains unknown.
- Malassezia cleave fatty acids from sebum → release inflammatory free fatty acids
- Aberrant keratinocyte production → abnormal stratum corneum → inflammatory response stimulated → skin eruption
- Other factors may include oxidative stress and cell-damaging oxygen radicals.
- Plugging of a hair follicle → sebaceous environment for yeast growth
- Degradation of lipids → inflammatory fatty acids → inflammatory response
Clinical Presentation and Diagnosis
- Generally asymptomatic, but mild pruritus can occur
- Evolving rash
- Affected areas do not tan (often noted during summer months).
- Rash appearance:
- Numerous well-demarcated oval or round lesions
- Macules, plaques, or patches
- Hypopigmented, hyperpigmented, or pink
- Moderate to severe pruritus
- Erythematous papules and plaques
- Thick, greasy scales
- Yellow crust
- Mustache/beard area
- Nasolabial folds
- Upper chest and back
- Intertriginous areas
This condition may appear similar to acne vulgaris or bacterial folliculitis:
- Monomorphic, erythematous papules or pustules
- Follicular pattern
- Upper arms
- Sides of the face
The diagnosis is most often made clinically on the basis of the history and examination. Additional evaluation can include:
- Visualization with Wood’s lamp:
- Yellow to yellow-green fluorescence
- Seen in only ⅓ of cases
- Skin scraping with KOH preparation
- “Spaghetti and meatballs” appearance of hyphae and spores
- Cultures may be obtained for invasive disease (e.g., meningitis, septic arthritis).
Management and Prevention
- Topical antifungals:
- Selenium sulfide shampoo
- Zinc pyrithione shampoo
- Ketoconazole cream or shampoo
- Oral antifungal (for widespread, recurrent, invasive, or refractory infections):
- Amphotericin B (for severe, invasive disease)
Recurrences of tinea versicolor and seborrheic dermatitis can be prevented with topical antifungal prophylaxis.
- Atopic dermatitis: chronic, relapsing, inflammatory skin condition. Patients present with pruritic, erythematous, thickened, scaly patches that frequently affect flexural regions. This distribution and appearance differentiates atopic dermatitis from tinea versicolor and seborrheic dermatitis. The diagnosis is clinical. Management focuses on avoiding potential triggers, topical steroids, and immunosuppressive therapy.
- Pityriasis alba: common skin disorder typically affecting children and adolescents. Pityriasis alba is often considered a manifestation of atopic dermatitis. Typically, patients present with erythema and scale, followed by round, hypopigmented macules and patches, commonly occurring on the face, upper trunk, or upper limbs. The diagnosis is clinical. Pityriasis alba is considered self-limiting, but it may take months to years to resolve. Topical steroids, emollients, and calcineurin inhibitors may be used to speed up resolution.
- Vitiligo: depigmenting disorder that causes destruction of melanocytes. The etiology of vitiligo is unknown, but genetic and autoimmune factors may play a role. Patients present with hypopigmented or depigmented macules or patches that often occur on the face, hands, knees, and/or genitalia. The diagnosis is clinical. Management can include topical corticosteroids, topical calcineurin inhibitors, immunosuppressants, and phototherapy.
- Pityriasis rosea: acute, self-limited skin disorder of unknown etiology. Pityriasis rosea presents with a single, ovoid “herald patch.” This presentation is followed by diffuse, pruritic, oval plaques with fine collarette scale in a Christmas-tree distribution on the trunk. The diagnosis is clinical. Treatment is not required, but pruritus can be managed with emollients, topical corticosteroids, and antihistamines.
- Guttate psoriasis: variant of psoriasis, which is an immune-mediated inflammatory skin condition. This form of psoriasis presents with small, salmon-colored papules that have a dew-drop appearance on the skin. The trunk and extremities are commonly involved. The diagnosis is clinical, and management includes topical corticosteroids, calcitriol, and phototherapy.
- Tinea corporis: superficial fungal infection of the skin that can affect the face, trunk, and extremities. The lesions of tinea corporis are characterized by peripheral scaling, central clearing, and erythema. The diagnosis is usually clinical, though a KOH examination would show fungal hyphae. Management includes topical or oral antifungal medications.
- Acne vulgaris: common disorder of the pilosebaceous units in adolescents and young adults. Acne vulgaris is caused by follicular hyperkeratinization, excess sebum production, follicular colonization by Cutibacterium acnes, and inflammation. Acne can present as open or closed comedones, papules, pustules, nodules, or cysts. The diagnosis is based on the clinical exam. Management depends on the severity, but includes skin care techniques, topical therapies, antibiotics, and retinoids.
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