Dwight A. Powell
The genus Malassezia includes 11 species associated with significant human disease1 (eTable 301.1 ). With the exception of M pachydermatis, all other Malassezia species require lipid supplementation of standard fungal growth media for isolation. When Sabouraud media is overlaid with sterile olive oil, Malassezia species grow within 5 to 14 days.2 Rapid identification techniques, such as identification of Malassezia DNA by polymerase chain reaction, have been utilized in study settings.3Malassezia species are normal residents of human skin, usually found in sebum-rich areas such as the trunk, face, and scalp. Extensive studies on skin colonization have shown that the skin of healthy newborn infants becomes colonized with Malassezia species within the first several months of life. Over 50% of prematurely born infants requiring prolonged hospitalization become colonized within 2 weeks of life.4,5Ninety to 100% of adolescents and adults have saprophytic skin colonization with Malassezia species.6
Skin diseases are the most common manifestation of Malassezia infection.7 Confirmed dermatoses include tinea versicolor, seborrheic dermatitis, and folliculitis. Tinea versicolor (Fig. 367-9) is disscussed in Chapter 367. M globosa, M restricta, and M sympodialis are most often associated with tinea versicolor.
Seborrheic dermatitis due to Malassezia occurs in 2% to 5% of normal hosts but is prevalent in 70% to 80% of persons with untreated AIDS. This condition varies from thick greasy scales covering the scalp of infants in the first 3 months of life (cradle cap) to an itchy, papular, erythematous, greasy, scaling rash most commonly found in the nasolabial folds, postauricular scalp, eyebrows, or chest.9 Dandruff, presenting as mildly pruritic scaling of the scalp without associated inflammation, is felt to represent a milder variant of seborrheic dermatitis. Diagnosis of seborrheic dermatitis and dandruff are usually made on a clinical basis. Culture for Malassezia does not confirm the diagnosis because the quantity of Malassezia may not differ from that normal skin.
Folliculitis resulting from Malassezia may resemble the lesion of disseminated candidiasis. This acneiform lesion presents as follicle-limited inflammatory papules or papulopustules. It is most commonly seen over the back and chest of patients with AIDS or of those receiving broad-spectrum antibiotics or steroids. M furfur is reported to cause eosinophilic pustular folliculitis with pruritus in patients with AIDS, and in its papular form, this lesion is pathologically a vasculitis of the dermis. This papulopustular dermatitis responds to topical or systemic imidazole therapy. Discontinuation of steroids or antibiotics also is helpful. Malassezia species were described as a cause of neonatal cephalic pustulosis, characterized by scattered erythematous papules and pustules on the face, scalp, and neck of infants in the first few weeks of life.10 Diagnosis can be confirmed by culture of purulent material or lesional biopsy where budding yeast are apparent.
Systemic Malassezia infections have most commonly been associated with catheter-associated fungemia due to M furfur in patients receiving intravenous lipid feedings or total parenteral nutrition. A characteristic syndrome is noted, most often in premature neonates, of fever, bilateral interstitial pulmonary infiltrates, leukocytosis, and thrombocytopenia.5,11 This syndrome also has been reported in immunocompromised adults and children with central venous catheters who were not receiving concurrent intravenous lipids.12 Complications from catheter-associated infections have included meningitis, peritonitis, endocarditis, and peripheral thromboembolism.13,14M pachydermatisis also associated with systemic sepsis in infants. At least 2 nursery outbreaks have been reported; in one, colonization of health care workers by their pet dogs was believed to be a possible source of infection.15 Diagnosis is generally made when blood from culture-negative cases of apparent catheter-associated sepsis is cultured on lipid-enriched media.
Malassezia species are generally susceptible to a wide range of topical and systemic antifungal treatments. Tinea versicolor and seborrheic dermatitis can be managed with topical 2.5% selenium sulfide, zinc pyrithione, or azole creams (ketoconazole, itraconazole, fluconazole).7,9 Susceptibility to terbinafine varies, but topical terbinafine is more effective than oral terbinafine. Oral itraconazole or fluconazole have been shown to be effective for tinea versicolor and seborrheic dermatitis. These drugs are probably more effective than topical medications for the treatment of Malassezia folliculitis. Topical corticosteroids may be effective in seborrheic dermatitis, but in children ages 2 years or older, tacrolimus or pimecrolimus may be more effective because of antifungal as well as anti-inflammatory activity. Recurrence within 1 to 2 years is common.
For sepsis, therapy includes removal of the venous catheter that was used for alimentation and interruption of lipid feedings. A short course of therapy with amphotericin B, fluconazole, or itraconazole may be indicated, particularly if a new deep line is placed.5,16Malassezia species are resistant to flucytosine.