Malassezia are common lipid-dependent fungi that grow on the sebaceous areas of human skin, including the face, scalp, and upper trunk. Although Malassezia are a part of the normal human skin flora, they may also cause or exacerbate several skin diseases, including tinea versicolor, Pityrosporum folliculitis, and seborrheic dermatitis. Topical antifungals are the mainstay of treating Malassezia-related diseases. Chronic prophylaxis is often required to prevent recurrences.

This paper briefly reviews the current knowledge of the epidemiology and modes of transmission of nosocomial fungal infections and some of the therapeutic options for treating these diseases. In the mid-1980s, many institutions reported that fungi were common pathogens in nosocomial infections. Most, if not all, hospitals care for patients at risk for nosocomial fungal infections. The proportion in all nosocomial infections reportedly caused by Candida spp. increased from 2% in 1980 to 5% in 1986 to 1989. Numerous studies have identified common risk factors for acquiring these infections, most of which are very common among hospitalized patients; some factors act primarily by inducing immunosuppression (e.g., corticosteroids, chemotherapy, malnutrition, malignancy, and neutropenia), while others primarily provide a route of infection (e.g., extensive burns, indwelling catheter), and some act in combination. Non-albicans Candida spp., including fluconazole-resistant C. krusei and Torulopsis (C.) glabrata, have become more common pathogens. Newer molecular typing techniques can assist in the determination of a common source of infection caused by several fungal pathogens. Continued epidemiologic and laboratory research is needed to better characterize these pathogens and allow for improved diagnostic and therapeutic strategies.

Pityriasis versicolor is a mild or chronic condition characterized by scaly hypopigmented or hyperpigmented lesions usually affecting the trunk. The lesions vary depending on tropical or temperate climates. The disease seems to occur mainly at adolescence when the sebaceous glands are more active. Malassezia yeasts have been implicated in the pathogenesis of this disease. The mycelial form of the fungus has been suggested to be the cause of lesions. Antifungal preparations have been used to treat the initial presentation effectively, although in a proportion of patients the disease tends to reoccur. They are available in a wide range of formulations and have been shown to be safe.

Pityriasis versicolor is a common superficial fungal infection of the skin. It is caused by Malassezia spp., which are normal human saprophytes. Under certain conditions, both exogenous and endogenous, the fungus can convert from a yeast to a pathogenic mycelial form. This alteration results in mild inflammation of the skin, and in characteristic clinical and histological changes. The taxonomy of Malassezia spp. has recently been modified to include six obligatorily lipophilic species, all of which can be found on human skin, plus one non-obligatorily lipophilic species, which only rarely colonizes human hosts. LEARNING OBJECTIVES: At the conclusion of this learning activity, participants should be aware of the role of Malassezia in the development of pityriasis versicolor, the clinical and histological changes arising from this dermatosis, and the diagnosis and treatment of this disorder.

Eighty-two patients with pityriasis versicolor were treated orally with ketoconazole in tablet form (200 mg). The tablets were taken at least 90 min before a meal, and patients who received only one tablet daily were told to refrain from bathing except immediately before ingestion of the drug and only once a day. Dosage of ketoconazole varied from a single dose of 400 mg to 200--400 mg per day for four weeks. Seventy-seven patients reported no adverse effects. There were reports from others of headache, gastralgia, nausea, dyspnea, dizziness, or tinnitus. In most affected patients, these symptoms stopped with the first meal eaten after initiation of treatment. Follow-up examinations were performed at different intervals. The maximal therapeutic effect of ketoconazole was seen three to six weeks after initiation of therapy. Seventy-eight patients were considered cured; one had received only one tablet. Only hypopigmented macules remained. Examination of these areas with a Wood lamp revealed no fluorescence, and scrapings examined with the light microscope did not contain Malassezia furfur. These results indicate that ketoconazole is effective in the treatment of pityriasis versicolor, but the problem of protecting susceptible persons from infection and reinfection remains.

Age of the patient, climate, season, and local environmental factors influence the onset and course of tinea versicolor (pityriasis versicolor). A number of effective topical therapies are available. In addition, a single dose of 400 mg of oral ketoconazole eliminates the disease and can be used prophylactically in some cases to prevent recurrence.

Twenty-four patients with extensive or recurrent pityriasis versicolor were treated with a single oral dose of 400 mg of fluconazole. Twenty-three patients returned for follow up. Seventeen or 74%, were free of lesions 3 weeks after treatment and no recurrences were seen 6 weeks after treatment. The majority of the patients found the treatment effective, safe and convenient.

Twenty patients with tinea versicolor were treated with propylene glycol 50% in water twice daily for 2 weeks. All of these were cured when seen 2 weeks after the last day of treatment. The patients found the treatment cosmetically attractive and only 2 patients complained of a slight burning sensation in the skin after application of the solution.

Malassezia furfur, the fungus causing pityriasis versicolor, has been reported to be sensitive to terbinafine in vitro but although topical therapy is effective in the treatment of pityriasis versicolor, oral therapy is not. This phenomenon was investigated by determining the susceptibility to terbinafine of different M. furfur subgroups in vivo (during topical or oral application) and in vitro. All M. furfur subgroups were suppressed (approximately 10-fold) by topical terbinafine. Oral treatment resulted in no significant suppression of cutaneous M. furfur populations with the exception of a single subgroup (A), which was reduced to undetectable levels on the skin of eight of 10 patients receiving oral terbinafine. Isolates of subgroup A were also markedly more susceptible to terbinafine in laboratory tests. The importance of the recognition of distinct subgroups within the cutaneous lipophilic yeasts when evaluating their antifungal susceptibility and their role in disease is discussed.