Malassezia Species

Microbiology

Malassezia (formerly called Pityrosporum ) is a genus of lipophilic, basidiomycetous yeasts lacking ballistospores and classified in the order Malasseziales . Its phylogenetic placement within the Ustilaginomycotina (Basidiomycota) is highly supported. Malassezia increasingly is recognized as an opportunist affecting both humans and animals. ^, Newer identification methods have made the characterization of several new species possible and also have enhanced our understanding of the ecology and clinical associations of the genus. The genus is responsible for various superficial skin infections of humans, including pityriasis (tinea) versicolor (PV), ^{, ,} and Malassezia folliculitis (MF). The association of Malassezia with seborrheic eczema/dermatitis also has been reconfirmed, although the implication of the immune system in this disease is critical. ^{, ,} Less commonly, members of the genus cause invasive disease in premature infants and other immunocompromised and debilitated individuals. Malassezia species also have been implicated in atopic dermatitis, confluent and reticulate papillomatosis, and neonatal cephalic pustulosis. ^{, ,} Various species of Malassezia form part of the normal microbial flora of the skin of humans and other warm-blooded animals, and most infections are endogenous in origin.

Until the 1990s only three Malassezia species were recognized: two lipid-dependent species, M. furfur and M. sympodialis, and one nonobligate lipophile, M. pachydermatis. After genomic and ribosomal sequence comparisons of a large number of human and animal isolates, the genus Malassezia was enlarged to seven species, consisting of the three former taxa ( M. furfur, M. pachydermatis, and M. sympodialis ) and four new taxa ( M. globosa, M. obtusa, M. restricta, and M. slooffiae ). More recently, eleven new species have been described and reported: M. dermatis, M . japonica, M . nana, M. yamatoensis, M. caprae, M. equina , M. cuniculi , M . psittaci , M . brasiliense , M . arunalokei, and M. vespertilionis. ^, With the exception of M. pachydermatis, 17 of the 18 Malassezia species are lipid dependent. Their isolation in culture requires the use of a lipid-enriched culture medium. If a conventional medium is used (e.g., Sabouraud dextrose agar), the surface must be covered with a thin layer of sterile olive oil; however, this method yields recovery only of M. furfur, M. pachydermatis, and M. yamatoensis . Other selective media useful for a wider range of species include Dixon, modified Dixon, and Leeming and Notman agars. M. pachydermatis, which most commonly is not lipid dependent, usually can be isolated on Sabouraud dextrose agar. The incubation temperature also is an important consideration because for many cutaneous species, the optimum growth temperature is 32°C–34°C, rather than 37°C. Methods have been developed to separate the species of Malassezia on the basis of morphologic and physiologic differences; however, these are somewhat cumbersome, and species identification can be difficult. Commonly used physiologic tests include urease, catalase, and β-glucosidase activities, growth at 37°C and 40°C, and evaluation of growth in four water-soluble lipid supplements (Tweens 20, 40, 60, 80) and in Cremophor EL (castor oil) using a diffusion method in Sabouraud glucose agar. The dependence on lipid precludes the use of conventional assimilation tests.

Molecular methods used to detect and characterize Malassezia species in humans and animals include biotyping using enzymatic methods, pulsed-field gel electrophoresis (PFGE), random amplification of polymorphic DNA (RAPD), DNA sequence analysis, restriction analysis of polymerase chain reaction (PCR) amplicon of ribosomal sequences, amplified fragment length polymorphism (AFLP), denaturing gradient gel electrophoresis (DGGE), and terminal fragment length polymorphism (tFLP). These methods have confirmed the robustness of the new classification of Malassezia species, all species having their own characteristic karyotype. DNA-based culture-independent methods, such as quantitative real-time PCR methods, can detect as few as 10 copies of Malassezia DNA and currently are the most reliable methods for detecting Malassezia .

Although 18 species of Malassezia thus far have been recovered from humans and animals, ^{, ,} they do not appear to have equal clinical importance. Although many clinicians previously have considered all clinical isolates to be M. furfur, this assumption is no longer valid because the host, sources of infection, and routes of transmission vary by species.

Epidemiology

Malassezia species form part of the normal cutaneous flora of humans and other warm-blooded animals. The prevalence of skin colonization depends on age, anatomic site, and, to a lesser extent, race. Cutaneous Malassezia is found immediately after birth. In a British study of skin swabs from 245 neonates, 31% were positive for Malassezia ; in 195 neonates from Iran, 68% tested positive, with a distribution of M. furfur and M. globosa of 60% and 7%, respectively.

The incidence of skin colonization with Malassezia species increases with age, rising from about 25% in children to almost 100% in adolescents and adults. ^, The density of colonization in postpubertal people is greater in anatomic sites that contain pilosebaceous glands; Malassezia species have been isolated from 100% of samples taken from the back of adults, but from only 75% taken from the face and scalp. Studies have shown that the degree of colonization with Malassezia species is closely aligned with age-related changes in sebaceous gland activity, ^, and increased fatty acid concentration occurs primarily at puberty. PV is worldwide in distribution but most prevalent in hot, humid, tropical and subtropical climates, where 30%–40% of the adult population can be affected. In temperate climates the disease affects 1%–4% of adults and is most common during the hot summer months. Malassezia folliculitis also is more prevalent in tropical countries and more common during the summer months in temperate regions.

The precise conditions that lead to the development of PV and other forms of superficial Malassezia infection have not been defined, but host-specific adaptations are important factors because the transition from commensal to pathogenic states appears to be a continuum rather than a discrete entity. ^, The lesions of PV and seborrheic dermatitis have a predilection for anatomic sites that are well supplied with sebaceous glands, and patients with the latter condition have been shown to have higher concentrations of lipids on their skin than other individuals. Instances in which members of the same family who are not cohabiting have demonstrated PV suggest a genetic predisposition. The higher incidence of Malassezia folliculitis and seborrheic dermatitis in people with immunosuppressive disorders, including AIDS, and in patients undergoing corticosteroid or other immunosuppressive treatment suggests that the relationship between Malassezia species and the immune system is important.

Exposure to lipid-rich intravenous infusions through a central venous catheter is the single most important risk factor for systemic Malassezia infection in both adults and infants. Among neonates, other risk factors include low birth weight (LBW), early gestational age, and length of hospitalization. An investigation of one outbreak of M. furfur infection among LBW infants, most of whom received intravenous lipids, identified long duration of antimicrobial treatment as an additional risk factor for disease.

Human-to-human transmission of Malassezia species is possible, either through direct contact or via contaminated clothing or bedding. In practice, however, cutaneous infection is endogenous in most cases, and spread from person to person is uncommon. No cases of occupational infection among healthcare personnel (HCP) have been reported.

Although most infections appear to be sporadic, healthcare-associated (HA) outbreaks of systemic Malassezia infection have been reported since the late 1980s in LBW infants and debilitated adults and children who were receiving parenteral lipid nutrition through indwelling vascular catheters. An investigation of one outbreak of M. furfur infection among LBW infants provided evidence that the organism can be transmitted from an infected or a colonized infant to other infants by the hands of HCP. HA outbreaks of M. pachydermatis infection also have been reported. ^{, ,} In one outbreak, patient-to-patient transmission of the organism was documented in a neonatal intensive care unit (NICU), but the source of the outbreak was not identified. In another outbreak involving 15 infants in a NICU, M. pachydermatis was introduced into the unit on the hands of HCP who were colonized from pet dogs at home. The organism persisted in the unit through patient-to-patient transmission.

Clinical Manifestations