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The role of Malassezia furfur in dermatology
The Role of Malassezia furfur in Dermatology ´ MD SUZANA LJUBOJEVIC, MIHAEL SKERLEV, MD, PhD ˘ C, ´ MD, PhD JASNA LIPOZENCI ˇ C, ´ MD, PhD ALEKSANDRA BASTA-JUZBASI
Y
easts of the genus Malassezia have been recognized as members of the microbiologic flora of the skin for over a century. Under certain conditions, they can cause superficial infection of the skin and associated structures, and they can become an opportunistic pathogen in patients with catheters.
Historical Perspective The earliest reports of Malassezia-like yeasts were those found in material from the infected scales of pityriasis versicolor (PV) patients reported by Eichstedt in 1846.1 In 1873, Rivolta reported yeast of similar type isolated from patients with psoriasis.2 The name Malassezia was used by Malassez,3 who first described typical round and oval budding yeast in the stratum corneum of patients with various skin diseases. In 1889, Baillon4 proposed the name Malassezia furfur for filamentous fungus observed in the skin lesions of PV. The genus Pityrosporum was proposed in 1904 by Sabouraud5 to describe budding yeast cells without hyphal elements observed in and isolated from normal skin and scalp. In 1913, Castelani and Chalmers6 used the species name P. ovale for the first time. In 1951, Gordon7 isolated a spherical to oval yeast from PV lesions and normal skin; he named it P. orbiculare.
Taxonomy Some authors believe P. ovale and P. orbiculare to be different organisms.8,9 Keddie and Barajas9 showed with volumetric analysis that the two species are much alike in regard to the volume of mitochondria and the nucleus, but on the other hand three-dimensional images disclosed variations in the cellular inclusions. The mitochondria of P. orbiculare appear to increase in size with cell volume, whereas in P. ovale, there may be an increase in number rather than in size. Later studies, From the Department of Dermatology and Venerology, Zagreb University Hospital Center, Croatia. Address correspondence to Suzana Ljubojevic´, MD, Department of Dermatology and Venereology, Zagreb University Hospital Center, Sˇalata 4, HR-10000 Zagreb, Croatia. E-mail address: [email protected]. © 2002 by Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
however, have revealed that the two yeasts are most likely identical10 and they represent different morphologic variants of M. furfur.11 The generic name P. ovale was used by dermatologist as an associated agent in seborrheic (SD) and atopic dermatitis (AD), and P. orbiculare as a causative agent for PV. The development of molecular techniques revealed that genus Malassezia is divided in to seven species12: M. furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta, and M. slooffiae. M. pachydermatis is the only nonlipophilic yeast and is adapted to animals (dogs), although it can be occasionally found in humans. M. globosa is found very frequently on both normal and diseased skin. M. restricta is very often found on the head region. M. slooffiae is isolated both from human and animal (pig) skin. M. sympodialis and M. furfur appeared as one of the most frequent residents of human skin, along with M. globosa and M. restricta.
Morphology M. furfur is a polymorphic lipophilic microorganism characterized by a thick, multilayered cell wall. Colonies are small and yellowish-brown (Fig 1) with an intact margin. M. furfur’s reproduction occurs by monopolar budding yeast cells,13 sometimes capable of forming filaments. Cultures were generally short-lived. The cultivation of M. furfur is not simple, because standard Sabouraud medium is not suitable. We are using our own modified Dixon medium for cultivation of M. furfur.14
Epidemiology Malassezia organisms are present in 75% to 98% of healthy individual.15 The organism is present in ⬎90% of adults. The colonization starts soon after birth16 and increases during the period when the sebaceus glands become active. The peak presence of these yeasts in our patients was in late adolescent and early adult life,17 the period when the sebaceus glands become active and the concentration of skin lipids increases (Table 1). During 1999, 1299 patients were examined in the Department of Dermatology and Venerology, Zagreb, 0738-081X/02/$–see front matter PII S0738-081X(01)00240-1
180 LJUBOJEVIC´ ET AL.
Clinics in Dermatology
Y
2002;20:179 –182
Malassezia Infection
Figure 1. Native microscopy preparation of Malassezia furfur from the skin scale lesion.
Croatia.17 Eighty-seven percent of the patients were positive for M. furfur in native preparations prepared with 20% potassium hydroxide from skin or scalp lesions suspected of SD, AD, or PV (Fig 1). The youngest patient was a 3-month-old female infant, and the oldest was an 88-year-old man. Majorities of the patients were in the age groups from 16 –30 and 31–50 years (70%) (Fig 2). The male/female ratio is approximately equal, although the results from our study suggested that there are twice as many females positive in native preparations for Malassezia. Earlier reports suggested that infections caused by M. furfur were uncommon in children; now they have been demonstrated in significant numbers of infants, especially in those receiving parenteral fat emulsions thought catheters.18 –20 M. furfur infections have also been associated with scalp scaling, cradle-cap dermatitis, and infantile seborrheic dermatitis.
Malassezia yeasts are members of the normal human cutaneus flora and can be found from almost all body areas but predominately on the face and scalp region. Usually they are found in the stratum corneum and in pillar folliculi, where free fatty acids and triglycerides from sebum provide the nutritive lipid source.21 Fatty acids from triglycerides are essential for Malassezia. They are opportunistic pathogen that, under the influence of several factors such as high temperature and relative humidity; and endogenous factors such as greasy skin, sweating, heredity, and immunosuppressive treatment, change from their saprophytic phase to their pathogenic mycelian phase.22 The cause of transformation of the yeast phase of M. furfur to the mycelial one is presumably because of the changes in the composition of fatty acids of the sebaceous glands due to increased androgen concentrations.23 The initiation and aggravation of several inflammatory skin diseases associated with M. furfur can be divided into at least two groups.24 The first group includes PV and Malassezia folliculitis. The growth of M. furfur directly triggers the development of the cutaneous lesions. The second group includes AD, SD, and psoriasis, cutaneous lesions already developed by other mechanisms, which are aggravated by the growth of M. furfur.24 The cause of SD is still unknown, although many attempts have been made to relate it to infection by Malassezia. According to some authors an inadequate or inappropriate immune response to Malassezia yeast leads to SD.25–27 Sohle and Collins-Lech26 have shown that Malassezia can activate complement by both classic and alternative pathways. Defective cell-mediated immunity to Malassezia in patients with SD has been dem-
Figure 2. The frequency of M. furfur according to age in total of 1132 patients in 1999
Clinics in Dermatology
Y
2002;20:179 –182
ROLE OF MALASSEZIA FURFUR IN DERMATOLOGY
Table 1. The Frequency of Malassezia furfur According to Age and Sex in a Total of 1132 Patients in 1999 Age ⱕ5 6–15 16–30 31–50 51–70 ⬎70 Total
Male
Female
Total
0 (0%) 14 (27%) 121 (37%) 133 (29%) 104 (45%) 25 (41%) 397 (35%)
1 (100%) 38 (73%) 205 (63%) 329 (71%) 126 (55%) 36 (59%) 735 (65%)
1 (1%) 52 (4%) 326 (29%) 462 (41%) 230 (20%) 61 (5%) 1132 (100%)
181
Conclusions The genus Malassezia is a part of normal skin flora. There is a wealth of evidence supporting the hypothesis that they can be implicated in the pathogenesis of various skin diseases such as SD, PV, and Malassezia folliculitis as well as “head and neck” form of AD and psoriasis. Further investigations are certainly necessary to elucidate the role of genus Malassezia in the pathogenesis of the above-mentioned diseases.
References onstrated by Wikler et al.27 Midgley and Hay28 found a slightly greater mean level of Malassezia-specific IgG in patients with SD than in healthy subjects. Broberg and Faergemann29 suspected Malassezia to be the etiologic agent for infantile seborrheic dermatitis. The relationship between Malassezia and the immune system can be found in patients with immunosuppressive diseases. In patients with AIDS who have diminished T-cell function, a higher incidence of SD and presence of Malassezia have been found.30,31 M. furfur yeasts may be a trigger factor for AD. This organism may produce positive skin-prick reactions in a higher rate in patients with AD of the head, scalp, and neck region.32 Waersted and Hjorth33 have shown that M. furfur can induce specific IgE antibodies against Malassezia, especially in patients with AD. PV is a chronic, mild infection of the skin characterized by various pigmentary changes, mainly located on the upper trunk, neck, and upper arms. The lesions of the face are unusual,34,35 especially in adult patients, but there have been several reports on face lesions in children.35 Due to predisposing factors (most commonly, high temperature and high relative humidity, greasy skin, hyperhidrosis, hereditary factors, immunodeficiency, and immunosuppressive treatment) the yeast changes from its round blastoconidia to the mycelial form.36 It is commonly found in AIDS patients.37 Malassezia (previously called Pityrosporum) folliculitis is a chronic disease caused by Malassezia colonization, characterized by pruritic follicular papules and pustules located primarily on the trunk, neck, and upper arms, often associated by itching.38,39 M. furfur can cause or be implicated as a causative organism of many other pathologic conditions, including onychomycosis40 and psoriasis.41 Systemic reactions (Malassezia sepsis) are rare and are usually connected to the colonization of the intravascular catheter in infants receiving parenteral fat emulsions.18 –20 Successful attempts at treating patients with AD, SD, and PV with antifungal local therapy confirm the involvement of these yeast in the etiology and pathogenesis of these diseases.
1. Eichstedt E. Piltzbildung in der Pityriasis versicolor. Froriep Neue Notis Nat Heilik 1846;39:270. 2. Rivolta S. Die parassiti vegetali come introduzione allo studio delle malattie parassitarie e delle alterazioni dell a´ limentano egli animali domestica. Torino, Italy, 1873. 3. Malassez L. Note sur le champignon du pityriasis simplex. Arch Psysiol Norm Pathol 1874;1:451– 64. 4. Baillon H. Traite´ de botanique me´ dicale cryprogamique. Paris: Octave Doir, 1889:234 –5. 5. Sabouraud R. Maladies due cuir chavelu, II: les maladies desquamatires pityriasis et alope´ cies pellicularis. Paris: Masson et cie, 1904. 6. Castellani A, Chalmers AJ. Manual of tropical medicine, 2nd ed. London: Baille´ re, Tindall, and Cox, 1913:1747. 7. Gordon MA. Lipophilic yeast-like organisms associated with tinea versicolor. J Invest Dermatol 1951;17:267. 8. Gordon MA. The lipophilic mycroflora of the skin. Mycologica 1951;43:524. 9. Keddie FM, Barajas L. Quantitative ultrastructural variations between Pityrosporum ovale and Pityrosporum orbiculare based on serial section electron microscopy. Int J Dermatol 1972;11:40. 10. Leeming JP, Notman FH. Improved methods for isolation and enumeration of Malassezia furfur on human and enumeration of Malassezia furfur on human skin. J Clin Microbiol 1987;25:2017–9. 11. Yarrow D, Ahren DG. Genus 7. Malassezia Baillon. In: Kreger-vab Rij NJW, editor. The yeasts: a taxonomic study, 3rd ed. Amsterdam: Elsevier Science Publishing Co, 1984:882–5. 12. Gue´ ho E, Midgley G, Guillot J. The genus Malassezia with description of four new species. Antonie van Leeuwenhoek 1996;69:337–55. 13. Takeo K, Nakai E. Mode of cell growth of Malassezia (Pityrosporum) as revealed by using plasma membrane configuration as natural makers. Can J Microbiol 1986;32: 389 –94. 14. Skerlev M, Lipozenc˘ ic´ J, Basta-Juzbasˇ ic´ A, Pasˇ ic´ A. The significance of Malassezia furfur (Pityrosporum ovale) in dermatology. Acta Dermatovenerol (Croat) 2000;8:107– 8. 15. McGinley KJ, Leyden JJ, Marples RR. Quantitative microbiology of the scalp in non-dandruff, dandruff and seborrheic dermatitis. J Invest Dermatol 1975;64:401–5. 16. Koseki S, Takahashi S. Serial observation on the colonization of Pityrosporum orbiculare (ovale) on the facial skin surface of newborn infants. Jpn J Med Mycol 1988;29:209 – 15. 17. Ljubojevic´ S, Sˇ tulhofer Buzina D, Skerlev M, Basta-Juz-
182 LJUBOJEVIC´ ET AL.
18.
19.
20.
21.
22. 23.
24.
25. 26. 27.
28.
Clinics in Dermatology
basˇ ic´ A. The frequency of Malassezia furfur (Pityrosporum ovale) according to age, sex and season at the Department of Dermatology and Venerology in Zagreb during 1999. Acta Dermatovenerol (Croat) 2000;8:108. Azimi PM, Leyermier K, Lefrak LM. Malassezia furfur: a cause of occulusion of percutaneous central venous catheters in infants in the intensive care nursery. Pediatr Infect Dis J 1988;7:100 –3. Dankner W, Spector S, Fierer J, Davis C. Malassezia fungemia in neonates and adults: complication of hyperalimentation. Rev Infect Dis 1987;4:743–53. Shek YH, Tucker MC, Viciana AL, et al. Massezia furfurdisseminated infection in premature infants. Am J Clin Pathol 1989;92:595– 603. Nazzaro-Porro M, Passi S, Caprilli F, et al. Growth requirements and lipid metabolism of Pityrosporum orbiculare. J Invest Dermatol 1976;60:178 – 82. Roberts SOB. Pityriasis versicolor: a clinical and mycological investigation. Br J Dermatol 1996;81:315–26. Mokronosova MA, Arzumanian VG, Gervazieva VB. Yeast-like fungi Malassezia (Pityrosporum): clinical and immunological aspects of the study. Vestn Ross Akad Med Nauk 1998;5:47–50. Terui T, Kudo K, Tagami H. Cutaneous immune and inflammatory reactions to Malassezia furfur. Nippon Ishinkin Gakkai Zasshi 1999;40:63–7. Bergbrant IM. Seborrhoeic dermatitis and Pityrosporum yeasts. Curr Top Med Mycol 1995;6:95–112. Sohle PG, Collins-Lech C. Activation of complement by Pityrosporum orbiculare. J Invest Dermatol 1983;80:93–7. Wikler JR, Trago E, de Haar P, Nieboer C. Cell-mediated deficiency to Pityrosporum orbiculare in patients with seborrhoeic dermatitis. Abstracts of ESDR-JSID-SID-Tricontinental Meeting. Washington, DC: April, 1989. Midgley G, Hay RJ. Serological responses to Pityrosporum (Malassezia) in seborrhoeic dermatitis demonstrated by ELISA and Western blotting. Bull Soc Fr Med Mycol 1988;17:267–76.
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29. Broberg A, Faergemann J. Infantile seborrhoeic dermatitis and Pityrosporum ovale. Br J Dermatol 1989;120:359 – 62. 30. Berger RS, Stoner MF, Hobbs ER. Cutaneous manifestation of early human immunodeficiency virus exposure. J Am Acad Dermatol 1988;19:298 –303. 31. Matis WL, Triana A, Shapiro R. Dermatologic findings associated with human immunodeficiency virus infection. J Am Acad Dermatol 1987;17:746 –51. 32. Devos SA, van der Valk PG. The relevance of skin prick test for Pityrosporum ovale in patients with head and neck dermatitis. Allergy 2000;55:1056 – 8. 33. Waersted A, Hjorth N. Pityrosporum orbiculare: a pathogenic factor in atopic dermatitis of face, scalp and neck. Acta Dermatol Venereol Stockholm 1985;114:146 – 8. 34. Terragni L, Lasagni A, Oriani A. Pityriasis versicolor of the face. Mycoses 1991;34:345–7. 35. Pontasch MJ, Kyanko ME, Brodell RT. Tinea versicolor of the face in black children in a temperate region. Cutis 1989;43:81– 4. 36. Gue´ ho E, Boekhout T, Ashbee R, et al. The role of Malassezia species in the ecology of human skin as pathogens. Med Mycol 1998;36:220 –9. 37. Aly R, Berger T. Common superficial fungal infections in patients with AIDS. Clin Infect Dis 1996;22:128 –32. 38. Potter SB, Burgoon FC, Johnson CW. Pityrosporum folliculitis: report of seven cases and review of the Pityrosporum organism relative to cutaneous disease. Arch Dermatol 1973;107:388 –391. 39. Ba¨ ck O, Faergemann J, Ho¨ rniquist R. Pityrosporum folliculitis: a common disease of the young and middle-aged. J Am Acad Dermatol 1985;12:56 – 61. 40. Crozier WJ, Wise KA. Onychomycosis due to Pityrosporum. Australas J Dermatol 1993;34:109 –12. 41. Squiquera L, Galimberti R, Morelli L, et al. Antibodies to proteins from Pityrosporum ovale in the sera from patients with psoriasis. Clin Exp Dermatol 1994;19:289 –93.
P
harmacy Label—From the collection of Lawrence Charles Parish, MD, Philadelphia, PA.
Y
easts of the genus Malassezia have been recognized as members of the microbiologic flora of the skin for over a century. Under certain conditions, they can cause superficial infection of the skin and associated structures, and they can become an opportunistic pathogen in patients with catheters.
Historical Perspective The earliest reports of Malassezia-like yeasts were those found in material from the infected scales of pityriasis versicolor (PV) patients reported by Eichstedt in 1846.1 In 1873, Rivolta reported yeast of similar type isolated from patients with psoriasis.2 The name Malassezia was used by Malassez,3 who first described typical round and oval budding yeast in the stratum corneum of patients with various skin diseases. In 1889, Baillon4 proposed the name Malassezia furfur for filamentous fungus observed in the skin lesions of PV. The genus Pityrosporum was proposed in 1904 by Sabouraud5 to describe budding yeast cells without hyphal elements observed in and isolated from normal skin and scalp. In 1913, Castelani and Chalmers6 used the species name P. ovale for the first time. In 1951, Gordon7 isolated a spherical to oval yeast from PV lesions and normal skin; he named it P. orbiculare.
Taxonomy Some authors believe P. ovale and P. orbiculare to be different organisms.8,9 Keddie and Barajas9 showed with volumetric analysis that the two species are much alike in regard to the volume of mitochondria and the nucleus, but on the other hand three-dimensional images disclosed variations in the cellular inclusions. The mitochondria of P. orbiculare appear to increase in size with cell volume, whereas in P. ovale, there may be an increase in number rather than in size. Later studies, From the Department of Dermatology and Venerology, Zagreb University Hospital Center, Croatia. Address correspondence to Suzana Ljubojevic´, MD, Department of Dermatology and Venereology, Zagreb University Hospital Center, Sˇalata 4, HR-10000 Zagreb, Croatia. E-mail address: [email protected]. © 2002 by Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
however, have revealed that the two yeasts are most likely identical10 and they represent different morphologic variants of M. furfur.11 The generic name P. ovale was used by dermatologist as an associated agent in seborrheic (SD) and atopic dermatitis (AD), and P. orbiculare as a causative agent for PV. The development of molecular techniques revealed that genus Malassezia is divided in to seven species12: M. furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta, and M. slooffiae. M. pachydermatis is the only nonlipophilic yeast and is adapted to animals (dogs), although it can be occasionally found in humans. M. globosa is found very frequently on both normal and diseased skin. M. restricta is very often found on the head region. M. slooffiae is isolated both from human and animal (pig) skin. M. sympodialis and M. furfur appeared as one of the most frequent residents of human skin, along with M. globosa and M. restricta.
Morphology M. furfur is a polymorphic lipophilic microorganism characterized by a thick, multilayered cell wall. Colonies are small and yellowish-brown (Fig 1) with an intact margin. M. furfur’s reproduction occurs by monopolar budding yeast cells,13 sometimes capable of forming filaments. Cultures were generally short-lived. The cultivation of M. furfur is not simple, because standard Sabouraud medium is not suitable. We are using our own modified Dixon medium for cultivation of M. furfur.14
Epidemiology Malassezia organisms are present in 75% to 98% of healthy individual.15 The organism is present in ⬎90% of adults. The colonization starts soon after birth16 and increases during the period when the sebaceus glands become active. The peak presence of these yeasts in our patients was in late adolescent and early adult life,17 the period when the sebaceus glands become active and the concentration of skin lipids increases (Table 1). During 1999, 1299 patients were examined in the Department of Dermatology and Venerology, Zagreb, 0738-081X/02/$–see front matter PII S0738-081X(01)00240-1
180 LJUBOJEVIC´ ET AL.
Clinics in Dermatology
Y
2002;20:179 –182
Malassezia Infection
Figure 1. Native microscopy preparation of Malassezia furfur from the skin scale lesion.
Croatia.17 Eighty-seven percent of the patients were positive for M. furfur in native preparations prepared with 20% potassium hydroxide from skin or scalp lesions suspected of SD, AD, or PV (Fig 1). The youngest patient was a 3-month-old female infant, and the oldest was an 88-year-old man. Majorities of the patients were in the age groups from 16 –30 and 31–50 years (70%) (Fig 2). The male/female ratio is approximately equal, although the results from our study suggested that there are twice as many females positive in native preparations for Malassezia. Earlier reports suggested that infections caused by M. furfur were uncommon in children; now they have been demonstrated in significant numbers of infants, especially in those receiving parenteral fat emulsions thought catheters.18 –20 M. furfur infections have also been associated with scalp scaling, cradle-cap dermatitis, and infantile seborrheic dermatitis.
Malassezia yeasts are members of the normal human cutaneus flora and can be found from almost all body areas but predominately on the face and scalp region. Usually they are found in the stratum corneum and in pillar folliculi, where free fatty acids and triglycerides from sebum provide the nutritive lipid source.21 Fatty acids from triglycerides are essential for Malassezia. They are opportunistic pathogen that, under the influence of several factors such as high temperature and relative humidity; and endogenous factors such as greasy skin, sweating, heredity, and immunosuppressive treatment, change from their saprophytic phase to their pathogenic mycelian phase.22 The cause of transformation of the yeast phase of M. furfur to the mycelial one is presumably because of the changes in the composition of fatty acids of the sebaceous glands due to increased androgen concentrations.23 The initiation and aggravation of several inflammatory skin diseases associated with M. furfur can be divided into at least two groups.24 The first group includes PV and Malassezia folliculitis. The growth of M. furfur directly triggers the development of the cutaneous lesions. The second group includes AD, SD, and psoriasis, cutaneous lesions already developed by other mechanisms, which are aggravated by the growth of M. furfur.24 The cause of SD is still unknown, although many attempts have been made to relate it to infection by Malassezia. According to some authors an inadequate or inappropriate immune response to Malassezia yeast leads to SD.25–27 Sohle and Collins-Lech26 have shown that Malassezia can activate complement by both classic and alternative pathways. Defective cell-mediated immunity to Malassezia in patients with SD has been dem-
Figure 2. The frequency of M. furfur according to age in total of 1132 patients in 1999
Clinics in Dermatology
Y
2002;20:179 –182
ROLE OF MALASSEZIA FURFUR IN DERMATOLOGY
Table 1. The Frequency of Malassezia furfur According to Age and Sex in a Total of 1132 Patients in 1999 Age ⱕ5 6–15 16–30 31–50 51–70 ⬎70 Total
Male
Female
Total
0 (0%) 14 (27%) 121 (37%) 133 (29%) 104 (45%) 25 (41%) 397 (35%)
1 (100%) 38 (73%) 205 (63%) 329 (71%) 126 (55%) 36 (59%) 735 (65%)
1 (1%) 52 (4%) 326 (29%) 462 (41%) 230 (20%) 61 (5%) 1132 (100%)
181
Conclusions The genus Malassezia is a part of normal skin flora. There is a wealth of evidence supporting the hypothesis that they can be implicated in the pathogenesis of various skin diseases such as SD, PV, and Malassezia folliculitis as well as “head and neck” form of AD and psoriasis. Further investigations are certainly necessary to elucidate the role of genus Malassezia in the pathogenesis of the above-mentioned diseases.
References onstrated by Wikler et al.27 Midgley and Hay28 found a slightly greater mean level of Malassezia-specific IgG in patients with SD than in healthy subjects. Broberg and Faergemann29 suspected Malassezia to be the etiologic agent for infantile seborrheic dermatitis. The relationship between Malassezia and the immune system can be found in patients with immunosuppressive diseases. In patients with AIDS who have diminished T-cell function, a higher incidence of SD and presence of Malassezia have been found.30,31 M. furfur yeasts may be a trigger factor for AD. This organism may produce positive skin-prick reactions in a higher rate in patients with AD of the head, scalp, and neck region.32 Waersted and Hjorth33 have shown that M. furfur can induce specific IgE antibodies against Malassezia, especially in patients with AD. PV is a chronic, mild infection of the skin characterized by various pigmentary changes, mainly located on the upper trunk, neck, and upper arms. The lesions of the face are unusual,34,35 especially in adult patients, but there have been several reports on face lesions in children.35 Due to predisposing factors (most commonly, high temperature and high relative humidity, greasy skin, hyperhidrosis, hereditary factors, immunodeficiency, and immunosuppressive treatment) the yeast changes from its round blastoconidia to the mycelial form.36 It is commonly found in AIDS patients.37 Malassezia (previously called Pityrosporum) folliculitis is a chronic disease caused by Malassezia colonization, characterized by pruritic follicular papules and pustules located primarily on the trunk, neck, and upper arms, often associated by itching.38,39 M. furfur can cause or be implicated as a causative organism of many other pathologic conditions, including onychomycosis40 and psoriasis.41 Systemic reactions (Malassezia sepsis) are rare and are usually connected to the colonization of the intravascular catheter in infants receiving parenteral fat emulsions.18 –20 Successful attempts at treating patients with AD, SD, and PV with antifungal local therapy confirm the involvement of these yeast in the etiology and pathogenesis of these diseases.
1. Eichstedt E. Piltzbildung in der Pityriasis versicolor. Froriep Neue Notis Nat Heilik 1846;39:270. 2. Rivolta S. Die parassiti vegetali come introduzione allo studio delle malattie parassitarie e delle alterazioni dell a´ limentano egli animali domestica. Torino, Italy, 1873. 3. Malassez L. Note sur le champignon du pityriasis simplex. Arch Psysiol Norm Pathol 1874;1:451– 64. 4. Baillon H. Traite´ de botanique me´ dicale cryprogamique. Paris: Octave Doir, 1889:234 –5. 5. Sabouraud R. Maladies due cuir chavelu, II: les maladies desquamatires pityriasis et alope´ cies pellicularis. Paris: Masson et cie, 1904. 6. Castellani A, Chalmers AJ. Manual of tropical medicine, 2nd ed. London: Baille´ re, Tindall, and Cox, 1913:1747. 7. Gordon MA. Lipophilic yeast-like organisms associated with tinea versicolor. J Invest Dermatol 1951;17:267. 8. Gordon MA. The lipophilic mycroflora of the skin. Mycologica 1951;43:524. 9. Keddie FM, Barajas L. Quantitative ultrastructural variations between Pityrosporum ovale and Pityrosporum orbiculare based on serial section electron microscopy. Int J Dermatol 1972;11:40. 10. Leeming JP, Notman FH. Improved methods for isolation and enumeration of Malassezia furfur on human and enumeration of Malassezia furfur on human skin. J Clin Microbiol 1987;25:2017–9. 11. Yarrow D, Ahren DG. Genus 7. Malassezia Baillon. In: Kreger-vab Rij NJW, editor. The yeasts: a taxonomic study, 3rd ed. Amsterdam: Elsevier Science Publishing Co, 1984:882–5. 12. Gue´ ho E, Midgley G, Guillot J. The genus Malassezia with description of four new species. Antonie van Leeuwenhoek 1996;69:337–55. 13. Takeo K, Nakai E. Mode of cell growth of Malassezia (Pityrosporum) as revealed by using plasma membrane configuration as natural makers. Can J Microbiol 1986;32: 389 –94. 14. Skerlev M, Lipozenc˘ ic´ J, Basta-Juzbasˇ ic´ A, Pasˇ ic´ A. The significance of Malassezia furfur (Pityrosporum ovale) in dermatology. Acta Dermatovenerol (Croat) 2000;8:107– 8. 15. McGinley KJ, Leyden JJ, Marples RR. Quantitative microbiology of the scalp in non-dandruff, dandruff and seborrheic dermatitis. J Invest Dermatol 1975;64:401–5. 16. Koseki S, Takahashi S. Serial observation on the colonization of Pityrosporum orbiculare (ovale) on the facial skin surface of newborn infants. Jpn J Med Mycol 1988;29:209 – 15. 17. Ljubojevic´ S, Sˇ tulhofer Buzina D, Skerlev M, Basta-Juz-
182 LJUBOJEVIC´ ET AL.
18.
19.
20.
21.
22. 23.
24.
25. 26. 27.
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harmacy Label—From the collection of Lawrence Charles Parish, MD, Philadelphia, PA.