SciELO - Scientific Electronic Library Online

vol.77 issue5Clinical experience assessing 284 cases of erisipelaComments on the XX International Dermatology Congress author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand




Related links


Anais Brasileiros de Dermatologia

Print version ISSN 0365-0596On-line version ISSN 1806-4841

An. Bras. Dermatol. vol.77 no.5 Rio de Janeiro Sept./Oct. 2002 



Pityriasis Versicolor*



Josenildo Rodrigues de OliveiraI; Viviane Tom MazoccoI; Denise SteinerII

IResident Doctor, Department of Dermatology, "Faculdade de Medicina de Jundiaí"
IIAssistant Professor, Doctor of Dermatology





Pityriasis versicolor is a superficial fungal infection characterized by changes in skin pigment due to colonization of the stratum corneum by a dimorphic lipophilic fungus of the normal flora of the skin, known as Malassezia furfur. This disease is most prevalent in the tropics, but is also common in temperate climates. Treatment is available and cure rates are high, although recurrence is common.

Key words: Fungi; Malassezia; pityriasis




Pityriasis Versicolor (PV) is a superficial fungal infection, characterized by changes in skin pigment due to colonization of the stratum corneum by a dimorphic lipophilic fungus of the normal flora of the skin, known as Malassezia furfur.1,2,3 The organism's yeast phase shows two morphologically distinct forms, one ovoid, the other spherical, in which the fungus is named Pityrosporum ovale and Pityrosporum orbiculare, respectively. PV is also known as tinea versicolor, dermatomycosis furfurácea and tinea flava. Although it may be distributed globally, it is more commonly found in the tropics. Often considered a post-pubescent disease, evidence shows that PV is not uncommon in children.1 Therapeutic advances are being realized in the treatment of this infection, like the substitution of topical antifungal drugs by systemic ones.4



PV was first recognized as a fungal disease by Eichsedt in 1846.5 In 1853, Robin described the fungus in scales, naming it Microsporum furfur.6 In 1853, Malassez observed "spores"7 that were then named Pityrosporum ovale by Castellani and Chalmers.8 In 1889, Baillon5 used the name Malassezia furfur in his text. In 1951, Gordon isolated other yeast, micromorphologically distinct from P. ovale, and named it Pityrosporum orbiculare.9



PV is most prevalent in the tropics with 40% incidence,10 but it is also common in temperate areas.11 It occurs in both sexes and all races, and shows variable distribution according to age range. Most cases of PV are in adults and post-pubescent children,12 its factors being a predisposition to hormonal changes and/or increase of sebum secretion.13 Quantitative cultures have shown much higher numbers of this fungus in children younger than one-year of age, and in pre-pubescents.14 Susceptibility in children is greater than what was initially believed. One study confirms about 4.9% of cases in children between five months and 13 years of age.15,16Distribution of PV in children is different, yet the most affected area is the face.16 It is important to remember that PV is not contagious and that precarious hygiene habits do not represent a factor in the development of this infection.



PV is caused by Malassezia furfur, which may appear in two forms: oval - Pityrosporum ovale-, often in the scalp, and cylindrical - Pityrosporum orbiculare-generally on the trunk.17These fungi require the addition of lipidic substances in the middle of culture,18 like olive oil. They grow better on average in 32-37°C environments. Filaments normally seen in areas of the skin affected by infection grow when the yeasts are incubated in stratum corneum.19P. orbiculare and P. ovale are similar in macromorphology, but differ in micromorphology. Observations show that the two forms are produced by the same organism, with the transformation of one into another possibly taking place;20 some antigenic similarities have also been reported. Three distinct forms of Malassezia furfur were recently described by Cunnigham et al.,22 and denominated serotypes A, B and C, which differ morphologically, physiologically and serologically, with distinct cellular membrane antigens.23,24 A recent study did not describe any difference between the distribution of serotypes in affected skin when compared to the control group.23,24

The organism is found in normal flora conditions,25,26 in percentages varying from 90 to 100% of individuals. It appears to be opportunistic, though the factors that increase susceptibility have not been completely defined yet. The simple fact of high growth does not seem to be the underlying cause,27,28 though some skin lesion cultures show much higher amounts of P. orbiculare in comparison of non-lesional skin with the skin of healthy volunteers.17,25

PV occurs when yeasts are converted by the micellar form due to certain predisposed factors, which may be classified as endogenic or exogenic. The exogenous factors include heat and humidity, contributing to higher disease prevalence in the tropics and during the summer in temperate climates. Other exogenous factor may be skin occlusion by clothing or cosmetics, resulting in an increase of carbon dioxide concentration29 and leading to microflora and pH changes. The infection has been experimentally induced by occlusive clothing.30 On the other hand, endogenic factors31-33 are responsible due to disease prevalence in temperate climates, including seborrheic dermatitis, Cushing's syndrome, treatment with immunosuppressor, malnutrition and (particularly flexural) hyperhydrosis. Hereditary factors appear to perform a certain role in the disease. Positive familial history was noted in various studies, while conjugal cases are less commonly reported.32,33

Malassezia furfur has been associated to folliculitis by Pityrosporum,34reticular and confluent papilloma (Gougerot-Carteaud),19seborrheic dermatitis, septicemic25 onychomycosis.36 In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis.

A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum.37 In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis.38

It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin.39 Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction.40 Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration.41These dicarboxilic acids may be causing the cytotoxic effects.42 The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.

The pathogenesis of hyperpigmentation in PV is not entirely understood. Two theories have been presented: (I) thickening of the keratine layer; and (II) presence of intense cellular inflamed infiltrate, which acts like a stimulus for melanocytes to produce more pigment, leading to an increase in the size of melanosomes and distribution changes in the epidermis.42



Skin biopsy is seldom necessary to confirm the diagnosis, though it may be useful in some cases. Staining due to hematoxiline-eosine reveals the presence of globose cells, bowling-pin-shaped cells and short pseudo-hyphae in the corneal layer, in addition to mild hyperkeratosis and acanthosis in the epidermis, perivascular lymphocytic infiltrate, and plasmocytes and histiocytes in the dermis. The electron microscope revealed melanocyte degeneration, epidermic reaction manifested by mitotic Langerhans cells, and allergic and inflammatory cellular reaction to the fungus,27 generalized in the dermis.



PV patients generally show multiple lesions on the trunk, with intercalated regions of normal skin.43 The lesions may also erupt on the throat and proximal upper extremities. Its distribution is normally parallel to that of the sebaceous glands,26 with higher occurrence on the thorax, back and face. However, the lesions are found in a higher number on the back. Those located on the face are more common in children (including newborns and infants) than in adults.44 A study revealed face lesions in children of PV-carriers in approximately 32% of cases,15 usually seen in the margins of the scalp, like achromic or hypopigmented, squamous and small macules. These lesions rarely remain limited to the lower limbs, were popliteal cavity, forearm, underarm, penis/genital,45 or in the area of radiotherapy.46 The distribution also occurs in areas normally covered by clothing, calling attention to the theory in which the occlusion of glands plays a role in this disease. The lesions may be hypo- or hyperpigmented (figures 1 and 2), erythematous or dark-brown; justifying the versicolor name. In the surface of lesions, a fine scaling is found, as evidenced by the stretched skin, a birthmark named after Zileri. Although at times mild pruritus occurs, patients' complaints are related to skin color changes more than to any other symptom.





PV as well as folliculities by Pityrosporum may occur in AIDS-patients. The disease then acquired an extended appearance, but does not differ clinically from PV in non-HIV patients.47,48



A study was performed in patients carrying PV with the objective of establishing the ultrastructural changes of hyper- and hypopigmented skin, and compare them with the same patients' non-affected skin. As such, four patients with confirmed diagnosis of PV were selected and submitted to skin biopsies.

The hyperpigmented skin showed the stratum corneum to be leaner than in the hypopigmented skin, but in both the stratum corneum was thinner than in non-affected skin. A large number of tonofilaments were present in the granulous layer of the hyperpigmented skin.

In the hypopigmented skin, the melanosomes were dispersed and in a smaller amount than in the non-affected skin. In the hyperpigmented skin, a large number of melanosomes occupying the cytoplasm of some melanoctyes, while adjacent keratinocytes demonstrated few melanosomes in its cytoplasm, which suggests difficulty in transferring the melanosome granules to the keratinosomes.

In the hypopigmented skin as in the hyperpigmented skin, the portion of the cell promptly affected is related to the cytoplasmatic organs, with a latent effect on the nucleus and nucleolus. 49



The diagnosis of PV is usually performed only through clinical examination. Wood's lamp is sometimes used to confirm the diagnosis and detect subclinical lesions. It presents yellow-gold fluorescence, probably due to excretion of (porphyrin) fungus metabolites, sensitive to ultraviolet radiation. The right mycological exam is performed on the lesion's scraping, after clarification of the scales by 10% potassium, which allows the encounter with spores and pseudo-hyphae. The negative result excludes the diagnosis. The characteristic distribution of PV on the trunk, throat and proximal extremities constitutes a relevant factor in the diagnosis.



Diagnosis differential includes other entities leading to cutaneous dispigmentation, namely vitiligo and alba pityriasis. None of them show furfuraceous scales or fluorescence under Wood's lamp. Another differential diagnoses that must not be forgotten is leprosy in its indeterminate form, located mainly on the face, in which alteration to sensitivity may not be present in an initial phase.

Other possibilities include psoriasis, seborrheic dermatitis (both able to coexist with PV), recticular and confluent papillomatosis (Gougerot-Carteaud), erythrasma and dermatophitosis. Wood's lamp examination is probably one of the most useful weapons in the differentiation of PV with erythrasma and dermatophitosis. Erythrasma acquires a red-coral tonality with Wood's lamp, and the dermatophitosis does not fluoresce.



PV treatment can be performed with a large amount of agents, subdivided into two groups: topical and systemic ones.

A -Topical Agents

In this group, the most frequently used agent has been selenium sulfide 2.5-5% in shampoo form applied once a day. Treatment must be realized over a period varying from seven to 14 days or more, and sometimes indefinitely.50

All topical "azoles" seems to be equally effective in treating PV. Still, none of them have been as fully studied as ketoconazol cream.50

B - Systemic Agents

¬ Ketoconazol. The suggested dose is 200 mg daily for 10 days. The cure rate is high (from 90 to 100%). Risk of hepatotoxicity exists and has been calculated in 1:500,000 patients who received oral ketoconazol for a short duration (10 days).

¬ Fluconazol. The recommended dose is 150 mg weekly for three weeks.

¬ Itraconazol. The suggested dose is 200 mg daily for seven days. This drug is well tolerated. When indicated for prolonged use, i.e. more than seven days, some gastrointestinal effects may be manifested. Cephalea, nausea and abdominal pain are possible side effects in 7% of cases.

¬ Terbinafine. Oral terbinafine is effective against many dermatofitoses, but not in PV treatment, due perhaps to not reaching a high enough concentration in the cornea layer. Topical terbinafine proved to be effective in treating M. furfur infection.

Topical therapy vs. systemic therapy

From the pharmacotherapeutic point of view, as a superficial infection PV should be treated with topical agents. Nonetheless, patients defend another point of view. For them treatment with topical agents has many disadvantages, e.g. the time needed and difficult application of the drug over large affected areas, especially on the trunk as well as the unpleasant odor of certain agents. For these reasons, patient adhesion is inadequate, which increases the rate of recurrence. Effectiveness of topical agents is lower, and rate of recurrence varies form 60 to 80%.50As such, the systemic agents are those recommended in short-term treatment for many patients, in spite of the side effects they may bring.

Hepatic effects with antifungal therapy

Hepatotoxicity is a rare side-effect that may be associated with some oral antifugal medications. The report on hepatotoxicity with ketoconazol use seems to be most common in women above the age of 50 who have been using the medication over long periods (from 51 to 60 days). Tests of hepatic function are found to be high, but normalization ensues by simply interrupting the drug.4



Pityriasis versicolor is a common superficial fungal infection caused by the Malassezia furfur fungus, incident mainly in the tropics. In the past it was thought to be a post-pubescent disease, however current evidence shows that versicolor pityriasis is not uncommon in school children. Diagnosis is easily performed by clinical exam.

Treatment shows changes in chronology, gradual substitution occurring of topical antifungal by systemic medication, for three reasons: (I) patient adhesion is inadequate for the topical drugs due to the required time of use, difficult applicability in extensor areas and the unpleasant odor of certain agents; (II) effectiveness of topical agents is lower, and the rate of recurrence varies from 60 to 80%; (III) the emergence of systemic antifungal drugs at a lower rate of adverse events.

After treatment, the affected area remained hypopigmented for a variable period of time. The mechanism of hypopigmentation has not been well established yet. But ultrastructural studies show severe damage to melanoctyes, which varies from melanosomes and altered mitochondria up to degeneration.



1. Michalowski R, Rodziewicz H. Pityriasis versicolor in children. Br J Dermatol 1963; 75: 397-400.        [ Links ]

2. Adamski Z. Studies of a role played by lipophilic yeasts Malassezia furfur (Pityrosporum ovale, Pityrosporum orbiculare) in different dermatoses. Postepy Dermatol (Poznan) 1995; 12: 349-454.        [ Links ]

3. Zaitz C - Dermatoses associadas às leveduras do gênero Malassezia. An Bras Dermatol 2000; 75 (2): 129-142.        [ Links ]

4. Sunenshine PJ, Schwartz RA, Janniger CK. Review. Tinea versicolor. Int J Dermatol 1998; 37: 648-655.        [ Links ]

5. Bailon H. Traite de Botanique Medicale Cryptogamique. Paris: Octave Doin, 1889: 234.        [ Links ]

6. Robin C. Historie Naturelle des Vegeaux Parasites. London: Balliere, 1853: 438.        [ Links ]

7. Gordon MA. The lipophilic mycoflora of the skin. Mycologica 1951; 43: 524-534.        [ Links ]

8. Castellani A, Chalmers AJ. Manual of Tropical Medicine, 2nd edn. New York: Wm. Wood & Co., 1913: 936-837.        [ Links ]

9. Gordon MA. Lipophilic yeastlike organisms associated with tinea versicolor. J Invest Dermatol 1951; 17: 267-272.        [ Links ]

10. Savin R. Diagnosis and treatment of tinea versicolor. J Fam Pract 1996; 43: 127-132.        [ Links ]

11. Nowiscki R, Sadowska E. Mycotic infections in the Gdansk area. Przegl Dermatol 1993; 80: 245-250.        [ Links ]

12. Akpata LE, Gugnani HC, Utsalo SJ. Pityriasis versicolor in school children in Cross River State of Nigeria. Mycoses 1990; 33: 549-551.        [ Links ]

13. Bergbrant IM, Faergemann J. Variations of Pityrosporum orbiculare in middle-aged and elderly individuals. Acta Derm Venereol 1988; 68: 537-540.        [ Links ]

14. Bergbrant IM, Brobeg A. Pityrosporum ovale culture from the forehead of healthy children. Acta Derm Venereol 1994; 74: 260-261.        [ Links ]

15. Terragni L, Lasagni A, Oriani A, Gelmetti C. Pityriasis versicolor in the pediatric age. Pediatr Dermatol 1991; 8: 9-12.        [ Links ]

16. Miskeen AK, Kelkar SS, Shroff HJ. Pityriasis versicolor in children. Indian J Dermatol Venereol Leprol 1984; 50: 144-146.        [ Links ]

17. Roberts SOB. Pityrosporum orbiculare: incidence and distribution on clinically normal skin. Br Dermatol 1969; 81: 264-269.        [ Links ]

18. Faergemann J. Lipophilic yeasts in skin disease. Semin Dermatol 1985; 4: 173-184.        [ Links ]

19. Faergemann J, Aly R, Maibach HI. Growth and filament production of Pityrosporum orbiculare and P. ovale on human stratum corneum in vitro. Acta Derm Venereol 1983; 63: 388-392.        [ Links ]

20. Salkin IF, Gordon MA. Polymorphism of Malassezia furfur. Can J Microbiol 1977; 23: 471-475.        [ Links ]

21. Faergemann J, Tjernlund U, Scheynius A, Sverker B. Antigenic similarities and differences in genus Pityrosporum. J Invest Dermatol 1982; 78: 28-31.        [ Links ]

22. Cunningham AC, Leeming JP, Ingham E, Gowland G. Differentiation of three serovars of Malassezia furfur. J Appl Bacteriol 1990; 68: 439-446.        [ Links ]

23. Ashbee HR, Ingham E, Holland KT, Cunliffe WJ. The carriage of Malassezia furfur serovars A, B, and C in patients with pityriasis versicolor, seborrhoeic dermatitis and controls. Br J Dermatol 1993; 129: 533-540.        [ Links ]

24. Ashbee HR, Ingham E, Holland KT, et al. The role of Malassezia furfur serovars A, B, and C in Pityriasis versicolor and seborrhoeic dermatitis. Br J Dermatol 1991; 125: 495.        [ Links ]

25. Schmidt A. Malassezia furfur: a fungus belonging to the physiological skin flora and its relevance in skin disorders. Cutis 1997; 59: 21-24.        [ Links ]

26. Leeming JP, Notman FH, Holland KT. The distribution and ecology of Malassezia furfur and cutaneous bacteria on human skin. J Appl Bacteriol 1989; 67: 47-52.        [ Links ]

27. Breathnach AS, Nazzaro Porro M, Martin B. Ultrastructure of skin in pityriasis versicolor. Giornale Italiano di Dermatologia-Minerva Dermatologica 1975; 110:457-469.        [ Links ]

28. Scheynius A, Faergemann J, Forsum U, Sjoberg O. Phenotypic characterization in situ of inflammatory cells in pityriasis (tinea) versicolor. Acta Derm Venereol 1984; 64: 473-479.        [ Links ]

29. King RD, Cunico RL, Maibach HI, et al. The effect of occlusion on carbon dioxide emission from human skin. Acta Derm Venereol 1978; 58: 135-138.        [ Links ]

30. Faergemann J, Bernander S. Tinea versicolor and Pityrosporum orbiculare. A mycological investigation. Sabouraudia 1979; 17: 171-179.        [ Links ]

31. Congly H. Pityriasis versicolor in a 3-month-old boy. Can Med Assoc J 1984; 130: 844-845.        [ Links ]

32. Roberts SOB. Pityriasis versicolor: a clinical and mycological investigation. Br J Dermatol 1969; 81: 315-326.        [ Links ]

33. Burke RC. Tinea versicolor: susceptibility factors and experimental infections in human beings. J Invest Dermatol 1961; 36: 389-402.        [ Links ]

34. Elewski BE, Hazen PG. The superficial mycoses and the dermatophytes. J Am Dermatol 1989; 21: 655-673.        [ Links ]

35. Heng MCY, Henderson CL, Barker DC, Haberfelde G. Correlation of Pityrosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique. J Am Acad Dermatol 1990; 23: 82-86.        [ Links ]

36. Crozier WJ, Wise KA. Onychomycosis due to Pityrosporum. Australas J Dermatol 1993; 34: 109-112.        [ Links ]

37. Sohnle PG, Collins-Lech C. Cell-mediated immunity to Pityrosporum orbiculare in tinea versicolor. J Clin Invest 1978; 62: 45-53.        [ Links ]

38. Hashim FA, Elhassan AM. Tinea versicolor and visceral leishmaniasis. Int J Dermatol 1994; 33: 258-259.        [ Links ]

39. De Luca C, Picardo M, Breathnach A, et al. Lipoperoxidase activity of Pityrosporum: characterization of by-products and possible role in pityriasis versicolor. Exper Dermatol 1996; 5: 49-56.        [ Links ]

40. Nazzaro-Porro M. Identification of tyrosinase inhibitors in cultures of Pityrosporum. J Invest Dermatol 1978; 71: 205-208.        [ Links ]

41. Soyer HP, Cerroni L. The significance of histopathology in the diagnosis of dermatomycoses. Acta Dermatovenerologica Alpina Pannonica et Adriatica 1992; 1: 84-87.        [ Links ]

42. Galadari I, El-Komy M, Mousa A, et al. Tinea versicolor: histologic and ultrastructural investigation of pigmentary changes. Int J Dermatol 1992; 31: 253-256.        [ Links ]

43. Schwartz RA, Fox MD. Office Dermatology. Kansas City, Missouri: American Academy of family Physicians Publications, 1992.        [ Links ]

44. Terragni L, Lasagni A, Oriani A. Pityriasis versicolor of the face. Mycoses 1991; 34: 345-347.        [ Links ]

45. Daneshvar SA, Hashimoto K. An unusual presentation of tinea versicolor in an immunosuppressed patient. J Am Acad Dermatol 1987; 17: 304-305.        [ Links ]

46. Conill C, Azón-Masoliver A, Verger E, et al. Pityriasis versicolor confined to the radiation therapy field. Acta Oncol 1990; 29: 949-950.        [ Links ]

47. Aly R, Berger T. Common superficial fungal infections in patients with AIDS. Clin Infect Dis 1996; 22: S128-S132.        [ Links ]

48. Elmets CA. Management of common superficial fungal infections in patients with AIDS. J Am Acad Dermatol 1994; 31: S60-S63.        [ Links ]

49. Karaoui R, Bou-Resli M, Al-Zaid NS, Mousa A. Tinea versicolor: Ultrastructural studies on hypopigmented and hyperpigmented skin. Dermatologica 1981; 132: 69-85.        [ Links ]

50. Savin R. Diagnosis and treatment of tinea versicolor. J Fam Pract 1996; 43: 127-132.        [ Links ]



Profa. Dra. Denise Steiner
Rua Eng° Edgar Egídio de Souza, 420 Pacaembú
São Paulo SP 01233-020
Tel.: (11) 825 9955 / 825 9968
Fax: (11) 825 9315

Received in March, 30th of 2001
Approved by the Consultive Council and accepted for publication in April, 2nd of 2002.



* Work done at "Serviço de Dermatologia do Hospital das Clínicas de Franco da Rocha, Faculdade de Medicina de Jundiaí".

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License