Figure. Hyperpigmented macules coalescing into patches with fine white scale on back.
A 65-year-old man presents with a recurring rash on his back. He has had the rash several times before, most often during the summer, and it was treated successfully with an antifungal shampoo prescribed by a prior dermatologist. The rash is not itchy or painful. He has a history of depression and hypertension. On physical examination, hyperpigmented macules coalescing into patches with very fine white scale are found. The lesions are scattered primarily on his upper chest and upper back.
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Tinea versicolor, also known as pityriasis versicolor, is a superficial fungal infection of the skin frequently affecting the trunk, neck, and proximal extremities.1 The infection is caused by Malassezia, a lipophilic dimorphic fungi also known as Pityrosporum.1 This fungus is a part of the normal skin flora, however, disease may occur when the fungus converts to its pathogenic hyphal form.2
Tinea versicolor was first identified as a distinct pathology in 1801. In 1846, Karl Ferdinand Eichstedt, MD, further delineated the mycotic nature of the disease, and Charles Robin, MD, identified the causative agent in 1853.3 Tinea versicolor was the first cutaneous condition associated with Malassezia to be discovered, although it was initially classified as a dermatophyte and erroneously named Microsporum furfur.
Malassezia globosa is the most commonly identified causative fungus of tinea versicolor, although species prevalence varies by region.4,5 Malassezia species proliferate in warm and humid conditions; thus, tinea versicolor is especially prevalent in tropical environments. No gender-specific predilection of tinea versicolor or ethnic predominance has been found.1 Incidence of disease increases significantly from childhood to adolescence as increasing sebum production creates a lipid-rich environment favorable to the fungus.1,2,6 Adolescents and adults who are physically active are also more likely to develop tinea versicolor.2
Malassezia yeasts isolated from tinea versicolor lesions are frequently found in their mycelial phase.5 Humidity, sweat, and heat, among other predisposing host factors such as Cushing syndrome prompt the yeasts to convert to their mycelial form, subsequently invading the stratum corneum and interacting with the host’s immune system.6 M globosa has a high degree of lipase activity and capacity for hyphal growth compared with other Malassezia species, explaining its significant role as a causative agent of tinea versicolor.5 The reasons for hyphal growth are still unclear, although the lack of inflammation within the lesions may result from T-cell inhibition caused by a lipid component associated with the yeast cell wall. 6
The rash associated with tinea versicolor typically presents on the torso, neck, and proximal extremities; this predilection for seborrheic areas is because of the lipophilic nature of the fungus.1 In pediatric populations, the face is often affected.2 The characteristic rash involves well-demarcated, finely scaling patches or plaques that may be hyperpigmented, hypopigmented, or erythematous.1,2 The lesions are generally asymptomatic but may become severely pruritic, especially in humid conditions. The hyperpigmentation or hypopigmentation associated with the rash may persist months after the rash is effectively treated. Though effective treatments exist for tinea versicolor, relapse is common.2
With its characteristic rash, tinea versicolor is often diagnosed clinically. If not initially appreciated, the fine scale of the rash is more readily identified when the affected skin is stretched or scraped.2 Skin scrapings can be soaked with potassium hydroxide or stained to aid in diagnosis. The numerous yeast cells and hyphae seen under direct microscopy are often said to resemble “spaghetti and meatballs.” After treatment initiation, microscopic evaluation is frequently nonsignificant and will no longer aid in diagnosis.2,6 The rash of tinea versicolor will also demonstrate coppery-orange fluorescence under Woods lamp, which may aid in diagnosis.1
Though punch biopsy is not required for diagnosis, histology of tinea versicolor shows hyperkeratosis and acanthosis of the epidermis and a mild superficial perivascular infiltrate in the dermis. The characteristic “spaghetti and meatball” appearing spores and hyphae of Malassezia are seen almost exclusively in the stratum corneum. The fungus can be seen in the stratum corneum with hematoxylin-eosin stain, though periodic-acid-Schiff stain may improve recognition.1
Should a patient fail to respond to treatment or if potassium hydroxide-treated scrapings do not support the diagnosis of tinea versicolor, alternative diseases should be considered. The differential diagnosis of tinea versicolor is broad and includes postinflammatory hypo- and hyperpigmentation (PIH), pityriasis rosea, tinea corporis, nummular eczema, vitiligo, confluent and reticulated papillomatosis, and progressive macular hypomelanosis.1,2
Topical antifungal creams or shampoos, particularly imidazoles such as ketoconazole, are first-line treatments for tinea versicolor with a typical recovery time of 2 to 3 weeks.6,7 Though ketoconazole is frequently used, no significant difference in results is achieved by various imidazoles.6 Alternative topical agents include the use of terbinafine 1% cream, sulfur plus salicylic acid, zinc pyrithione shampoo, and selenium sulfide shampoo. Duration may vary depending on treatment modality, however, longer treatment durations and increased concentration of active agents are associated with higher cure rates.2 The oral medications fluconazole and itraconazole are second-line treatments and may be used in patients with extensive skin disease or recalcitrant or recurrent cases.1,2 In patients with recurrent tinea versicolor, topical treatments may be used once weekly for prophylaxis.2
This patient was diagnosed clinically with tinea versicolor. Given the widespread and recurrent nature of tinea versicolor, he was treated with oral fluconazole and was prescribed ketoconazole shampoo to use weekly as a body wash for prophylaxis.
Rosemary Demet is a medical student at Baylor College of Medicine in Houston, Texas. Tara L. Braun, MD, is a dermatologist at Elite Dermatology in Houston, Texas.
1. Karray M, McKinney WP. Tinea versicolor. In: StatPearls. StatPearls Publishing LLC; 2022.
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3. Negroni R. Historical aspects of dermatomycoses. Clin Dermatol. 2010;28(2):125-132. doi:10.1016/j.clindermatol.2009.12.010
4. Nenoff P, Krüger C, Ginter-Hanselmayer G, Tietz HJ. Mycology – an update. Part 1: Dermatomycoses: causative agents, epidemiology and pathogenesis. J Dtsch Dermatol Ges. 2014;12(3):188-211.doi:10.1111/ddg.12245
5. Prohic A, Jovovic Sadikovic T, Krupalija-Fazlic M, Kuskunovic-Vlahovljak S. Malassezia species in healthy skin and in dermatological conditions. Int J Dermatol. 2016;55(5):494-504. doi:10.1111/ijd.13116.
6. Saunte DML, Gaitanis G, Hay RJ. Malassezia-associated skin diseases, the use of diagnostics and treatment. Front Cell Infect Microbiol. 2020;10:112. doi:10.3389/fcimb.2020.00112.
7. Hu SW, Bigby M. Pityriasis versicolor: a systematic review of interventions. Arch Dermatol. 2010;146(10):1132-1140. doi:10.1001/archdermatol.2010.259.