A dark lesion on the finger

Tinea nigra is a rare superficial mycosis most commonly caused by the organism Hortaea werneckii.1-8 Less commonly, tinea nigra is caused by the amorphic fungus Stenella araguata.3 Tinea nigra is characterized by a single, asymptomatic, dark, macule located on the...

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Tinea nigra is a rare superficial mycosis most commonly caused by the organism Hortaea werneckii.^1-8 Less commonly, tinea nigra is caused by the amorphic fungus Stenella araguata.³ Tinea nigra is characterized by a single, asymptomatic, dark, macule located on the palms or soles of the feet.^1,4,8

H werneckii (formerly Phaeoannellomyces werneckii) is a black yeast-like fungus that is typically found in humid environments.^4,6 This organism is considered an environmental pathogen and is not part of the normal human flora. It is transmitted via direct contact with infested substances, such as soil or sewage.^1,2 The fungus is lipophilic and extremely halotolerant in character, which encourages adhesion to human skin, especially in areas such as the palms or soles.^2,6 There is no documented human to human transmission of H werneckii.^1,4

Because the causative organism thrives in hot, humid environments, tinea nigra is typically seen in tropical climates such as the southeastern United States (especially along the Gulf Coast). Central America, South America, Asia, and Africa are also common locations for infection, due to their tropical or subtropical climates.^1-4,7,8 These infections can also be present in more temperate climates, as people travel from endemic regions.^2,7 Tinea nigra can infect people of any age, race, or sex. However, it is most common in children and young adults.^1,2,4 The most common predisposing factors for infection with H werneckii are hyperhidrosis of the palms or soles, frequent exposure to soil or sewage, and exposure to a high-salinity environment. Because of these factors, farmers frequently contract tinea nigra.^2,4

Tinea nigra typically presents as a single, darkly pigmented, well-demarcated macule located on the palm.^1,4,8 Because H werneckii yeast cells are highly halotolerant and hydrophobic in nature, they tend to colonize the palms of the hand more often than other locations. Less common sites of infection include the palmar side of the fingers, soles of the feet, and the trunk.^2,4 These macules are often brown to black in coloration and sometimes present with hyperpigmentation of the advancing border.^1,4 Some patients report a decrease in pigmentation throughout the day, which can be attributed to clearance of the causative agent due to routine activities.² Tinea nigra lesions vary in texture, ranging from a mild scale to a velvet-like texture. These lesions are usually not associated with any other symptoms (eg, pruritus, erythema) and thus are often not immediately brought to a physician’s attention.^1,2,4

Tinea nigra is classically diagnosed based on clinical findings and then confirmed with potassium hydroxide (KOH) examination and/or culture.^1,2 Patients may have a history of travel to an area of tropical climate⁷ or contact with commonly infested materials.² KOH examination of skin scrapings reveals brown- or gold-pigmented septate hyphae.^1,2,4 Occasionally, hyperchromic blastoconidia can be seen under KOH examination.⁴ After a 10- to 15-day incubation period, cultures of H werneckii grow in a yeast-like manner with glossy black colonies. After 2 weeks of growth, H werneckii cultures take on a mold-like appearance and morph into a filamentous, melanized growth.^1,2,4 Biopsies are not often performed because clinical impressions and KOH preparations are usually diagnostic.⁴ The histopathology of tinea nigra shows darkly pigmented hyphae confined to the stratum corneum with minimal to no associated inflammatory processes.¹ Polymerase chain reaction testing is available for H werneckii but is rarely utilized in the clinical setting.^2,8

Tinea nigra is most commonly mistaken for other melanocytic lesions, such as acral nevi, acral melanoma, junctional nevi, and lentigines.⁴ Because H werneckii is limited to the stratum corneum, the areas of hyperpigmentation are easily scraped off, as compared with other pigmented lesions.⁸ Skin scrapings of tinea nigra reveal positive findings under KOH examination, whereas other melanocytic lesions do not. This test performed by scraping the active border of the lesion, then treating the scrapings with 10% KOH and observing them under a light microscope. Under dermoscopy, tinea nigra presents as patches of pigment that are not restricted to the dermatoglyphs of the palms or soles. This contrasts with the dermoscopic examination of acral nevi or acral melanomas, in which the pigmentation is either constrained to the ridges, as in acral nevi, or constrained to the furrows, as in acral melanoma. Both acral nevi and acral melanoma follow a characteristic parallel-like pattern that is not seen in tinea nigra.⁵ Other possible causes of lesions that are similar to tinea nigra include skin staining with chemicals or dyes, postinflammatory hyperpigmentation, Addison disease, secondary syphilis, and fixed drug eruption.⁴ All are easily excluded based on the patient’s history, physical findings, or KOH examination or culture results.

Patients with tinea nigra are often cured with topical keratolytic agents, such as Whitfield ointment (6% benzoic acid, 3% salicyclic acid), as the superficial layer containing the causative agent is subsequently sloughed off.^1,2 Similarly, simple scraping of the skin is often curative. Topical imidazoles and allylamines have also proven to be an effective means of treating tinea nigra.^1,2,8 Specific drugs that have been proven effective include ketoconazole, miconazole, and terbinafine.^9-11 Both topical keratolytic agents and topical antifungal medications are applied once or twice daily, usually for a duration of approximately 2 weeks, or until the lesion has resolved. Oral antifungal treatment is not recommended, as topical agents are sufficiently effective.^1,2 Once treated, most cases of tinea nigra do not recur.² Those with recurring infections are most likely due to re-exposure rather than recurrence of the initial infection.¹

In this clinical case, a KOH scraping was performed in the office, results of which showed the presence of brown-pigmented septate hyphae, confirming the diagnosis. The patient was treated with topical terbinafine for 3 weeks, which led to the resolution of the lesion.

Sydney Dunn, BS, is a medical student, and Christopher Rizk, MD, is a dermatology resident at the Baylor College of Medicine in Houston. 

References

1. Bolognia JL, Jorizzo JL, Schaffer J. Dermatology. 3rd ed. London: Saunders; 2012.
2. Bonifaz A, Badali H, de Hoog GS, et al. Tinea nigra by Hortaea Werneckii, a report of 22 cases from Mexico. Stud Mycol. 2008;61:77-82. 
3. Perez C, Colella MT, Olaizola C, Hartung de Capriles C, Magaldi S, Mata-Essayag S. Tinea nigra: report of twelve cases in Venezuela. Mycopathologia. 2005;160:235-238. 
4. Bonifaz A. Tinea nigra. In Arenas R, Estrada R, eds. Handbook of Tropical Dermatology. Austin, TX: Landes Bioscience; 2001:24-26.
5. Piliouras P, Allison S, Rosendahl C, Buettner PG, Weedon D. Dermoscopy improves diagnosis of tinea nigra: a study of 50 cases. Australas J Dermatol. 2011;52:191-194.
6. Zalar P, de Hoog GS, Gunde-Cimerman N. Ecology of halotolerant dothideaceous yeasts. Stud Mycol. 1999;43:38-48.
7. Rezusta A, Gilaberte Y, Betran A, et al. Tinea nigra: a rare imported infection. J Eur Acad Dermatol Venereol. 2010;24:89-91.
8. James WD, Berger TG, Elston DM, eds. Andrews’ Diseases of the Skin: Clinical Dermatology. 11th ed. Philadelphia, PA: Saunders-Elsevier; 2011.
9. Burke WA. Tinea nigra: treatment with topical ketoconazole. Cutis. 1993;52:209-211.
10. Marks JG Jr, King RD, Davis BM. Treatment of tinea nigra palmaris with miconazole. Arch Dermatol. 1980;116:321-322.
11. Shannon PL, Ramos-Caro FA, Cosgrove BF, Flowers FP. Treatment of tinea nigra with terbinafine. Cutis. 1999;64:199-201.