Figure 1. A 3×3-cm tan patch with central clearing is present on the left palm.
Figure 2. Olive hyphae are present on the potassium hydroxide preparation.
Tinea nigra, also known as "tinea nigra palmaris" because of its predilection for the palm, is an asymptomatic superficial fungal infection of the stratum corneum caused by Phaeoannellomyces werneckii, also known asExophiala werneckii and Cladosporium werneckii. Tinea nigra is uncommon in the United States, being much more prevalent in warm, humid parts of the world such as the Central and South Americas, Africa, and Asia. The asymptomatic nature of this infection probably accounts for the infrequent recognition and reports from the United States. Most cases in the United States have been reported from the Atlantic coastal areas and the Gulf of Mexico.1 Children and adolescents, particularly girls, are most likely to become infected with this fungus.
The incubation period may be very long, up to 20 years in some cases.1 The most common presentation is a brown-black, sharply demarcated macula or patch on the palmar surface or volar surface of the fingers; it appears less commonly on the feet or other cutaneous surfaces. The reason for the predilection for the palmar surface is unknown. The macula enlarges slowly over a period of weeks to months.
Because of its appearance, tinea nigra is frequently misdiagnosed as a melanocytic lesion, such as a junctional nevus, or even a melanoma.2 Pigmentation from various chemicals and dyes can also mimic this infection, particularly a silver nitrate stain.
A potassium hydroxide–prepared scraping from a lesion will display the characteristic brown or olive hyphae and sporelike yeast cells. The fungus can be grown on Sabouraud agar, forming black, shiny, tarlike colonies.3
Antifungal creams such as clotrimazole or ketoconazole are effective therapy. Keratolytic agents such as salicylic acid may also be effective.4 Oral antifungal drugs such as griseofulvin and terbinafine hydrochloride are not effective treatment for this disorder.
Accepted for publication November 11, 1997.
Reprints: LCDR Joseph R. McKinlay, MC, USNR, c/o Clinical Investigation Department, Naval Medical Center San Diego, 34800 Bob Wilson Dr, San Diego, CA 92134-5000.
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