Tinea Nigra 

Updated: Apr 09, 2021
Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD 



Tinea nigra is an uncommon superficial dermatomycosis usually caused by Hortaea werneckii (see the image below), formerly known as Phaeoannellomyces werneckii, (formerly classified as Exophiala werneckii and Cladosporium werneckii).[1]

Micrograph of the Hortaea werneckii fungus, which Micrograph of the Hortaea werneckii fungus, which is a causative agent of tinea nigra. Courtesy of CDC Public Health Information Library (PHIL) and Wikimedia Commons.

Tinea nigra may also be due to Stenella araguata, first described and named Cladosporium castellanii in 1973.[2] Tinea nigra appears as a hyperpigmented macule, which usually occurs on the palms. The soles and, more rarely, other areas of the body, can also be affected.

Cequeira first described tinea nigra in 1891, calling the infection keratomycosis nigricans palmaris. In 1921, Horta isolated the pathogen and gave it its original name, C werneckii.

Although H werneckii has been established as the causative fungus in most cases of tinea nigra, other species of dematiaceous fungi, such as S araguata, may produce a similar clinical picture.

A Cladophialophora strain, allegedly a new species, Cladophialophora saturnica, has been described that caused an interdigital tinea nigra – like lesion in a HIV-positive Brazilian child, successfully treated with oxiconazole.[3]


Tinea nigra is a superficial mycosis of the stratum corneum. Infection is believed to occur as a result of inoculation from a contamination source such as soil, sewage, wood, or compost subsequent to trauma in the affected area.

Typically, the incubation period for tinea nigra is 2-7 weeks, although in experimental inoculation, the incubation period was 20 years.[4] The fungus exhibits lipophilic adhesion to human skin; it is exclusively found in the stratum corneum and does not extend into the stratum lucidum.

H werneckii receives nourishment from its use of decomposed lipids. Its tolerance to an environment with a high salt concentration and a low pH allows the fungus to thrive in human skin. It has been isolated from the hypersaline waters of salterns as one of the predominant species of a group of halophilic and halotolerant melanized yeastlike fungi.[5]  H werneckii has distinct mechanisms of adaptation to high-salinity environments that are not seen in salt-sensitive and only moderately salt–tolerant fungi.

A pigmentary change in the skin results in a dark-colored macule due to the accumulation of a melaninlike substance in the fungus.


Tinea nigra is due to infection by the fungus, H werneckii, which is classified in the family Dematiaceae, class Hyphomycetes, phylum Deuteromycota. Infection occurs after inoculation subsequent to trauma. The dermatomycosis tends to occur in areas with an increased concentration of eccrine sweat glands. Hyperhidrosis appears to be a risk factor for this disease.



United States

Tinea nigra is relatively uncommon in the United States. However, numerous cases are reported in the dermatologic literature. Tinea nigra typically affects people who reside in the coastal states such as Florida, Texas, Alabama, Louisiana, Virginia, and North Carolina. Although cases of tinea nigra are also reported in patients from northern and inland regions of the United States, including New York City, Chicago, and Boston, patients often report a history of foreign travel, frequently to the Caribbean Islands.[6]


Tinea nigra is not uncommon in tropical regions of Central America, South America, Africa, and Asia. Epidemiologic studies of skin diseases in schoolchildren performed by direct inspection using dermatologists in Magong, Penghu, Republic of China on the island of Formosa found the prevalence of fungal infection, including tinea nigra, tinea versicolor, and tinea corporis, to be 0.24% (95% confidence interval, 0.07-0.41%).[7] Tinea nigra may present as an imported infection from endemic areas into temperate climate regions,[6] including Chile.[8]


Tinea nigra appears to occur less often in the black population than in others, although this observation may reflect impaired recognition of the disease.


The female-to-male predilection for tinea nigra is 3:1.


Tinea nigra most often occurs in pediatric and adolescent populations; however, individuals of any age may be affected. In a study of 12 patients in Venezuela, it was found to be more prevalent among young people with fair skin aged 3-28 years who visited beaches.[2]


Although the appearance of tinea nigra may be alarming because of its uncommon occurrence and its potential confusion with a more serious medical disorder (eg, malignant melanoma[9, 10] ), tinea nigra is a benign disease that is easily curable.

Patient Education

Tinea nigra may be psychologically distressing, especially because of its potential confusion with a melanoma. Therefore, the patient should be reassured of the benign nature of this condition.




Generally, patients with tinea nigra are asymptomatic. Rarely, pruritus may be reported. The absence of any discomfort often delays the patient's decision to seek medical advice.

Patients who live in the inland areas of the United States generally report a history of foreign travel, most often to the Caribbean islands. In addition, patients may have acquired this infection while visiting the tropical regions of Asia or Africa. Those who reside in the coastal regions do not necessarily report any travel outside of the United States.

Uezato et al[11] reported a case of tinea nigra palmaris from Okinawa, Japan on the left palm of a 13-year-old girl, who had noticed the pigmented, asymptomatic macule on her left palm approximately 4-5 years prior to presentation. She stated the lesion became lighter after a bath and darkened some time later. Physical examination revealed a 4 X 5-cm, dark brown, and irregularly shaped macule.

Histological findings were reported as follows: "Direct potassium hydroxide (KOH) microscopic examination from skin scrapings revealed branched brown hyphae with light brown septa. A fungal culture on Sabouraud's agar media produced wet, medium brown, yeast-like colonies, the surface of which later became black and shiny. A slide culture disclosed light brown, elliptic or peanut-shaped conidia comprised of one to two ampullaceous cells. Scanning electron microscopic examination of the conidia showed both annellation [sic] conidia with lunate bud scars and sympodial conidiogenesis."

DNA was extracted from separately cultured fungi, and polymerase chain reaction with primers specific to H werneckii was performed; results showed positive bands. Direct sequencing was performed with the DNA segments from the positive bands. Type C H werneckii was determined to be the causative fungus, based on the base sequences obtained, and tinea nigra due to H werneckii was diagnosed.

Physical Examination

Tinea nigra is characterized by the presence of a painless brown-to-black macule, as shown in the image below. The macule appears insidiously as a small dark spot.

Tinea nigra, evident as a painless cluster of brow Tinea nigra, evident as a painless cluster of brown-to-black macules. Courtesy of Dr. Peter Santalucia.

Hyperpigmentation of the macule ranges from light brown to black discoloration, resembling silver nitrate or India ink stains. The borders are typically discrete. The pigmentary change may appear mottled or velvety.

The lesions are typically solitary, although more than one lesion can be present. Solitary lesions are typically located on the palmar surfaces of the hands or plantar surfaces of the feet, and they may extend to the fingers or toes, respectively. Other areas of the body, such as the neck and chest wall, are more rarely affected.

The shape of the lesion varies, and they may appear ovoid, round, or irregular. The lesion slowly grows over weeks to months. The size may range from a few millimeters to several centimeters in diameter, depending on the duration of the infection.

Other physical findings, such as erythema or induration, are absent. Rarely, scaling is present. Dermoscopic examination may facilitate the in vivo diagnosis of tinea nigra.[12, 13] Manual and digital dermatoscopic images show irregularly distributed dark brown-pigmented dots with a filamentous aspect,[14] that is, brown strands or spicules.[15] There may also be a parallel ridge pattern, one associated with melanomas.[16] In some, a parallel ridge pattern may be evident, with fine, wispy, brown spicules characteristic for tinea nigra.[17]

Although tinea nigra is often easily diagnosed on clinical grounds alone,[18] the use of dermoscopy for palmar or plantar pigmentation may enhance the recognition of tinea nigra.[19, 20, 21] Characteristic features evident on dermoscopy are superficial fine, wispy, light-brown strands forming a reticularlike patch with a uniform brown color. These strands do not follow the furrows and ridges normally observed in this skin. There are no pigment network, globules, and stripes that would suggest a melanocytic neoplasm.[22] Reflectance confocal microscopy (RCM) examination may show multiple elongated and round bright structures at the stratum corneum, probably representing filamentous septate hyphae and arthroconidia.[23]


Tinea nigra is a benign superficial fungal infection that does not have any serious complications.

Tinea nigra palmaris–associated peritonitis, caused by Hortaea werneckii has been described, with the suggestion that gloving should be employed during peritoneal dialysis bag exchange in patients or caregivers who have tinea nigra palmaris.[24]



Diagnostic Considerations

Consider the following:

  • Hyperpigmentation due to pinta

  • Chemical stains

  • Junctional nevi, postinflammatory pigmentation, melanoma, and melanosis of syphilis and pinta[25]

  • Superficial phaeohyphomycosis: Even in an immunocompetent individual, clinical and microscopic patterns may be similar to tinea nigra, but with the culture showing Aureobasidium melanogenum.[26]

  • Tattooing from dirt or other substances[27]

Lichen planus may rarely be evident as asymptomatic black patches on both palms, simulating tinea nigra.[28]

The recognition of tinea nigra is crucial to prevent any unnecessary diagnostic procedures for the evaluation of pigmented lesions. Tinea nigra may easily be confused with a junctional nevus or acral lentiginous melanoma,[29] which would require excisional biopsy. Furthermore, suspicion of a melanoma may cause unnecessary anxiety in a patient. A simple microscopic examination of the skin scrapings of the affected area readily aids the distinction between tinea nigra and other serious medical disorders that result in pigmentary changes.

Differential Diagnoses




Microscopic examination of skin scrapings treated with 20% KOH reveals thick, septate, branching hyphae that contain a dark pigment in their walls. Blastospores or chlamydoconidia may also be present.

Culture of skin scrapings on Sabouraud agar at 25°C yields growth in approximately 1 week. Initially, yeastlike colonies that are shiny, black, and mucoid are present. Subsequently, the colonies become olivaceous brown and develop aerial mycelia in 2-3 weeks. Microscopic examination of the colonies reveals dematiaceous 2-celled yeast that produce annelloconidia in addition to dematiaceous, septate hyphae with conidia on intercalary annelides.

Histologic Findings

Examination of biopsy specimens reveals hyperkeratosis and mild acanthosis. Periodic acid-Schiff (PAS)–positive septate hyphae are present in the stratum corneum. A scant amount of perivascular lymphocytic infiltrate may be found in the papillary and subpapillary layers of the dermis. Note the images below.

Tinea nigra, showing hyperkeratosis and mild acant Tinea nigra, showing hyperkeratosis and mild acanthosis. A scant amount of perivascular lymphocytic infiltrate may be found in the papillary and subpapillary layers of the dermis (hematoxylin and eosin stain). Courtesy of Thomas N. Helm, MD.
Tinea nigra, with histologic section demonstrating Tinea nigra, with histologic section demonstrating periodic acid-Schiff–positive septate hyphae within the stratum corneum. Courtesy of Thomas N. Helm, MD.


Medical Care

After tinea nigra is diagnosed on the basis of the findings from the patient's history, physical examination, and appropriate laboratory test, a topical medication designed to eradicate the fungal infection should be applied to the respective area. Topical application of antifungal agents usually resolves tinea nigra within 2-4 weeks. Topical ketoconazole cream may be a good choice,[16, 30]  as well other antifungals.[31, 32, 33] Prolonged therapy may be necessary to prevent relapse. Repeated vigorous scrubbing or topical application of keratolytic agents can reduce pigmentation.[25]

Spontaneous healing has been described but is rare.[34]

Surgical Care

To aid the effectiveness of the topical medication in eradicating the dermatomycosis, the affected skin area should be scraped with a No. 15 scalpel blade prior to the initial application of the medicine.


Because infection is believed to occur after inoculation subsequent to trauma, patients should avoid potentially contaminated sources, such as soil, sewage, compost, and decaying wood.



Medication Summary

Because tinea nigra is caused by a superficial fungal infection of the skin, topical medicines designed to eradicate the dermatomycosis are used,[35] including topical butenafine.[31]

Dermatologic agents

Class Summary

These agents are used to treat tinea nigra because of their action on the skin. They may either aid in the removal of excessive keratin in hyperkeratotic skin disorders or increase epithelial cell turnover. These agents are used in conjunction with fungicidal or fungistatic medications.

Salicylic acid topical (Compound W, Salactic Film, Sal-Plant, Panscol)

Salicylic acid topical causes desquamation of the horny layer of skin by dissolving intercellular cement substance, while not affecting structure of viable epidermis. Hydrate the skin and enhance the effects of medication; soak the affected area in warm water for 5 minutes prior to use; remove any loose tissue with a brush, washcloth, or emery board, and dry thoroughly. Improvement should occur in 1-2 weeks.

Tretinoin topical (Avita, Retin-A)

Topical tretinoin decreases the cohesiveness of follicular epithelial cells and stimulates their mitotic activity, resulting in quicker turnover of the epithelial layer.

Topical imidazoles

Class Summary

These medications are broad-spectrum antifungals that are commonly used in the treatment of tinea pedis, but they are also effective in the treatment of tinea nigra.

Clotrimazole (Lotrimin, Mycelex, Femizole-7)

Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. Reevaluate the diagnosis if no clinical improvement is see after 4 weeks.

Ketoconazole topical (Nizoral)

Ketoconazole is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Miconazole (Micatin, Femizol-M)

Miconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. It increases membrane permeability, causing nutrients to leak out and resulting in fungal cell death.

Topical pyridones

Class Summary

Topical pyridones are broad-spectrum agents with antidermatophyte, antibacterial, and anticandidal activity.

Ciclopirox (Loprox)

Ciclopirox interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

Topical allylamines

Class Summary

These drugs are effective in treating a variety of fungal infections. Because they have demonstrated potent activity against dermatophytes, they are often used in recalcitrant infections.

Terbinafine topical (Lamisil)

Terbinafine is an allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. This effect results in a deficiency in ergosterol in the fungal cell wall, causing fungal cell death.

Fungistatic agents

Class Summary

These medications do not kill the fungus, but rather, they prevent their growth and replication.

Undecylenic acid & derivatives (Blis-To-Sol powder, Caldesene, Cruex)

These are fungistatic. They are indicated for superficial dermal fungal infections.