eMedicine Specialties > Dermatology > Fungal Infections

Tinea Nigra

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital

Updated: Jul 24, 2009

Introduction

Background

Tinea nigra is an uncommon superficial dermatomycosis usually caused by Hortaea werneckii, formerly known as Phaeoannellomyces werneckii, (formerly classified as Exophiala werneckii and Cladosporium werneckii).¹ 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 P 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

Pathophysiology

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.

P 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 P 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.

Frequency

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.

International

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%).⁶

Mortality/Morbidity

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^7,8 ), tinea nigra is a benign disease that is easily curable.

Race

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

Sex

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

Age

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

Clinical

History

• 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 al⁹ 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

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

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.¹⁰

Causes

• Tinea nigra is due to infection by the fungus, P 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.

Differential Diagnoses

Addison Disease
Atypical Mole (Dysplastic Nevus)
Malignant Melanoma
Nevi, Melanocytic
Syphilis
Yaws

Other Problems to Be Considered

Hyperpigmentation due to pinta
Chemical stains

Workup

Procedures

• 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.

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 periodic acid-Schiff–positive septate hyphae within the stratum corneum. Courtesy of Thomas N. Helm, MD.

Treatment

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.

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.

Medication

Because tinea nigra is caused by a superficial fungal infection of the skin, topical medicines designed to eradicate the dermatomycosis are used.

Dermatologic agents

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 (Compound W, Salactic Film, Sal-Plant, Panscol)

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

Dosing

Adult

Apply to affected area; maximum resolution expected after 4-6 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; prolonged use in infants, patients with diabetes, and those with impaired circulation not recommended; do not use on moles, birthmarks, warts with hair growing from them, genital or facial warts, warts on mucous membranes, irritated skin or any area infected or reddened

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid contact with mucous membranes, normal skin surrounding tinea nigra lesion, and eyes; immediately flush with water for 15 min if contact with eyes or mucous membranes occurs; avoid inhaling vapors

Tretinoin (Avita, Retin-A)

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

Dosing

Adult

Apply 0.1% cream or gel bid/qid; decrease frequency if irritation develops

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Toxicity increases with coadministration of benzoyl peroxide, salicylic acid, and resorcinol; avoid topical sulfur, resorcinol, salicylic acid, other keratolytics, abrasives, astringents, spices, and lime

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with excessive sunlight exposure; caution in eczema; do not apply to mucous membranes, mouth, and angles of nose

Topical imidazoles

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.^11,12

Clotrimazole (Lotrimin, Mycelex, Femizole-7)

Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells. Reevaluate diagnosis if no clinical improvement after 4 wk.

Dosing

Adult

Gently massage onto affected area and surrounding skin bid for 2-4 wk

Pediatric

Children: Not established
Adolescents: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not for treatment of systemic fungal infections; avoid contact with the eyes; if irritation or sensitivity develops, discontinue and initiate appropriate therapy

Ketoconazole (Nizoral)

Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Dosing

Adult

Rub gently into affected area qd/bid for 2-4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue if sensitivity or irritation develops; for external use only; avoid contact with eyes

Miconazole (Micatin, Femizol-M)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Increases membrane permeability, causing nutrients to leak out and resulting in fungal cell death.

Dosing

Adult

Apply cream or lotion to affected areas bid for 2-4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

If sensitivity or chemical irritation occurs, discontinue use; for external use only; avoid contact with eyes

Topical pyridones

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

Ciclopirox (Loprox)

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

Dosing

Adult

Massage into affected areas bid; reevaluate diagnosis if no improvement after 4 wk

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid contact with eyes and other internal routes

Topical allylamines

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.¹³

Terbinafine (Lamisil)

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.

Dosing

Adult

Apply to affected area bid for at least 1-2 wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if sensitivity or irritation occurs; for external use only; avoid contact with eyes

Fungistatic agents

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

Undecylenic acid

Fungistatic agent.

Dosing

Adult

Cleanse and dry affected areas; apply a thin film of 25% solution to the affected area bid

Pediatric

<2 years: Not recommended
>2 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue if reaction suggesting hypersensitivity or chemical irritation occurs; not for ophthalmic or optic use; avoid inhalation and contact with eyes or other mucous membranes; not to be applied over blistered, raw, or oozing areas of skin or over deep puncture wounds

Follow-up

Deterrence/Prevention

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.

Complications

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

Prognosis

Tinea nigra is curable, and, with appropriate medication, it does not recur.

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.

Miscellaneous

Medicolegal Pitfalls

• 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,¹⁴ 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.

Multimedia

Media file 1: Tinea nigra, evident as a painless cluster of brown-to-black macules. Courtesy of Dr. Peter Santalucia.

Media file 2: 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.

Media file 3: Tinea nigra, with histologic section demonstrating periodic acid-Schiff–positive septate hyphae within the stratum corneum. Courtesy of Thomas N. Helm, MD.

References

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3. Badali H, Carvalho VO, Vicente V, et al. Cladophialophora saturnica sp. nov., a new opportunistic species of Chaetothyriales revealed using molecular data. Med Mycol. Feb 2009;47(1):51-62. [Medline].

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5. Lenassi M, Vaupotic T, Gunde-Cimerman N, Plemenitas A. The MAP kinase HwHog1 from the halophilic black yeast Hortaea werneckii: coping with stresses in solar salterns. Saline Systems. 2007;3:3. [Medline].

6. Chen GY, Cheng YW, Wang CY, Hsu TJ, Hsu MM, Yang PT, et al. Prevalence of skin diseases among schoolchildren in Magong, Penghu, Taiwan: a community-based clinical survey. J Formos Med Assoc. Jan 2008;107(1):21-9. [Medline].

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10. Zalaudek I, Giacomel J, Cabo H, Di Stefani A, Ferrara G, Hofmann-Wellenhof R, et al. Entodermoscopy: a new tool for diagnosing skin infections and infestations. Dermatology. 2008;216(1):14-23. [Medline].

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21. Meletiadis J, Meis JF, de Hoog GS, Verweij PE. In vitro susceptibilities of 11 clinical isolates of Exophiala species to six antifungal drugs. Mycoses. Sep 2000;43(7-8):309-12. [Medline].

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Keywords

tinea nigra palmaris, tinea nigra plantaris, keratomycosis nigricans palmaris, dermatomycosis nigricans, mycosis of the stratum corneum, Hortaea werneckii, H werneckii, Phaeoannellomyces werneckii, P werneckii, Exophiala werneckii, E werneckii, Cladosporium werneckii, C werneckii

Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital
George Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Medical Editor

Neil Shear, MD, Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada
Neil Shear, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics, Canadian Dermatology Association, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Vinay Arya, MD, and previous Chief Editor, William D. James, MD, to the development and writing of this article.

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