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 It may also be due to Stenella araguata, first described and named Cladosporium castellanii in 1973.2 This infection 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.
Two Medscape CME courses of possible interest are Fungal Skin and Nail Infections: Practical Advice for Advanced Practice Clinicians and Selecting Effective Treatment in the Antibiotic-Resistant Emergency Room Patient.
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 is 2-7 weeks, although in experimental inoculation, the incubation period was 20 years.3 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.4 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%).5
Mortality/Morbidity
Although the fungal infection may be alarming because of its uncommon occurrence and its potential confusion with a more serious medical disorder (eg, malignant melanoma6,7 ), 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 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 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 al8 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.
- 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.9
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.
More on Tinea Nigra |
Overview: Tinea Nigra |
| Differential Diagnoses & Workup: Tinea Nigra |
| Treatment & Medication: Tinea Nigra |
| Follow-up: Tinea Nigra |
| Multimedia: Tinea Nigra |
| References |
| Next Page » |
References
Schwartz RA. Superficial fungal infections. Lancet. Sep 25-Oct 1 2004;364(9440):1173-82. [Medline].
Perez C, Colella MT, Olaizola C, Hartung de Capriles C, Magaldi S, Mata-Essayag S. Tinea nigra: report of twelve cases in Venezuela. Mycopathologia. Oct 2005;160(3):235-8. [Medline].
Blank H. Tinea nigra: a twenty-year incubation period?. J Am Acad Dermatol. Jul 1979;1(1):49-51. [Medline].
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].
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].
Hall J, Perry VE. Tinea nigra palmaris: differentiation from malignant melanoma or junctional nevi. Cutis. Jul 1998;62(1):45-6. [Medline].
Tseng SS, Whittier S, Miller SR, Zalar GL. Bilateral tinea nigra plantaris and tinea nigra plantaris mimicking melanoma. Cutis. Oct 1999;64(4):265-8. [Medline].
Uezato H, Gushi M, Hagiwara K, Kayo S, Hosokawa A, Nonaka S. A case of tinea nigra palmaris in Okinawa, Japan. J Dermatol. Jan 2006;33(1):23-9. [Medline].
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].
Burke WA. Tinea nigra: treatment with topical ketoconazole. Cutis. Oct 1993;52(4):209-11. [Medline].
Marks JG Jr, King RD, Davis BM. Treatment of tinea nigra palmaris with miconazole. Arch Dermatol. Mar 1980;116(3):321-2. [Medline].
Shannon PL, Ramos-Caro FA, Cosgrove BF, Flowers FP. Treatment of tinea nigra with terbinafine. Cutis. Sep 1999;64(3):199-201. [Medline].
Babel DE, Pelachyk JM, Hurley JP. Tinea nigra masquerading as acral lentiginous melanoma. J Dermatol Surg Oncol. May 1986;12(5):502-4. [Medline].
Carr JF, Lewis CW. Tinea nigra palmaris. Treatment with thiabendazole topically. Arch Dermatol. Jul 1975;111(7):904-5. [Medline].
Cutlip BD Jr, Varkonyi NT, Grant D. Tinea nigra palmaris. Mil Med. Mar 1970;135(3):192-3. [Medline].
Feng B, Wang X, Hauser M, Kaufmann S, Jentsch S, Haase G, et al. Molecular cloning and characterization of WdPKS1, a gene involved in dihydroxynaphthalene melanin biosynthesis and virulence in Wangiella (Exophiala) dermatitidis. Infect Immun. Mar 2001;69(3):1781-94. [Medline].
Gupta G, Burden AD, Shankland GS, Fallowfield ME, Richardson MD. Tinea nigra secondary to Exophiala werneckii responding to itraconazole. Br J Dermatol. Sep 1997;137(3):483-4. [Medline].
Hughes JR, Moore MK, Pembroke AC. Tinea nigra palmaris. Clin Exp Dermatol. Sep 1993;18(5):481-2. [Medline].
McKinlay JR, Barrett TL, Ross EV. Picture of the month. Tinea nigra. Arch Pediatr Adolesc Med. Mar 1999;153(3):305-6. [Medline].
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].
Merwin CF. Tinea nigra palmaris. Review of literature and case report. Pediatrics. Oct 1965;36(4):537-41. [Medline].
Mok WY. Nature and identification of Exophiala werneckii. J Clin Microbiol. Nov 1982;16(5):976-8. [Medline].
Palmer SR, Bass JW, Mandojana R, Wittler RR. Tinea nigra palmaris and plantaris: a black fungus producing black spots on the palms and soles. Pediatr Infect Dis J. Jan 1989;8(1):48-50. [Medline].
Reid BJ. Exophiala werneckii causing tinea nigra in Scotland. Br J Dermatol. Jul 1998;139(1):157-8. [Medline].
Sayegh-Carreño R, Abramovits-Ackerman W, Girón GP. Therapy of tinea nigra plantaris. Int J Dermatol. Jan-Feb 1989;28(1):46-8. [Medline].
Whiting DA, Bisset EA. Tinea nigra. S Afr Med J. Sep 15 1973;47(36):1659-61. [Medline].
Further Reading
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
Overview: Tinea Nigra