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Piedra, which means “stone” in Spanish, is an asymptomatic superficial fungal infection of the hair shaft. In 1865, Beigel [1] first described piedra in The Human Hair: Its Structure, Growth, Diseases, and Their Treatment; although, he may have been describing Aspergillus infection.

In 1911, Horta classified piedra into two types. The first is black piedra, which is caused by Piedraia hortae. The second is white piedra. The etiological agents of white piedra, originally named Pleurococcus beigelii and later Trichosporon beigelii, are now called Trichosporon asahii and 5 other species: Trichosporon ovoides, Trichosporon inkin, Trichosporon mucoides, Trichosporon asteroides, and Trichosporon cutaneum. These 6 organisms are all causative agents of white piedra. T asahii is considered most closely linked to white piedra, although some authorities believe T ovoides is the main agent of white piedra of the scalp. Use of the term T beigelli should be avoided. [2]

The two types of piedra occur in different climatic conditions. Black piedra is most common in the tropical regions of the world that have high temperatures and humidity. For example, black piedra may occur in many central South American countries, including Brazil, as well as in Southeast Asia. Black piedra is rare in the United States. White piedra is more common in temperate and semitropical climates, such as those in South America, Asia, Europe, Japan, and parts of the southern United States.

In addition, the black piedra and white piedra affect the hair in different body locations. Black piedra usually affects scalp hair, whereas white piedra more commonly affects pubic hair, axillary hair, beards, mustaches, and eyebrows and/or eyelashes. However, in Brazil, white piedra is reported to affect scalp hair most commonly. [3] White piedra affects horses and monkeys, in addition to humans. Black piedra occurs in monkeys and humans.

Both types of piedra ultimately may lead to hair breaking because the shaft is weakened by cuticular penetration. In patients who are immunocompromised, dissemination of T asahii can occur, causing purpuric or necrotic cutaneous papules and nodules. Culture or biopsy samples from skin lesions may reveal the causative organism. Related organisms may be found on animal hair, in soil, or in stagnant water. [4] Gonzalez et al documented outbreaks of clinical mastitis caused by T asahii in dairy herds. This intramammary infection of affected cows causes hyperthermia, swelling of the udder, and decreased milk production or agalactia; this infection can be fatal in cows. [5]

The environment and typical skin flora are the 2 main sources of infectious agents that cause piedra. The source of infection in black piedra, P hortae, appears to be in the soil; however, infection also has been traced to organisms in stagnant water and crops. [6, 7] The source of infection for white piedra, typically T asahii, can be present in the soil, air, water, vegetable matter, or sputum or on body surfaces. [4] However, the mode of infection in humans is not clear. Trichosporon inkin and Trichosporon mucoides have also been documented as unusual causes of scalp hair white piedra. [8, 9] White piedra has been described in horses, monkeys, and dogs. [10]

Trichosporon species may also be causative agents of onychomycosis. A German study showed that among yeasts, they represented 10% of such infections. [11] T inkin and T ovoides may be human nail disease pathogens in Brazil. [12, 13] In addition, T asahii fungemia may develop in clinically deteriorated patients with or without an underlying hematological malignancy, [14] as in a neutropenic patient with acute leukemia. [15]

T asahii can cause white piedra and occasionally an onychomycosis. [16, 17] The genus Trichosporon Behrend consists of 6 human pathogenic species: T asahii, T mucoides, T ovoides, T asteroides, T cutaneum, and T inkin and all of which belong to the class Basidiomycetes. [10, 18] These species are the causative agents of piedra and other superficial infections as well as mucosa-associated systemic mycosis. [18] Cladosporium cladosporioides may also cause white piedra. [19]

In Brazil Trichosporon ovoides and Trichosporon inkin are common causative agents of white piedra, producing nodules in genital hair or on the scalp. [20] Of Trichosporon species isolated from 10 clinical samples in a 2008 study, T ovoides was predominant, being found in 7 samples, while T inkin was identified just in two of them.

United States

White piedra is quite common in parts of the southern United States and less so elsewhere in America. However, white piedra may be emerging as a commonly seen hair and scalp infection in the northeastern United States. [21, 22]


Black piedra is most common in tropical regions such as South America, Far East, and the Pacific Islands. At one time, black piedra reportedly was endemic in Brazilian Indians living in the northern area of midwestern Brazil. [23] This trend may have been linked to the Brazilian Indians’ cultural use of plant oils in their hair.

White piedra is more common in temperate and semitropical climates, such as those in Asia, Europe, Japan, and parts of the southern United States. [24, 25] White piedra caused by T cutaneum was identified in 5.8% of the children frequenting a day care in northeastern São Paulo State, Brazil. [26]

A combination of black and white (mixed) piedra has been speculated to represent a unique and probably underreported variety mainly restricted to scalp hair in young Muslim women who wear a scarf (hijab). [27]

In the United States, the occurrence of piedra may be higher in blacks than in whites; however, many cases may be underreported because nodules of piedra may be inconspicuous. [28]

Both sexes are affected equally. Black piedra initially was believed to be more common in men than in women; however, a study among the Zoro Indians of Brazil revealed no significant differences between the sexes. [6] In another study among Brazilian Indians, black piedra affected both sexes equally. [23]

Twenty-three cases of scalp white piedra were described in Brazil, with a high incidence in women (87%) and preschool children aged 2-6 years (74%). [10]

Individuals of all ages are affected. In a study of Brazilian Indians, persons of all ages were affected, from young children to adults older than 70 years, although black piedra infected young adults most frequently. [23] In one series of 23 Brazilian patients with scalp white piedra, a high incidence was found in preschool children aged 2-6 years (74%). [10]

The prognosis after treatment is good. Removal of the affected hair is usually curative, with few recurrences. Even without treatment, spontaneous remissions can occur.

Cosmetic morbidity occurs because piedra may affect the patient’s body image; the hair shaft may break and/or the patient may need to shave the affected hair.

Trichosporon, a causative pathogen of white piedra and summer-type hypersensitivity pneumonitis, can rarely produce a fatal disseminated trichosporonosis, a concern in immunocompromised persons. [29]

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Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Rachel Altman, MD Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School

Rachel Altman, MD is a member of the following medical societies: Alpha Omega Alpha, Sigma Xi

Disclosure: Nothing to disclose.

Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.


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