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]
International
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] Trichosporon inkin meningitis has been described.[30]
White piedra shows irregular, white, cream-colored, or brown soft nodules or gelatinous sheaths along the hair shaft. They can be easily detached from the hair shaft. White piedra is found in the hair of the beard, moustache, genitals, and axilla. Eyebrow and eyelash involvement can also be present, while on the scalp, white piedra appears to be less common.
Piedra may be asymptomatic in many patients. Patients may not be able to see the minute nodules that haphazardly develop on the hair shaft; however, they may feel the gritty nodules. Patients may hear a metallic sound when they brush their hair.[31]
Assess the immune status of the patient because of the possibility of disseminated infection in a patient who is immunocompromised; T asahii, which is the most typical agent for white piedra, can cause disseminated infection in these patients. These systemic infections occur primarily in patients who have neutropenia and, rarely, in patients with AIDS.[32] Cutaneous disseminated papulae or purpural nodules are frequently present in these patients.
Black piedra may be used as a hair dye to darken hair; at least one San Blas (Panama) Cuna albino Indian chanter has been described as deliberately cultivating black piedra for cosmetic reasons.[33] She was careful to avoid oil use on her scalp, since it apparently removed this fungus.
White piedra may have a synergistic coryneform bacterial infection.[34] White piedra, although not commonly reported to infect scalp hair in North America, is an important consideration in the evaluation of scalp hair concretions. White piedra may affect the scalp, and in one case, it was the only site affected and was extensive.[35] Rarely, Trichosporon species may be accompanied by Candida parapsilosis along hair shafts, although it is unclear if this is really a co-infection.
A peculiar case has been described with white piedra spores packed inside empty pedicular nits were accidentally found on microscopic examination in a 42-year-old Indian woman who presented with hair loss.[36] It is remarkable to have pedicular nits impregnated with spores of white piedra.
Black piedra consists of darkly pigmented, firmly attached nodules that vary in size to as large as a few millimeters in diameter. The nodules feel hard. The most commonly affected area of the body is the scalp hair. Black piedra less frequently affects beards, mustaches, and the pubic hair. The fungus grows into the hair shaft; ultimately, it may cause hair breakage because of structural instability.
White piedra consists of lightly pigmented, loosely attached nodules or gelatinous sheaths that have a soft texture. The most commonly affected areas of the body are beards, mustaches, pubic and axillary hair, and eyelashes and eyebrows. It may rarely appear on the scalp,[37] where it can be extensive.[38, 39]
Hair breakage occurs in both forms of piedra. In both varieties of piedra, the surrounding skin is healthy.
The most common complication is the loss of the structural integrity of the hair shaft, which leads to breakage.
Place hair shaft nodules into a 10-15% potassium hydroxide preparation on a glass slide. A fungal stain, such as chlorazol black E stain or Parker blue-black ink may be added to highlight the hyphae. If the nodule is from black piedra, tightly packed and pigmented hyphae, asci, and ascospores are seen attached to the hair shaft. If the nodule is from white piedra, darkly stained and loosely arranged hyphae, blastoconidia, and arthroconidia are seen attached to the hair shaft.
P hortae, the cause of black piedra, grows slowly on Sabouraud dextrose agar and is not inhibited by cycloheximide. Microscopic examination reveals septate hyphae, chlamydospores, and irregularly shaped hyphal elements.[46] These cultures are of the asexual phase of the fungus. Organisms in the sexual phase are difficult to grow in culture.
T asahii, the typical cause of white piedra, rarely grows on Sabouraud dextrose agar because of inhibition by cycloheximide, which is present in dermatophyte test medium and in Mycosel and mycobiotic agars. In addition, Trichosporon species grow best at 28-30°C.
Mycological culture on Mycosel plus molecular identification may be used to confirm the diagnosis.[47]
Morphological and physiological analysis may provide inconsistent identification of Trichosporon to species level. For example, sequencing of the intergenic spacer 1 region of ribosomal DNA may be necessary accurately identify T inkin.[9] Such molecular identification is desirable for suitable epidemiological surveillance of superficial mycoses from Trichosporon species.
In black piedra, the dark nodules are composed of different components based on the area of the body in which they are located. Black piedra is distinguished by ascospores borne in a subglobose ascus in groups of 8. The periphery of the nodule has regularly aligned hyphae and arthroconidia.[48] P hortae is one of the few pathogenic human fungi that produce sexual spores in its parasitic phase.
White piedra is characterized by discrete-to-coalesced nodules that typically are white, cream, or brown.[28, 49] Nodules on the hair shaft often appear amorphous, but may be outlined by hyaline arthroconidia, 2-4 septate hyphae, and differentiated blastoconidia that arise from loosely packed hyphae. Sexual spores are not known to be present.[28] Fungal structures stain easily with Parker blue-black ink.
Shaving or cutting the hair is the treatment of choice. Antifungal agents and terbinafine also are used in the treatment of piedra.
Black piedra is treated by using oral terbinafine.
White piedra can be treated by using topical antifungals, including imidazoles, ciclopirox olamine, 2% selenium sulfide, 6% precipitated sulfur in petroleum, chlorhexidine solution, Castellani paint, zinc pyrithione, and amphotericin B lotion.
Spontaneous remissions are common. Treatment is effective in patients without spontaneous remission. Removal of hair is curative and requires no follow-up treatment. Recurrences are rare.
Treatment of white piedra can be a therapeutic challenge. Several topical and systemic antifungal agents may not eradicate the disorder. However, they should be tried, as scalp and hair infection may sometimes be successfully treated with a combination of oral azole antifungals and shampoos without shaving the scalp.[21] Therapy with oral itraconazole for the treatment of uncomplicated white piedra affecting the scalp hair may be a good choice if topical remedies fail.[50]
Disseminated trichosporosis can be difficult to treat, but itraconazole is often used. In one study, in vitro interactions of itraconazole with caspofungin suggested enhanced antifungal activity against T asahii; this combination may be of value for treating disseminated trichosporosis.[51]
Clinical Context: Clotrimazole 1% is often a first-line drug used in the treatment of tinea cruris. It is available by prescription only. Cream, solution or spray, and lotion forms are available.
Clinical Context: Miconazole 2% is an imidazole used in the treatment of tinea cruris. It is available over the counter. Cream, solution or spray, lotion, and powder forms are available.
Clinical Context: Ketoconazole topical is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.
Clinical Context: Econazole 1% is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell-wall permeability, causing fungal cell death.
Clinical Context: Terbinafine is an allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. This inhibition results in a deficiency in ergosterol within the fungal cell wall that causes fungal cell death. Terbinafine is available by prescription only. Some clinicians reserve the use of this drug for more widespread and/or resistant infections because of its broad coverage and cost. This medication is effective and well tolerated in children.
Clinical Context: Oxiconazole 1% damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. It increases membrane permeability, causing nutrients to leak out, resulting in fungal cell death.
Clinical Context: Sulconazole 1% is a broad-spectrum imidazole derivative with antifungal and antiyeast activity. It is for topical use. It inhibits the growth of common pathogenic dermatophytes.
Clinical Context: Itraconazole has fungistatic activity. It is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Absorption is improved with food and in the presence of normal gastric acidity. Patients should be cautioned against ingesting grapefruit juice while on itraconazole therapy (decreased oral bioavailability of itraconazole). Discontinue if sensitivity or chemical irritation occurs; for external use only; avoid contact with eyes.
Clinical Context: Ciclopirox interferes with DNA, RNA, and protein synthesis by inhibiting the transport of essential elements in fungal cells.
Clinical Context: Naftifine is indicated for tinea corporis, tinea cruris, and tinea pedis. It is a broad-spectrum antifungal agent that appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition results in decreased amounts of sterols, causing cell death. If no clinical improvement occurs after 4 weeks of treatment, reevaluate the patient.
The mechanism of action of antifungals may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.
Clinical Context: Selenium sulfide blocks enzymes involved in the growth of epithelial tissue.
Clinical Context: Chlorhexidine is an effective, relatively safe, and reliable topical antiseptic. It is a polybiguanide with bactericidal activity; usually it is supplied as a gluconate salt. At physiologic pH, the salt dissociates to a cation that binds to bacterial cell walls.
Clinical Context: Pyrithione zinc is a cytostatic agent that reduces cell the turnover rate. It strongly binds to hair and external skin layers.