eMedicine Specialties > Dermatology > Fungal Infections

Piedra

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

Updated: Jun 12, 2009

Introduction

Background

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 2 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 2 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 ]}

Pathophysiology

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 man is not clear. White piedra has been described in horses, monkeys, and dogs.^{[8 ]}

Trichosporon species may also be causative agents of onychomycosis. A German study showed that among yeasts, they represented 10% of such infections.^{[9 ]}In addition, T asahii fungemia may develop in clinically deteriorated patients with or without an underlying hematological malignancy,^{[10 ]}as in a neutropenic patient with acute leukemia.^{[11 ]}

Frequency

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.^{[12 ]}

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.^{[13 ]}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.^{[14,15 ]}White piedra caused by T cutaneum was identified in 5.8% of the children frequenting a day care in northeastern São Paulo State, Brazil.^{[16 ]}

Mortality/Morbidity

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.

Race

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.^{[17 ]}

Sex

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.^{[13 ]}

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%).^{[8 ]}

Age

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.^{[13 ]}In one series of 23 Brazilian patients with scalp white piedra, a high incidence was found in preschool children aged 2-6 years (74%).^{[8 ]}

Clinical

History

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.^{[18 ]}
• 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.^{[19 ]}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.^{[20 ]}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.^{[21 ]}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.^{[22 ]}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.^{[23 ]}It is remarkable to have pedicular nits impregnated with spores of white piedra.

Physical

• Findings in black piedra may include the following:
  • 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.
• Findings in white piedra may include the following:
  • 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.
• Hair breakage occurs in both forms of piedra.
• In both varieties of piedra, the surrounding skin is healthy.

Causes

T asahii can cause white piedra and occasionally an onychomycosis.^{[24,25 ]}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.^{[8,26 ]}These species are the causative agents of piedra and other superficial infections as well as mucosa-associated systemic mycosis.^{[26 ]}

In Brazil Trichosporon ovoides and Trichosporon inkin are common causative agents of white piedra, producing nodules in genital hair or on the scalp.^{[27 ]}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 2 of them.

Differential Diagnoses

Lice
Monilethrix
Tinea Capitis
Trichomycosis Axillaris
Trichorrhexis Nodosa

Other Problems to Be Considered

Pediculosis
Nits^{[28,29 ]}
Hair casts
Developmental defects of the hair shaft
Trichomycosis axillaris infection: Unlike the organisms that cause piedra, T axillaris fluoresces under ultraviolet illumination.
Tinea capitis: Unlike piedra, tinea capitis affects the base of the hair shaft and the follicle.
Monilethrix, trichorrhexis nodosa, and trichoptilosis: White piedra can be clinically indistinguishable from these conditions.
Hand eczema: This condition is a superficial infection caused by Trichosporon species that can mimic hand eczema in one who is immunocompromised.^{[30 ]}

Workup

Laboratory Studies

• Staining
  • 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.
• Culturing
  • 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.^{[31 ]}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.

Histologic Findings

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.^{[32 ]} 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.^{[17,33 ]}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.^{[17 ]}Fungal structures stain easily with Parker blue-black ink.

Treatment

Medical Care

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.
• The American Academy of Dermatology has published guidelines for treating this superficial mycotic infection.^{[34 ]}

Medication

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.^{[12 ]}Therapy with oral itraconazole for the treatment of uncomplicated white piedra affecting the scalp hair may be a good choice if topical remedies fail.^{[35 ]}

Antifungal agents

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.

Clotrimazole 1% (Lotrimin, Mycelex)

Often a first-line drug used in the treatment of tinea cruris. Available by prescription only. Cream, solution or spray, and lotion forms are available.

Dosing

Adult

Apply topically to affected areas bid for 4 wk or until condition resolves

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

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

Miconazole 2% (Micatin, Monistat-Derm, Femizole-7, Lotrimin)

Imidazole used in the treatment of tinea cruris. Available over the counter. Cream, solution or spray, lotion, and powder forms are available.

Dosing

Adult

Apply topically to affected areas bid for 4 wk or until condition resolves

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 chemical irritation occurs; for external use only; avoid contact with eyes

Ketoconazole 2% cream (Nizoral cream)

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

Dosing

Adult

Apply topically to affected areas qd for 2-4 wk or until condition resolves

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

Econazole 1% (Spectazole)

Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell-wall permeability, causing fungal cell death.

Dosing

Adult

Apply topically to affected areas qd until condition resolves

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

Terbinafine (Lamisil)

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.

Dosing

Adult

White piedra: Apply topically to the affected area qd for 2 wk or until condition resolves
Black piedra: 250 mg/d PO; not to exceed 12 wk

Pediatric

Topical: Administer as in adults
Oral:
12-20 kg: 62.5 mg/d
20-40 kg: 125 mg/d
>40 kg: 250 mg/d
Treatment duration as in adults

Interactions

Possible interactions with drugs metabolized by the CYP-450 (P-450) 2D6 enzyme (eg, tricyclic antidepressants, propranolol, theophylline); may decrease cyclosporin levels; rifampin increases clearance; cimetidine may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Reduce oral dose in renal insufficiency; discontinue if hepatobiliary dysfunction, neutropenia, Stevens-Johnson syndrome, or changes in ocular lens or retina develop; discontinue topical use if chemical irritation develops
Monitor patient response and adjust caffeine dosage during combined treatment with terbinafine; observe for signs of caffeine toxicity (headache, agitation, insomnia, diuresis, fever)

Oxiconazole 1% (Oxistat)

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

Dosing

Adult

Apply to affected area qd/bid until condition resolves

Pediatric

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

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

Sulconazole 1% (Exelderm)

Broad-spectrum imidazole derivative with antifungal and antiyeast activity. For topical use. Inhibits growth of common pathogenic dermatophytes.

Dosing

Adult

Apply to affected areas qd/bid for 2-4 wk or until condition resolves

Pediatric

Not established

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 chemical irritation occurs; for external use only; avoid contact with eyes

Itraconazole (Sporanox)

Fungistatic activity. 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 improved with food and in 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.

Dosing

Adult

100 mg PO qd until culture negativity achieved

Pediatric

Not established

Interactions

As CYP3A4 inhibitor (P450 metabolism), many drugs have interactions when coadministered with itraconazole; avoid alcohol use because disulfiramlike reaction may occur; antacids may reduce absorption; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; high doses may increase tacrolimus and cyclosporine plasma concentrations; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (eg, lovastatin, simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death; may increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce levels (phenytoin metabolism may be altered)
Reduced itraconazole plasma concentrations reported with concurrent use of H2 antagonist and aluminum-, calcium-, or magnesium-containing products (administer aluminum-, calcium-, or magnesium-containing products at least 1 h before or 2 h after itraconazole cap); enhances anticoagulant effects of coumarinlike drugs

Contraindications

Documented hypersensitivity; congestive heart failure or history of congestive heart failure (itraconazole cap for treatment of superficial fungal infections), concurrent administration with cisapride, midazolam, triazolam, lovastatin, dofetilide, pimozide, levacetylmethadol (levomethadyl), quinidine, lovastatin, simvastatin, and ergot alkaloids metabolized by CYP3A4 (eg, dihydroergotamine, ergometrine [ergonovine], ergotamine, methylergometrine [methylergonovine]); women contemplating pregnancy

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

Caution in hepatic insufficiencies; adverse effects include headache, nausea, vomiting, reversible elevation of liver enzyme levels, hepatotoxicity, hallucinations, hypokalemia, heart failure, edema, congestive heart failure, and neutropenic disorder; oral solution and oral capsules not to be used interchangeably; injection not for use in patients with CrCl <30 mL/min, and use with caution in patients with CrCl of 30-80 mL/min

Ciclopirox (Loprox)

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

Dosing

Adult

Massage into affected area bid until condition resolves

Pediatric

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

Naftifine (Naftin)

Indicated for the treatment of tinea corporis, tinea cruris, and tinea pedis. 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 wk of treatment, reevaluate patient.

Dosing

Adult

Gently and sparingly massage the cream or gel into affected area and surrounding skin qd/bid for 2-4 wk or until condition resolves

Pediatric

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

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

Dermatologic agents

These agents may be effective in treating white piedra.

Selenium sulfide 1-2.5% lotion (Exsel, Selsun)

Blocks enzymes involved in growth of epithelial tissue.

Dosing

Adult

Massage for 5-10 min into wet hair, wait for 2-3 min, then rinse; repeat application and rinse; wash hands after treatment; qd until resolved

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

To avoid systemic toxicity, do not use in broken or open skin; avoid use in very young children

Carbol-fuchsin (Castellani Paint)

First-aid antiseptic and drying agent. Active ingredient is phenol 1.5%. Inactive ingredients are water, SD alcohol 40B (13%), resorcinol, acetone, and basic fuchsin.

Dosing

Adult

Spray or apply to affected area qd/bid

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

Avoid contact with clothing; stain slowly wears off; not for application on eroded skin, or large areas; infants may be more sensitive than adults to phenol component

Chlorhexidine (Hibiclens, PerioGard)

Effective, relatively safe, and reliable topical antiseptic. A polybiguanide with bactericidal activity; usually is supplied as a gluconate salt. At physiologic pH, the salt dissociates to a cation that binds to bacterial cell walls.

Dosing

Adult

Rinse affected area with water, apply sufficient amount to cover affected area, wash gently, then rinse

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

Corneal damage may occur; skin irritation, ototoxicity resulting in deafness (when used around the ear), phototoxicity, and/or allergic reactions rare when used to clean superficial wounds (does not cause additional tissue injury or delay healing)

Pyrithione zinc (DHS Zinc, Zincon, Head & Shoulders)

Cytostatic agent that reduces cell turnover rate. Strongly binds to hair and external skin layers.

Dosing

Adult

Apply shampoo and rinse; use qd until condition resolves; use as with selenium sulfide

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

For external use only; do not apply to eyes

Follow-up

Further Outpatient Care

• 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.

Complications

• The most common complication is the loss of the structural integrity of the hair shaft, which leads to breakage.

Prognosis

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

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnosis piedra may lead to broken hair in patients and subsequent emotional distress.
• Misdiagnosis of pediculosis or tinea capitis may result in unwarranted emotional distress in patients.
• Misdiagnosis of pediculosis in children may result in their being banned from attending school because of the infectious nature of pediculosis and the possibility of an epidemic in the school.

References

1. Beigel H. The Human Hair. In: Its Structure, Growth, Diseases, and Their Treatment. London, England: Renshaw; 1869.

2. Schwartz RA. Superficial fungal infections. Lancet. Sep 25-Oct 1 2004;364(9440):1173-82. [Medline].

3. Londero AT, Ramos CD, Fischman O. White piedra of unusual localization. Sabouraudia. Oct 1966;5(2):132-3. [Medline].

4. Rippon JW. Medical Mycology. In: The Pathogenic Fungi and the Pathogenic Actinomycetes. 142. 3^rd ed. Philadelphia, Pa: WB Saunders; 1988:163-8.

5. González RN, Wilson DJ, Sickles SA, Zurakowski MJ, Weybrecht PM, Walsh AK. Outbreaks of clinical mastitis caused by Trichosporon beigelii in dairy herds. J Am Vet Med Assoc. Jan 15 2001;218(2):238-42. [Medline].

6. Coimbra Junior CE, Santos RV. Black piedra among the Zoró Indians from Amazônia (Brazil). Mycopathologia. Jul 1989;107(1):57-60. [Medline].

7. Kwon-Chung KJ, Bennett JE. Piedra (tinea nodosa trichomycosis nodularis, trichomycosis nodosa, Beigel's disease, Chignon disease). In: Medical Mycology. Philadelphia, Pa: Lea & Febiger; 1992:183-90.

8. Pontes ZB, Ramos AL, Lima Ede O, Guerra Mde F, Oliveira NM, Santos JP. Clinical and mycological study of scalp white piedra in the State of Paraíba, Brazil. Mem Inst Oswaldo Cruz. Jul 2002;97(5):747-50. [Medline].

9. Mugge C, Haustein UF, Nenoff P. [Causative agents of onychomycosis--a retrospective study]. J Dtsch Dermatol Ges. Mar 2006;4(3):218-28. [Medline].

10. Karabay O, Madariaga MG, Kocoglu E, Ince N, Kandirali E. Trichosporon asahii fungemia in a patient with non-hematological malignancy. Jpn J Infect Dis. Apr 2006;59(2):129-31. [Medline].

11. Bayramoglu G, Sonmez M, Tosun I, Aydin K, Aydin F. Breakthrough Trichosporon asahii fungemia in neutropenic patient with acute leukemia while receiving caspofungin. Infection. Feb 2008;36(1):68-70. [Medline].

12. Kiken DA, Sekaran A, Antaya RJ, Davis A, Imaeda S, Silverberg NB. White piedra in children. J Am Acad Dermatol. Dec 2006;55(6):956-61. [Medline].

13. Fischman O. Black piedra among Brazilian Indians. Rev Inst Med Trop Sao Paulo. Mar-Apr 1973;15(2):103-6. [Medline].

14. Kubec K, Dvorak R, Alsaleh QA. Trichosporosis (white piedra) in Kuwait. Int J Dermatol. Mar 1998;37(3):186-7. [Medline].

15. Therizol-Ferly M, Kombila M, Gomez de Diaz M, Duong TH, Richard-Lenoble D. White piedra and Trichosporon species in equatorial Africa. I. History and clinical aspects: an analysis of 449 superficial inguinal specimens. Mycoses. Jul-Aug 1994;37(7-8):249-53. [Medline].

16. Roselino AM, Seixas AB, Thomazini JA, Maffei CM. An outbreak of scalp white piedra in a Brazilian children day care. Rev Inst Med Trop Sao Paulo. Sep-Oct 2008;50(5):307-9. [Medline].

17. Kalter DC, Tschen JA, Cernoch PL, et al. Genital white piedra: epidemiology, microbiology, and therapy. J Am Acad Dermatol. Jun 1986;14(6):982-93. [Medline].

18. Elgart ML. Unusual subcutaneous infections. Dermatol Clin. Jan 1996;14(1):105-11. [Medline].

19. Lascaux AS, Bouscarat F, Descamps V, et al. [Cutaneous manifestations during disseminated trichosporonosis in an AIDS patient]. Ann Dermatol Venereol. Feb 1998;125(2):111-3. [Medline].

20. Moyer DG, Keeler C. Nnote on culture of black peidra for cosmetic reasons. Arch Dermatol. Mar 1964;89:436. [Medline].

21. Youker SR, Andreozzi RJ, Appelbaum PC, Credito K, Miller JJ. White piedra: further evidence of a synergistic infection. J Am Acad Dermatol. Oct 2003;49(4):746-9. [Medline].

22. Taj-Aldeen SJ, Al-Ansari HI, Boekhout T, Theelen B. Co-isolation of Trichosporon inkin and Candida parapsilosis from a scalp white piedra case. Med Mycol. Feb 2004;42(1):87-92. [Medline].

23. Ghorpade A. Surrogate nits impregnated with white piedra--a case report. J Eur Acad Dermatol Venereol. Jul 2004;18(4):474-6. [Medline].

24. Elmer KB, Elston DM, Libow LF. Trichosporon beigelii infection presenting as white piedra and onychomycosis in the same patient. Cutis. Oct 2002;70(4):209-11. [Medline].

25. Manzano-Gayosso P, Hernandez-Hernandez F, Mendez-Tovar LJ, et al. Onychomycosis incidence in type 2 diabetes mellitus patients. Mycopathologia. Jul 2008;166(1):41-5. [Medline].

26. Gueho E, Improvisi L, de Hoog GS, Dupont B. Trichosporon on humans: a practical account. Mycoses. Jan-Feb 1994;37(1-2):3-10. [Medline].

27. Magalhaes AR, Mondino SS, Silva M, Nishikawa MM. Morphological and biochemical characterization of the aetiological agents of white piedra. Mem Inst Oswaldo Cruz. Dec 2008;103(8):786-90. [Medline].

28. Child Health Alert. Head lice vs. white piedra: something to consider. Child Health Alert. Jan 2007;25:1. [Medline].

29. Lebwohl M, Clark L, Levitt J. Therapy for head lice based on life cycle, resistance, and safety considerations. Pediatrics. May 2007;119(5):965-74. [Medline].

30. Nakagawa T, Nakashima K, Takaiwa T, Negayama K. Trichosporon cutaneum (Trichosporon asahii) infection mimicking hand eczema in a patient with leukemia. J Am Acad Dermatol. May 2000;42(5 Pt 2):929-31. [Medline].

31. Castro RM, Jaeger RG, Talhari S, de Araujo NS. [Black piedra: the study of its etiological agent using scanning electron microscopy]. Rev Inst Med Trop Sao Paulo. Jul-Aug 1987;29(4):251-2. [Medline].

32. Hay RJ, Moore M. Mycology. In: Rook/Wilkinson/Ebling Textbook of Dermatology. 6^th ed. Oxford, England: Blackwell Science; 1998:1291-3.

33. Roberts SOB, Hay RJ, Mackenzie DWR. The superficial mycoses: tropical superficial infections. In: A Clinician's Guide to Fungal Disease. New York, NY: Marcel Dekker; 1984:92-4.

34. [Guideline] American Academy of Dermatology, Guidelines/Outcomes Committee. Guidelines of care for superficial mycotic infections of the skin: Piedra. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. Jan 1996;34(1):122-4. [Medline].

35. Khandpur S, Reddy BS. Itraconazole therapy for white piedra affecting scalp hair. J Am Acad Dermatol. Sep 2002;47(3):415-8. [Medline].

36. Figueras MJ, Guarro J, Zaror L. New findings in black piedra infection. Br J Dermatol. Jul 1996;135(1):157-8. [Medline].

37. Fischman O, Pires de Camargo Z, Meireles MCA. Genital white piedra: an emerging fungal disease? 5th International Conference on Mycoses. PAHO Sci Publ. 1989;396:70-6.

38. Fishman HC. White piedra. Int J Dermatol. Oct 1987;26(8):538. [Medline].

39. Gueho E, Faergemann J, Lyman C, Anaissie EJ. Malassezia and Trichosporon: two emerging pathogenic basidiomycetous yeast-like fungi. J Med Vet Mycol. 1994;32 Suppl 1:367-78. [Medline].

40. Odom RB, James WD, Berger TG. Andrews' Diseases of the Skin: Clinical Dermatology. 9^th ed. Philadelphia, Pa: WB Saunders; 2000:387-8.

41. Sugita T, Nishikawa A, Ichikawa T, Ikeda R, Shinoda T. Isolation of Trichosporon asahii from environmental materials. Med Mycol. Feb 2000;38(1):27-30. [Medline].

Keywords

black piedra, white piedra, trichosporosis, asymptomatic superficial fungal infection of the hair shaft, Pleurococcus beigelii, P beigelii, Trichosporon beigelii, T beigelii, Piedraia hortae, P hortae, Trichosporon cutaneum, T cutaneum

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)

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 and Sigma Xi
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

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Christen M Mowad, MD, Associate Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
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.

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