Are You Confident of the Diagnosis?
Characteristic findings on physical examination
The clinical presentation of tinea capitis varies. There are three main clinical forms:
Noninflammatory (tinea capitis superficialis)
Inflammatory (tinea capitis profunda)
Favus (tinea capitis favosa)
The noninflammatory form has a number of patterns, ranging from diffuse scaling to black dot alopecia (Figure 1). The inflammatory form may present as a kerion (kerion celsi), a boggy plaque on the scalp (Figure 2). Favus is a rare form with yellow crusting. Both inflammatory and favus types can lead to scarring and permanent alopecia.
Expected results of diagnostic studies
Dermatophyte screen/fungal cultures using a toothbrush, brush, or cotton swab to rub the scalp for a sample helps identify tinea. The most common medium is Sabourad’s agar with chloramphenicol and cycloheximide to inhibit bacterial and saprophytic fungal contamination. Cultures are incubated for 3-4 weeks at 20-25 degrees Celsius, and screened one to two times per week for growth. The edge of the lesion has the highest yield. Crusts can also be removed with forceps or tweezers.
Some labs will do sensitivities testing for medications if resistance is noted. Polymerase chain reaction (PCR) is used in a limited number of laboratories. Direct microscopic exam of hair and scale in 10%-20% potassium hydroxide with or without dimethyl sulfoxide (DMSO) is the fastest test but can have a false negative result in 10%-15% of cases.
Physical exam typically will reveal cervical lymphadenlopathy. Wood lamp utility is dependent on whether the dermatophyte is ectothrix or endothrix. Ectothrix dermatophytes such as Microsporum canis, Microsporum audouinii, and Microsporum distortum produce infection, which cause the hair to fluoresce bright green.
Alopecia areata, atopic dermatitis with superinfection with bacteria of the scalp, seborrheic dermatitis, and secondary syphilis can sometimes mimic tinea capitis.
Alopecia areata should show a nonscarring alopecia with exclamation point hairs and no scaling or broken hairs.
Atopic dermatitis with bacterial superinfection can be distinguished by a negative dermatophyte screen and positive bacterial culture. Seborrheic dermatitis occurs in older children. It can be distinguished with a negative dermatophyte screen, and thick white scale on the scalp, eyebrows, and within the ears, without breakage of hairs.
Secondary syphilis can also mimic tinea capitis. The areas of alopecia appear more “moth-eaten” in appearance. If suspected, serologic tests for treponmenal antibody can be performed.
Who is at Risk for Developing this Disease?
Pre-adolescent children (between the ages of 3 and 7) are at highest risk in the United States, accounting for greater than 90% of the dermatophytoses in children under 10 years of age. The disease is rare in adults, but can be found in immunocompromised and elderly adults.
There is a higher incidence in urban areas and in children of African or Caribbean descent. Girls and boys are affected equally by Trichophyton infections of the scalp. Microsporum species are five times more common in boys.
What is the Cause of the Disease?
Tinea capitis is a dermatophyte infection of the hair follicles and skin of the scalp caused by Trichophyton tonsurans and Microsporum. Trichophyton tonsurans is the most common cause of tinea capitis in the United States.
Dermatophytes, which are keratinophilic fungi, are the causative agents. These are molds that live in the cornified layers of the skin and are capable of invading the outermost layer of skin, hair, and nails. From the area of inoculation, they grow concentrically, creating the typical “ringworm” appearance. The fungus can grow downward into the hair, and invades the keratin as it forms. It becomes visible on the surface two weeks after inoculation, when hairs become brittle and begin to break.
Dermatophytes can invade hairs in a number of ways. The endothrix (Trichophyton tonsurans, Trichophyton violaceum) leads to development of arthroconidia within the hair shaft. The ectothrix (Microsporum canis, Microsporum gypseum, Trichophyton equinum and Trichophyton verrucosum) create arthroconidia on the outside of the hair shaft, destroying the cuticle of the hair. Ectothrix infection fluoresces green under a Wood lamp.
Trichophtyon schoenleini causes favus. Favus is a severe tinea capitis infection seen predominantly in Africa and the Middle East, and is characterized by yellow crusts (scutula). Hairs appear yellow.
Anthrophilic organisms are fungi that preferentially grow on humans and form large conidia within the hair shafts. Zoophilic organisms are acquired by direct contact with infected animals; they produce smaller conidia on the outside of the hair shaft.
Person-to-person transmission is the most common means of acquiring the infection. The dermatophytes also can live on combs, brushes, hats, and furniture for long periods of time.
Systemic Implications and Complications
Suppuration and kerion formation is commonly associated with T. tonsurans infection. Untreated infections can lead to scarring alopecia.
A dermatophytid reaction or Id reaction are manifestations of the immune response to dermatophytosis (Figure 3). They can occur at sites distant from the tinea infection. They can also be triggered by antifungal therapy. These reactions are often eczematous, papular, and/or vesicular, and start on the face and spread to the trunk. Erythema nodusum is a rare manifestation of an Id reaction.
Tinea capitis requires systemic treatment because antifungal topical agents cannot penetrate hair follicles. Topical therapies, including shampoos and creams, are used as adjunct therapy.
Griseofulvin has been the gold standard of therapy because of its efficacy, tolerability, safety, cost, and availability in liquid form. The main disadvantage is the length of therapy, which requires 6-12 weeks or longer.
Newer agents such as terbinafine, itraconazole, and fluconazole have efficacy similar to griseofulvin in children with Trichophyton species. These agents also have the benefit of a shorter duration of treatment; however, they are typically more expensive and terbinafine is not as effective against Microsporum species. Clinical and mycologic examination can be performed every 4-8 weeks and therapy can be discontinued with a negative fungal culture or dermatophyte screen, or when hair growth is evident.
Treatment options are summarized in Table I.
|Agent||Dose||Duration of Treatment|
|Griseofulvin||20mg/kg/day||8-12 weeks (longer if cultures are still positive)|
|Microsize Griseofulvin||10-15mg/kg/day||8-12 weeks|
|Terbinafine||10-20kg: 62.5mg/day||Trichophtyon: 2-4 weeks|
|20-40kg: 125mg/day||Microsporum: 8-12 weeks*|
|Itraconazole||Oral solution: 3mg/kg/day***||2-6 weeks*|
|Capsules 5mg/kg/day||Alternative is pulse therapy**|
|Fluconazole||5mg/kg/day (daily dosing)||2-6 weeks|
|8mg/kg once weekly||8-12 weeks|
|Selenium Sulfide||2 applications/week||2-4 weeks|
|Ketoconazole (1% or 2%)||2 applications/week||2-4 weeks|
|Topical fungicidal lotions/creams:|
|Ketoconazole||1-2 applications daily||2-4 weeks|
|Other azoles||1-2 applications daily||2-4 weeks|
*Periodic monitoring of hepatic enzymes and complete blood count is recommended in children, when using prolonged therapy with itraconazole or terbinafine (>4 weeks)
**Pulse therapy: Itraconazole 5mg/kg/day (capsules) or 3mg/kg/day (liquid) for 1 week, repeated once a month for three cycles.
***Cyclodextrin, a component in itraconazole oral solution, can cause diarrhea in children.
Optimal Therapeutic Approach for this Disease
Assess the patient clinically for breakage of hair, black dot tinea, scarring alopecia, superinfection of scalp, and cervical lymphadenlopathy. If fungal infection is suspected, perform a dermatophyte screen and potassium hydroxide (KOH) exam.
Dermatophyte screens can take 1-2 weeks to come back positive. While waiting for the result, start the patient on topical therapies, including shampoos and creams, which have been shown to reduce carriage of viable spores.
If the patient is positive for a dermatophyte, start griseofulvin for 8 weeks, to be taken with fatty foods for better absorption. If the patient doesn’t tolerate the griseofulvin, is allergic to griseofulvin, or if resistance to griseofulvin is noted, start terbinafine as an alternative therapy.
During therapy with oral antifungals, continue the topical shampoo and/or cream for a minimum of 2 weeks. Clinically examine the patient 4-6 weeks after the initiation of therapy to assess for response (hair growth). At 6-8 weeks, repeat the dermatophyte screen. If negative, therapy can be discontinued.
If a kerion is noted, it can be managed by treating the fungal infection. Bacterial culture should be performed because often there is a mixed infection. Some advise treating with steroid medications. There is no evidence that steroids taken by mouth or injected into kerions improve cure rates or time to cure. Steroids have been shown to make patients more comfortable from the inflammation of a kerion.
Prednisolone has been used as an oral treatment at 1mg/kg per day for 7 days.
Oral antibiotics can be helpful if there is a mixed infection.
In patients with pruritus, antihistamines can provide some relief and prevent spreading from scratching.
Household members that may be carriers should be treated (at a minimum) with selenium sulfide or ketoconazole shampoo. Asymptomatic carriage is higher with Trichophyton tonsurans, Trichophyton violaceum, and Microsporum audouinii.
Household items such as brushes and combs should be replaced and then boiled for 5 minutes once a week while the patient is on therapy to prevent reinfection. Patients should not share brushes, combs, or hats with other family members.
If a household pet is suspected of infection, the pet should be treated for tinea infection.
Many patients develop a rash after starting griseofulvin. This Id reaction should be explained to parents so they do not stop therapy because of a presumed drug reaction.
Unusual Clinical Scenarios to Consider in Patient Management
Tinea infection in patients under the age of 1 is uncommon but can occur. Though most infants who develop a tinea infection have a normal immune system, assessing the child for immune problems should be considered.
Fluconazole is the only antifungal oral medication that is approved for patients under the age of 1 year, although reports of successfully using griseofulvin and terbinafine have been reported.
What is the Evidence?
Elewski, E. “Tinea capitis: a current perspective”. J Am Acad Dermatol. vol. 42. 2000. pp. 1-20. (This is a review of the epidemiology of tinea capitis with emphasis on Western Europe. It highlights the change in predominant dermatophyte over the last 50 years and focuses on alternate antifungal therapies to griseofulvin, including terbinafine, fluconazole, and intraconazole.)
Elewski, BE, Caceres, HW, DeLeon, L, El Shimy, S, Hunter, JA, Korotkiy, N. “Terbinafine hydrochloride oral granules versus griseofulvin suspension in children with tinea capitis: result of two randomized, investigator blinded, multicenter, international, controlled trials”. J Am Acad Dermatol. vol. 59. 2008. pp. 41-54. (This is a randomized control trial of children taken terbinafine granules (5-8mg/kg a day for 6 weeks) versus oral griseofulvin suspension 20mg/kg/day for 6 weeks. Rates of complete cure and mycologic cure were significantly higher for terbinafine than for griseofulvin. There were some differences in the type of dermatophyte infecting patients in the two groups.)
Gupta, AK, Summerbell, RC. “Tinea capitis”. Med Mycol. vol. 38. 2000. pp. 255-87. (This review focuses on causes and epidemiology of tinea capitis in North America. It also highlights the efficacy of multiple oral antifungal agents for tinea capitis.)
Kakourou, T, Uksal, U. “Guidelines for the management of tinea capitis in children”. Ped Dermatol. vol. 27. 2010. pp. 226-8.
Gupta, AK, Solomon, RS, Adam, P. “Itraconazole oral solution for the treatment of tinea capitis”. Br J Dermatol. vol. 139. 1998. pp. 104-6. (This article highlights the use of itraconazole in twenty-seven children given a pulsed treatment of 3mg/kg once a week for up to three doses. The first two doses were separated by 2 weeks and the last dose was separated by 3 weeks. Children with severe disease required three doses, whereas children with less severe disease required only one. No side effects were noted from administration.)
Robert, R, Pihet, M. “Conventional methods for the diagnosis of dermatophytes”. Mycopathologia. vol. 166. 2008. pp. 295-306. (Reviews methods for diagnosing dermatophytes, including direct microscopic exam and stains that highlight dermatophytes. Also reviews culture methods, including useful culture media and growth.)
Honig, PJ, Caputo, GL, Leyden, JJ, McGinley, K, Selbst, SM, McGravey, AR. “Treatment of kerions”. Pediatr Dermatol. vol. 11. 1994. pp. 69-71. (Seminal article on the treatment of kerions with oral griseofulvin and oral steroids. This was pilot study to compare systemic antibiotics and/or systemic steroids in children with kerions. Children in the group treated with griseofulvin alone improved the most.)
Pomeranz, AJ, Sabnis, SS, McGrath, GJ, Esterly, NB. “Asymptomatic dermatophyte carriers in the households of children with tinea capitis”. Arch Pediatr Adolesc Med. vol. 153. 1999. pp. 483-6. (This paper looked at asymptomatic carriers as source for tinea capitis in children and as sources for recurrence of tinea after treatment.)
Roberts, BJ, Friedlander, SF. “Tinea capitis: a treatment update”. Pedatr Ann. vol. 34. 2005. pp. 191-200. (Highlights oral therapies, but additionally highlights the importance of the adjuvant use of antifungal shampoos for all patients in order to decrease the viability of fungal spores present on the hair, as well as for all household contacts to prevent infection or eliminate the carrier state.)
Romano, C, Gianni, C, Papini, M. “Tinea capitis in infants less than 1 year of age”. Pediatr Dermatol. vol. 18. 2001. pp. 465-8. (This is a report of fifteen cases of tinea capitis observed in Italy in infants less than 1 year of age. There were ten boys and five girls (mean age 6 months). Diagnosis was confirmed by mycologic examination. Microsporum canis was isolated in nine cases and Trichophyton mentagrophytes in three. These twelve infants were Italian; animals were the source of infection.)
Seebacher, C, Bouchara, JP, Mignon, B. “Updates on the epidemiology of dermatophyte infections”. Mycopathologia.. vol. 166. 2008. pp. 335-52. (Highlights the change in epidemiology of dermatophyte species over the last 100 years. Identifies trends in North America, Europe, and developing countries.)
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