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This case is about "black-dot" ringworm, a form of tinea capitis.
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A 9-year-old boy is brought to you by his mother to evaluate a bald spot that appeared one week ago behind his left ear. The area of hair loss is not symptomatic, but he has nontender left postauricular adenopathy. He appears healthy, takes no medications, and has no family history of hair loss.
1. What's the differential diagnosis of focal hair loss in a healthy child of this age?
2. What's the most likely diagnosis?
3. How would you confirm the diagnosis?
This 9-year-old boy has classic findings of black-dot ringworm from endothrix fungal infection of the hair shaftthe form of tinea capitis in the United States most commonly caused by Trichophyton tonsurans. The microorganism grows, then forms arthrospores within the hair shaft. The result is increased shaft fragility and breakage, which leaves a small nubbin of residual hair, or a black dot, at the surface.1-3 Little or no inflammation, scale, or pruritus may occur, but striking patches of hair loss often prompt a visit to a pediatrician.
Prevalence. An epidemic of tinea capitis has been recognized recently in the United States and throughout the world.1-4 In North America, the prevalence of infection is highest among African-Americans, but it may also be increasing in Hispanic and Caucasian children. Several surveys of African-American school children show positive fungal cultures among approximately 13% to 15%.5,6 Some experts propose that the rate may be as high as 25% in some settings. Those statistics also include a number of carriers who lack clinical evidence of disease but undoubtedly act as a reservoir for the organism.
Differential diagnosis. About 60% of tinea capitis presents as chronic, persistent scale, often mistaken for dandruff or seborrheic dermatitis.4 Therefore, any school-age African-American child who is given a diagnosis of seborrheic dermatitis should first be evaluated for fungal infection.
The differential diagnosis of localized hair loss in this age group should also include external trauma (such as hair pulling or traumatic hair grooming) and alopecia areata. Clinically, the presence of adenopathy and "black dots" helps exclude those disorders.
Diagnosis. Tinea capitis can be diagnosed by finding arthrospores packed inside fragments of hair. Obtain the hair by gently, but firmly, scraping patches of scale or alopecia with a #15 scalpel blade.1-3 Place the specimen on a glass slide with a drop of potassium hydroxide and a cover slip, and examine it under low power. Sending scrapings for fungal culture on a moistened cotton swab or sterile plastic plate is still the gold standard for confirming the diagnosis.
Close examination of our patient (see photo) reveals a small area of almost complete alopecia and a larger area of more subtle hair loss on the left parietal and temporal scalp. Potassium hydroxide scrapings from both areas show hair fragments filled with arthrospores.
Clinical course. Over weeks or months, some patients develop inflammation and increasing erythema, crusting, and pustules. Patients who become highly sensitized to the organism may develop a severe inflammatory reaction referred to as "kerion." This reaction appears as painful, edematous, boggy, and purulent nodules and plaques ranging from 1.0 cm to more than 10 cm in diameter. Patients with both noninflammatory and inflammatory disease often develop postauricular adenopathy. During the course of infection, either before or after initiating antifungal therapy, many patients develop an id, or autoeczematization, reactionan itchy, papular, eczematous eruption that usually starts on the face and neck and disseminates to the trunk and extremities.1 The clinician should discuss the id reaction with parents when oral antifungal medications are started. Informing parents prevents them from confusing uncommon adverse medication reactions with id features, which may erroneously lead them to discontinue treatment.
Treatment. Griseofulvin (Grifulvin V, Gris-PEG, Grisactin) in two divided doses, taken with fatty food, is the most effective treatment and the only drug approved by the FDA for treating tinea capitis. Therapy should continue for at least two months. When the patient looks clinically clear, some experts recommend obtaining a proof-of-cure culture before discontinuing treatment. In recurrent cases, siblings and parents should be evaluated and, possibly, cultured to identify clinical cases and carriers in the home so that concomitant therapy may be started. Caution against sharing hairbrushes, hats, combs, and other fomites, which may be a source of reinfection.
A number of newer oral antifungal medicationsincluding fluconazole (Diflucan), terbinafine (Lamisil), and itraconazole (Sporanox)may require a shorter period of treatment than griseofulvin, but guidelines on using these medications in children have not yet been established (nor has FDA approval been granted for a pediatric indication). Results of domestic and international studies are pending.1-3
1. Elewski BE: Tinea capitis: A current perspective. J Am Acad Dermatol 2000;42(1Pt1):1
2. Gupta AK, Summerbell RC: Tinea capitis. Med Mycol 2000;38:255
3. Ceburkovas O, Schwartz PA, Janniger CK: Tinea capitis: Current concepts. J Dermatol 2000;27:144
4. Laude TA: Epidemiology of tinea capitis. Pediatr Dermatol 1988;2:234
5. Williams JV, Honig PJ, McGinley KJ, et al: Semiquantitative study of tinea capitis and the asymptomatic carrier state in inner-city school children. Pediatrics 1995;96:265
6. Vargo K, Cohen BA: Prevalence of undetected tinea capitis in household members of children with disease. Pediatrics 1993;92:155
Bernard Cohen. Pediatric dermatology: What's your Dx?.