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Dermatology quiz NANETTE B. SILVERBERG, MD aSpring 1999 A SEVEN-YEAR-OLD African-American male presents with a five-month history of scalp pruritus and hair loss. Four months ago, the patient was given a one-month course of griseofulvin suspension at 10 mg/kg. Despite some initial improvement, the scalp hairs have not regrown and the scalp remains scaly. The patient's mother believes that the scalp pruritus and alopecia were caused by a new hair product that she had applied to the scalp to treat "dryness." The patient is otherwise healthy and has no pets. He has three siblings and five friends with whom he plays frequently.  FIGURE 1 On physical examination there is a diffuse patchy alopecia of the occipital scalp with pustules and short broken hairs (Figures 1 and 2). The posterior occipital nodes are somewhat enlarged. The rest of the physical examination is significant for diffuse xerosis and follicular prominence of the back and upper arms.  FIGURE 2 Questions What is your diagnosis?
What is the most appropriate course of work-up?
All of the following are appropriate therapy except:
Answers D, B and B, respectively. DISCUSSION AND DENOUMENT Tinea capitis is a common scalp infection of school-age children. The recent increase in incidence of this disorder, primarily in African-American children, has been documented by rising numbers of oral griseofulvin prescriptions.1 The infection is reaching epidemic proportions because it is highly contagious. Tinea capitis is caused by dermatophytes, or skin fungi, that are able to invade the hair shaft. The two major forms of hair shaft invasion are ectothrix and endothrix infections. Ectothrix infections leave most of their fungal spores on the outside of the hair shaft, allowing them to flouresce under UVA light (e.g. Wood’s light), while endothrix infections are predominantly within the hair shaft, protected from a UVA light source. In the 1940s the most common pathogen was Microsporum audoinii, an ectothrix infection. As a result, mass screening in schools could be performed using the Wood’s light. Currently the most common scalp pathogen in the United States is Trichophyton tonsurans, an endothrix infection of humans (but not animals); it does not fluoresce. As a result, mass screening is no longer possible.2 Most tinea capitis is acquired from human fomites. Shared combs, hats, and close play with contact have been shown to be sources of infection. Siblings, classmates, and parents of infected individuals may become carriers of the organism, and later develop the infection, or just pass it on to others. Animal-acquired infection in the United States is usually of the Microsporum canis variant and is generally very inflammatory. Often there is a history of a kitten with hair loss to which the child has been exposed. Tinea capitis occurs in three clinical variants: non-inflammatory; inflammatory, or kerion; and seborrheic. Non-inflammatory tinea capitis produces a typical black dot appearance due to hair weakening and breakage near the scalp. Kerions may cause scarring of the scalp and permanent hair loss, which may simulate such scarring processes as discoid lupus. Diffuse "dandruff" in a young school-age child is far more likely to signify tinea than seborrheic dermatitis. A clue to the diagnosis is the age of the patient and the presence of occipital lymphadenopathy. Potassium hydroxide preparation may allow the diagnosis to be made in the office. Culture should always be performed to confirm the diagnosis. Culture yields are improved through use of brushing with a cytology brush or toothbrush. Scraping the affected scalp or swabbing with a sterile cotton swab moistened with saline are alternate means. Hair pulls are usually not an appropriate way to culture, since the infected, broken hairs are the most difficult to obtain. Cultures should be repeated at the time of clinical clearance to confirm mycological cure. The gold standard of treatment continues to be griseofulvin, which has been used safely for more than 20 years. Griseofulvin is available in a 125 mg/5ml microsized suspension. Effective dosing of this medication has increased to 20 to 25 mg/kg/day. Absorption of the medication is improved when taken with fatty foods, and compliance is enhanced by once-daily dosing. Therapy should be continued until fungal culture is negative, which is a minimum of six weeks and may be as long as 12 weeks. When initiating therapy, there may be a strong immunological response, and a diffuse id reaction may develop, manifesting as small pruritic, erythematous papules on the extremities and trunk. If this occurs, antihistamines and emollient therapy may be used until the reaction resolves. Bacterial superinfection may occur and requires oral antibiotic therapy as concurrent therapy for a kerion. A short course of prednisone is rarely indicated.2 In recent years, there has been an increase of dermatophyte resistance to griseofulvin. In this case, fluconazole,3 itraconazole, or lamisil4 may be used for a three- to four-week course. Reduction of spread by fomites reduces familial infections. Selenium sulfide shampoo should be used two to three times per week to reduce spore carriage and consequent infectivity.5 Patients should have separate hats and combs; pillowcases should be washed frequently in hot water. Children may attend school once therapy has been initiated. REFERENCES 1. Lobato MN, Vugia DJ, Frieden IJ. Tinea capitis in California children: A population-based study of a growing epidemic. Pediatrics 1997;99:551–554. 2. Frieden IL, Howard R. Tinea capitis: Epidemiology, diagnosis, treatment and control. J Am Acad Dermatol 1994;31:S42–46. 3. Solomon BA, Collins R, Sharma J, Silverberg NB, Laude TA. Fluconazole for the treatment of tinea capitis. J Am Acad Dermatol 1997;38:128–129. 4. Elewski B. Tinea capitis. Dermatol Clin 1996;14:23–31. 5. Allen HB, Honig PJ, Leyden JJ, McGinley KJ. Selenium sulfide: Adjunctive therapy for tinea capitis. Pediatrics 1982;69:1–3. |
