CASE #2: Black dot alopecia
Tinea capitis, a condition common in children but rare in adults, is caused by an infection of the scalp with a dermatophyte fungus.17-21 It is the most common dermatophyte infection found in children younger than age 12 years and is especially prevalent in blacks.
The etiologic classes of fungi that result in tinea capitis infections are anthropophilic, zoophilic, and geophilic. The anthropophilic fungi are endemic in humans, cause mild inflammation, and grow inside the hair shaft, forming large hyphae (branches) and arthroconidia (spores). Anthropophilic infections are more common among people in crowded living conditions. Zoophilic fungi are endemic in animals, grow outside the hair shaft, form smaller hyphae and spores, and elicit brisk inflammation in the form of pustules and abscesses, as do geophilic fungi, which grow in the soil.
There are three genera of dermatophytes: Epidermophyton, Microsporum, and Trichophyton. Approximately 40 species are either anthropophilic, zoophilic, or geophilic.
Three types of invasion of the scalp’s hair follicles occur in tinea capitis: (1) endothrix (inside the follicle); (2) ectothrix (outside the follicle); and (3) favus (honeycomb/abscess-type destruction of the hair shaft).
Endothrix tinea capitis is usually caused by anthropophilic fungi, which include T. tonsurans, T. violaceum, and T. soudanense. The hair shaft is filled with fungal branches and spores. Endothrix infections do not fluoresce under a Wood’s lamp.
Ectothrix tinea capitis is caused by zoophilic fungi that include M. canis (from an infected kitten or, rarely, an older cat or dog), M. audouinii, M. distortum (cats), M. ferrugineum, T. mentagrophytes var. equinum (horses), M. nanum (pigs), and T. verrucosum (cattle). The geophilic fungi M. gypseum and M. fulvum are infrequent causes of tinea capitis. Fungal branches and spores coat the outside of the hair shaft in this type of tinea capitis.
Favus is caused by an abscess-like destruction of the hair follicle that results in large, boggy plaques on the scalp with yellow crusts and matted hair. It is brought on by T. schoenleinii infection.
T. tonsurans is most common in white children in the United States and occurs equally in boys and girls. Infection with this dermatophyte results in black dot alopecia, which responds well to oral terbinafine (Lamisil, Terbinex) or griseofulvin (Fulvicin, Grifulvin). T. verrucosum is found most often in Africa and Eastern Europe and responds well to oral terbinafine or griseofulvin. M. canis is most common in black boys. It can cause severe scaling of the scalp, cuticle breakage, and brittle hair. Treatment requires high-dose griseofulvin for three months and results in gray-patch tinea capitis and kerions. M. audouinii is the most common cause of tinea capitis in Western Europe.
There are six clinical variants of tinea capitis: (1) dry scaling, which mimics the scale of seborrheic dermatitis and occasionally the moth-eaten alopecia of syphilis; (2) black dot, in which the hairs are broken off at the scalp, leaving a scaly or smooth surface; (3) smooth areas of hair loss that mimic alopecia areata; (4) kerion, which is a very inflamed mass similar to an abscess; (5) favus, characterized by yellow crusts and matted hair; and (6) mild scaling, which indicates a carrier state has no symptoms and no swollen lymph nodes. Untreated kerion and favus may result in permanent scarring and hair loss.
The main findings associated with tinea capitis are the id reaction, an eczematous eruption of juicy papules on the body distant from the scalp (especially just after the start of antifungal treatment), and swollen lymph glands at the sides of the back of the neck and around the ears.
Dermatophytes that cause tinea capitis can be spread person-to-person or transferred from fomites on hairbrushes, clothing, towels, and furniture. Fungal spores are long-lived and can infect another individual months after being shed.
Diagnosis of tinea capitis can usually be made clinically based on the findings discussed previously. A KOH preparation or examination with a Wood’s lamp can also help in the diagnosis. M. audouinii and M. canis infections appear as green-blue fluorescence under a Wood’s lamp. The confirmatory diagnosis, if needed, may be obtained by culturing the hair on Sabouraud medium.
Oral treatment is required to clear tinea capitis.22,23 Griseofulvin is the mainstay of oral treatment in the United States. The manner in which dermatologists and pediatricians treat tinea capitis differs. Dermatologists dealing with more complex cases often use griseofulvin at a dose of 20 to 25 mg/kg for 12 weeks. Pediatricians tend to treat for six to eight weeks at 10 mg/kg with a higher rate of clinical failure. Griseofulvin is available in suspension and pill forms and should always be taken with such fatty foods as whole milk or ice cream. Griseofulvin rarely precipitates lupus erythematosus and should not be used in patients with porphyria or liver disorders.
Although topical medications are not approved to treat tinea capitis, they do have a role to play. Shampoos and lotions (e.g., ketoconazole 2% or selenium sulfide 2.5%) used daily appear to prevent the spread of tinea capitis among infected children and household contacts who may be asymptomatic carriers of dermatophytes in their scalps.
Terbinafine, a recently approved treatment, is available in granules taken in the following dosage: 125 mg/day in patients weighing <25 kg, 187.5 mg/day in patients weighing 25-35 kg; and 250 mg/day in patients weighing >35 kg. The granules should be sprinkled on a spoonful of soft, nonacidic food (e.g., pudding or mashed potatoes) and swallowed without chewing. Do not use with applesauce or other fruit-based foods. Check liver function tests before starting terbinafine treatment.
Non-FDA approved treatments for tinea capitis include fluconazole (Diflucan) 5 mg/kg/day for up to six weeks and itraconazole (Sporanox) at varying dosages (depending on the weight of the child) for four to six weeks.
Dr. Scheinfeld is assistant clinical professor of dermatology at Columbia University in New York City, where he has a private practice. The author has no relationship to disclose relating to the content of this article.
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