Tinea Capitis

Tinea capitis most commonly occurs in prepubertal children.
In the United States, African-American children are disproportionately affected by this superficial fungal infection of the hair shaft. Tinea capitis appears most often in overcrowded, impoverished inner-city communities.
Trichophyton tonsurans is, by far, the most common etiologic agent; more than 90% of cases are caused by it. Other species, such as Microsporum audouinii, which is spread from human to human, and Microsporum canis, which is spread from animals (cats and dogs), are more often seen in white children. Patients frequently have a family member, pet, or playmate with tinea.
Tinea capitis is quite contagious and is generally spread by person-to-person contact. Studies have demonstrated a 30% carrier state of adults exposed to a child with T. tonsurans. The organism has also been isolated from such inanimate objects as hairbrushes and pillows.

There are essentially five clinical expressions of tinea capitis, with some overlapping physical presentations:

Inflamed, scaly, often alopecic patches, mimicking seborrheic dermatitis, are especially common in infancy until the age of 6 to 8 months (Fig. 9.8).
A diffuse scaling is seen with multiple round areas, characterized by alopecia that occurs secondary to broken hair shafts, leaving residual black stumps (“black dot” ringworm) (Fig. 9.9A,B). It is seen uncommonly and is often mistaken for alopecia areata.
The “gray patch” type (Fig. 9.10) consists of round, scaly plaques of alopecia in which hairs are broken off close to the surface of the scalp.
A kerion is a boggy, pustular, indurated, tumor-like mass, which represents an inflammatory hypersensitivity reaction to the fungus. It typically appears on the scalp. Such inflammation can result in localized scarring (Fig. 9.11).
Secondary bacterial invaders such as Staphylococcus aureus and some gram-negative organisms may sometimes be recovered from a kerion. Often, there is accompanying nontender regional adenopathy.
Occasionally, a pustular variety, with or without alopecia, can mimic a bacterial infection.

A KOH preparation or fungal culture confirms the diagnosis.
When in doubt, or when a KOH preparation is negative, a fungal culture placed on Sabouraud's agar should be done. This can be performed by obtaining broken hairs and scale by stroking the affected area with a sterile toothbrush, a familiar object to a child and one that is less frightening than a surgical blade or forceps (see Chapter 35: Diagnostic and Therapeutic Techniques). The collected material is then tapped onto the surface of Sabouraud's agar.
An alternative method of harvesting broken hairs is by rubbing a moistened gauze pad on the involved area of scalp and then using forceps to place the hairs on the culture medium or slide. Pustules generally are sterile or grow bacterial contaminants.
A biopsy is rarely necessary.
In the past, Wood's light examination was a valuable screening tool to diagnose tinea capitis easily (because Microsporum species are usually fluorescent), but it has largely lost its usefulness because most cases are caused by the nonfluorescing T. tonsurans.

Differential Diagnosis

Alopecia Areata

Atopic Dermatitis

Seborrheic Dermatitis

Tinea amiantacea

KOH-negative local patch or plaque of thick adherent scale (“tinea” is a misnomer for this condition) (Fig. 9.12).

Management

Topical therapy is of little or no value in treating tinea capitis; although an adjunctive antifungal shampoo such as ketoconazole 1% to 2% (Nizoral) or selenium sulfide 1% to 2.5% (Selsun) may be used by the infected person and contacts to prevent reinfection and spread.

Griseofulvin

In children, systemic therapy with a liquid suspension of griseofulvin has been the mainstay of therapy.
Dosing: The effective dose of microsized griseofulvin = 20 to 25 mg/kg/day; sometimes as high as 25 mg/kg/day in divided doses. Ultramicrosized griseofulvin = 15 to 20 mg/kg/day.
Should be given with milk or food to increase its absorption and continued until the patient is clinically cured, generally 6 to 8 weeks. Some patients may require longer therapy.
Treatment failure may indicate inadequate doses or duration of therapy, drug resistance, reinfection from another family member, poor compliance, or immune incompetence.
Terbinafine, itraconazole, and fluconazole are more efficacious agents. They have been used in some cases of griseofulvin treatment failure.

Terbinafine (Lamisil)

Available as a 250 mg tablet or a 125 or 187.5 mg granule packet.
Dosing: weight-based, <20 kg take 62.5 mg/day; 20 to 40 kg take 125 mg/day; >40 kg take 250 mg/day.
Granules are child friendly and parents can be instructed to sprinkle it on the food.

Itraconazole (Sporanox)

Fluconazole (Diflucan)

Available in 100, 150, and 200 mg tablets and as an oral solution of 10 and 40 mg/mL.
Dosing: 6 mg/kg/day for 3 to 6 weeks
Occasionally, concomitant systemic steroid therapy is warranted in addition to griseofulvin or other systemic antifungal when the patient is experiencing a severe, tender, or painful kerion. A short course (usually 5 to 7 days) of oral prednisone, 1 mg/kg/day, is sufficient.

Helpful Hints

A pustular presentation of tinea capitis can mimic a bacterial infection.
When a child has scaling alopecia and enlarged lymph nodes in the posterior auricular or occipital area, obtain a fungal culture and consider starting empiric antifungal treatment.
In many instances, therapy may have to be initiated in a patient with negative KOH examination and fungal cultures, based solely on clinical appearance.
Siblings of tinea capitis patients should be evaluated, or else the infection might be “ping-ponged” back and forth within the family.
Occasionally, an “id-like” reaction occurs shortly after the initiation of griseofulvin therapy. This consists of multiple small sterile papules on the face or body, and it probably represents a hypersensitivity response.

Points to Remember