Tinea Capitis

Tinea capitis is a dermatophytosis of the scalp and associated hair. It may be caused by any pathogenic dermatophyte from the genera Trichophyton and Microsporum excepting T. concentricum. The most common cause worldwide is M. canis, whereas in the United States T. tonsurans is most prevalent followed by M. canis.

EPIDEMIOLOGY

The incidence of tinea capitis remains unknown, but it is most commonly found in children aged 3 to 14 years old. It is uncommon in adults. For unknown reasons, tinea capitis is more common in children of African descent. Transmission is increased with decreased personal hygiene, overcrowding, and low socioeconomic status. Organisms responsible for tinea capitis have been cultured from fomites such as combs, caps, pillowcases, toys, and theater seats. Even after shedding, hairs may harbor infectious organisms for more than 1 year. Asymptomatic carriers are common, making tinea capitis difficult to eradicate.

PATHOGENESIS

Ectothrix dermatophytes  typically establish infection in the perifollicular stratum corneum, spreading around and into the hair shaft of mid- to late-anagen hairs before descending into the follicle to penetrate the cortex of the hair. Arthroconidia then reach the cortex of the hair and are transported upward on its surface. Microscopically, only the ectothrix arthroconidia may be visualized on plucked hairs, although intrapilary hyphae are present as well.

The pathogenesis of endothrix infections is the same except that arthroconidia remain within the hair shaft, replacing the intrapilary keratin and leaving the cortex intact. As a result, the hair is very fragile and breaks at the surface of the scalp where support from the follicular wall is lost, leaving behind a tiny black dot. Thus, “black dot” tinea capitis is observed.

CLINICAL FINDINGS

The clinical appearance of tinea capitis depends on its etiology .

Noninflammatory, Human, or Epidemic Type.

The noninflammatory pattern of tinea capitis is seen most commonly with the anthropophilic ectothrix organisms such as M. audouinii or M. canis. This form of tinea capitis is also known as the seborrheic form secondary to prominent scaling. Inflammation is minimal. Hairs in the affected area turn gray and lusterless secondary to their sheath of arthroconidia and break off just above the level of the scalp . Often there is no noticeable hair loss. Frequently, however, these lesions appear as well-defined, round hyperkeratotic, scaly areas of alopecia, due to the breaking off of hairs . Appearance is like a “wheat field.” Remaining hairs and scales exhibit green fluorescence under Wood's light . Lesions usually occur on the occiput.

Inflammatory Type.

The inflammatory type of tinea capitis is usually seen with zoophilic or geophilic pathogens, with common examples being M. canis and M. gypseum. Inflammatory tinea capitis is the result of a hypersensitivity reaction to the infection. The spectrum of inflammation ranges from a pustular folliculitis to kerion , which is a boggy, inflammatory mass studded with broken hairs and follicular orifices oozing with pus. Such inflammation often results in scarring alopecia. Inflammatory lesions are usually pruritic, and may be associated with pain, posterior cervical lymphadenopathy, fever, and additional lesions on glabrous skin.

“Black Dot” Tinea Capitis.

The “black dot” form of tinea capitis is caused by the anthropophilic endothrix organisms T. tonsurans and T. violaceum. This is the least inflammatory form of tinea capitis. Hair loss may or may not occur. When it does, hairs broken at the level of the scalp leave behind grouped black dots in the areas of alopecia . Diffuse scaling is again typically present, but inflammation varies from minimal to pustular folliculitis or furuncle-like lesions to kerion.Affected areas are usually multiple or polygonal with poorly demarcated, finger-like margins. Normal hairs commonly remain within patches of alopecia.

DIFFERENTIAL DIAGNOSIS

HISTOPATHOLOGY

In tinea capitis, methenamine silver and periodic acid-Schiff (PAS) stains reveal hyphae around and within the hair shaft. The dermis demonstrates a perifollicular infiltrate of mixed lymphocytes, histiocytes, plasma cells, and eosinophils. Follicular disruption leads to an adjacent foreign-body giant cell reaction.

Markedly inflammatory lesions, such as a kerion, demonstrate a more intense infiltrate of polymorphonuclear leukocyte abscesses within the dermis and follicle. Organisms are difficult to visualize, but fungal antigens are detectable with immunofluorescent techniques.