Tinea Capitis
Tinea capitis is a dermatophyte infection of the scalp hair caused primarily by Trichophyton and Microsporum species. The fungi invade keratinized tissue, including the hair follicle and hair shaft, leading to brittle hair, scaling, and alopecia. Tinea capitis most commonly affects children, particularly those between three and 14 years of age, although adult cases can occur. In adults, tinea capitis infection is uncommon but has been reported most often in postmenopausal women, with Black women described as a particularly at-risk group.
Transmission may occur through direct contact with infected humans, animals, or soil, as well as indirectly through fomites such as hats, hairbrushes, towels, bedding, and hair-grooming tools. Adults at increased risk include those with exposure
to infected children or animals, crowded living conditions, immunosuppression, or shared haircare environments.
Clinical presentation varies depending on the infecting organism and host inflammatory response. Noninflammatory tinea capitis includes the gray patch, black dot, and seborrheic dermatitis-like variants with the gray patch typically caused by ectothrix Microsporum species and the black dot variantby Trichophyton species. Inflammatory variants include diffuse pustular tinea capitis, which presents with patchy alopecia accompanied by scattered pustulesor folliculitis, and kerion, a painful, boggy inflammatorylaque that may be mistaken for a bacterial abscess (Figure 12). Another distinct clinical subtype is favus, a chronic inflammatory form caused primarily by Trichophyton schoenleinii. It is characterized by yellow cup-shaped crusts (scutula) surrounding hair follicles and remains endemic in parts of Africa and Asia despite declining worldwide incidence. Delayed diagnosis, particularly in inflammatory disease, may result in permanent scarring alopecia.
Diagnosis should be substantiated by confirmatory evaluation such as trichoscopy, potassium hydroxide preparation, fungal culture, or Wood’s light examination. Potassium hydroxide (KOH) preparation allows rapid visualization of fungal elements, while fungal culture can confirm the causative organism. Wood’s light fluorescence depends on the organism; some Microsporum species fluoresce green to yellow–green, whereas Trichophyton tonsurans typically does not fluoresce.
Trichoscopy is a valuable adjunct in the evaluation of suspected tinea capitis and may facilitate diagnosis before fungal culture results become available. Common findings include black dots, broken hairs, comma hairs, corkscrew hairs, Morse code-like (barcode-like) hairs, zigzag hairs, bent hairs, and interfollicular/perifollicular scaling. Corkscrew hairs are observed most frequently in patients with tightly coiled hair and serve as a particularly helpful trichoscopic clue in Black patients. Trichoscopy may also be used to monitor treatment response over time.
Since topical therapy cannot adequately penetrate infected hair, systemic antifungal therapy is required. Oral griseofulvin and terbinafine are commonly used, while itraconazoleand fluconazole are less common alternatives. Although griseofulvin is generally preferred for Microsporum infections and terbinafine may offer greater efficacy against Trichophyton species, both remain effective first-line therapies. In one cohort comprised predominantly of Black children, Trichophyton tonsurans was the most commonly identified pathogen, and approximately 81% of patients achieved long-term mycologic cure, and 89% achieved long-term clinical cure following griseofulvin-based therapy. Adjunctive antifungal or selenium sulfide shampoos may reduce spread but should not be used as monotherapy. Patients and families should be counseledto avoid sharing hairbrushes, combs, hats, and other personal haircare items, and household contacts may need screening to prevent ongoing transmission.

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