History
Tinea capitis begins as a small erythematous papule around a hair shaft on the scalp, eyebrows, or eyelashes. Within a few days, the red papule becomes paler and scaly, and the hairs appear discolored, lusterless, and brittle. They break off a few millimeters above the scalp skin surface. The lesion spreads, forming numerous papules in a typical ring form. Ring-shaped lesions may coalesce with other infected areas.
Pruritus usually is minimal but may be intense at times. Alopecia is common in infected areas. Inflammation may be mild or severe. Deep boggy red areas characterized by a severe acute inflammatory infiltrate with pustule formation are termed kerions or kerion celsi (see the image below).

Favus (also termed tinea favosa) is a severe form of tinea capitis. Favus is a chronic infection caused most commonly by T schoenleinii and, occasionally, by T violaceum or Microsporum gypsum. Scalp lesions are characterized by the presence of yellow cup-shaped crusts termed scutula, which surround the infected hair follicles. Favus is seen predominantly in Africa, the Mediterranean, and the Middle East and, rarely, in North America and South America, usually in descendants of immigrants from endemic areas. Favus usually is acquired early in life and has a tendency to cluster in families. In favus, infected hairs appear yellow.
Physical Examination
A variety of clinical presentations of tinea capitis are recognized as being inflammatory or noninflammatory and are usually associated with patchy alopecia. Physical examination with a hand lens or trichoscopy may be helpful in demonstrating the affected hairs. [15, 16, 17] The infection may be widespread, and the clinical appearances can be subtle, especially in black children with Trichophyton tonsurans infection, in whom the findings may mimic patches of seborrheic dermatitis with hair loss. In urban areas, tinea capitis should be considered in the differential diagnosis of children older than 3 months with a scaly scalp until proven negative by mycological examination. Infection may also be associated with painful regional lymphadenopathy, especially in the inflammatory variants.
T tonsurans is the most common pathogen causing tinea capitis in the United States. As T tonsurans is an endothrix, its spores remain inside the hair shaft and do not fluoresce at Wood lamp examination. Thus, diagnosis should be made with mycological analysis by scraping scale from the scalp and sending it to the laboratory for confirmation of diagnosis. As M canis and M audouinii do exist in the United States, as with other species that cause tinea capitis, it is suggested to perform a Wood lamp examination, evaluating for an ectothrix infection of the hairs. If positive, the hairs fluoresce. [14]
Pertinent physical findings are limited to the skin of scalp, eyebrows, and eyelashes. [18]
Primary skin lesions of tinea capitis
Lesions begin as red papules with progression to grayish ring-formed patches containing perifollicular papules. Pustules with inflamed crusts, exudate, matted infected hairs, and debris may be seen. Black dot tinea capitis refers to an infection with fracture of the hair, leaving the infected dark stubs visible in the follicular orifices. Kerion celsi may progress to a patchy or diffuse distribution and to severe hair loss with scarring alopecia (see the image below). This is often described as having a “moth-eaten" appearance.

Id reaction
Dermatophyte idiosyncratic or id reactions are manifestations of the immune response to dermatophytosis. Id reactions occur at a distant site, and the lesions are devoid of organisms. Id reactions may be triggered by antifungal treatment.
The most common type of id reaction is an acute vesicular dermatitis of the hands and feet. The grouped vesicles are tense, pruritic, and sometimes painful. Id reactions are noted in patients with inflammatory ringworm of the feet, primarily resulting from infection by Trichophyton mentagrophytes. Similar lesions may occur on the trunk in tinea capitis. Vesicular lesions may evolve into a scaly eczematoid reaction or a follicular papulovesicular eruption.
Other less common types of id reactions include annular erythema and erythema nodosum. These patients have a strong delayed-type hypersensitivity reaction to intradermal trichophytin.
Distribution of tinea capitis lesions
Skin lesions appear on the scalp with extension to the eyebrows and/or eyelashes.
Regional lymph nodes
Cervical lymphadenopathy may develop in patients with severe inflammation associated with kerion formation.
Complications
The causative fungal organisms of tinea capitis destroy hair and pilosebaceous structures, resulting in severe hair loss and scarring alopecia. Since tinea capitis is the most common dermatophyte infection in the pediatric population in the United States, without accurate diagnosis and proper treatment, the disease is detrimental, both physically and mentally, to children who are affected. Young patients with itchy scalp and patchy or total hair loss frequently are ridiculed, isolated, and bullied by classmates or playmates. In some cases, the disease can cause severe emotional impairment in vulnerable children and can destabilize family relationships.
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Gray-patch ringworm (microsporosis) is an ectothrix infection or prepubertal tinea capitis seen here in an African American male child. Gray patch refers to the scaling with lack of inflammation, as noted in this patient. Hairs in the involved areas assume a characteristic dull, grayish, discolored appearance. Infected hairs are broken and shorter. Papular lesions around hair shafts spread and form typical patches of ring forms, as shown. Culture from the lesional hair grew Microsporum canis.
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Typical lesions of kerion celsi on the vertex scalp of a young Chinese boy. Note numerous bright yellow purulent areas on skin surface, surrounded by adjacent edematous, erythematous, alopecic areas. Culture from the lesion grew Trichophyton mentagrophytes. Courtesy of Skin Diseases in Chinese by Yau-Chin Lu, MD. Permission granted by Medicine Today Publishing Co, Taipei, Taiwan, 1981.
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Discrete patches of hair loss or alopecia caused by Trichophyton violaceum infection of the vertex scalp of a young Taiwanese boy. Courtesy of Skin Diseases in Chinese by Yau-Chin Lu, MD. Permission granted by Medicine Today Publishing Co, Taipei, Taiwan, 1981.
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Photomicrograph depicting an endoectothrix invasion of a hair shaft by Microsporum audouinii. Intrapilary hyphae and spores around the hair shaft are seen (hematoxylin and eosin stain with Periodic acid-Schiff counterstain, magnification X 250).
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Fungal hyphae and yeast cells of Trichophyton rubrum seen on the stratum corneum of tinea capitis. Periodic acid-Schiff stain, magnification 250X.
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Pronounced inflammatory tissue reaction with follicular pustule formation surrounding a hair follicle seen in a patient with clinical form of infection, termed kerion celsi. No fungal hyphae or spores were identified in the lesion in either tissue sections or culture. Fluorescein-labeled Trichophyton mentagrophytes antiserum cross-reacted with antigens of dermatophyte in the infected hairs within the pustule (hematoxylin and eosin stain, magnification X 75).
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Wood lamp examination of a gray-patch area on the scalp. In Microsporum canis infection, scalp hairs emit a diagnostic brilliant green fluorescence. Trichophyton tonsurans does not fluoresce with Wood lamp.
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Tinea capitis, presenting as alopecia with scale, in an African American child.