Practice Essentials
Tinea capitis is a disease caused by superficial fungal infection of the skin of the scalp, eyebrows, and eyelashes, with a propensity for attacking hair shafts and follicles. The disease is considered to be a form of superficial mycosis or dermatophytosis. Several synonyms are used, including ringworm of the scalp and tinea tonsurans. In the United States and other regions of the world, the incidence of tinea capitis is increasing. [1]
Dermatophytosis includes several distinct clinical entities, depending on the anatomic site and etiologic agents involved. Clinically, the conditions include tinea capitis, tinea favosa (favus resulting from infection by Trichophyton schoenleinii), tinea corporis (ringworm of glabrous skin), tinea imbricata (ringworm resulting from infection by Trichophyton concentricum), tinea cruris (ringworm of the groin), tinea unguium or onychomycosis (ringworm of the nail), tinea pedis (ringworm of the feet), tinea barbae (ringworm of the beard), and tinea manuum (ringworm of the hand).
Clinical presentation of tinea capitis varies from a scaly noninflamed dermatosis resembling seborrheic dermatitis to an inflammatory disease with scaly erythematous lesions and hair loss or alopecia that may progress to severely inflamed deep abscesses termed kerion, with the potential for scarring and permanent alopecia. (See Presentation.) The type of disease elicited depends on interaction between the host and the etiologic agents. Workup may include culture, Wood lamp examination, dermoscopy/videodermatoscopy, or skin biopsy. (See Workup.)
Treatment is governed by the species of fungus concerned, the degree of inflammation, and in some cases, by the patient's immunologic and nutritional status. (See Treatment.) Topical treatment alone usually is ineffective and is not recommended. Griseofulvin, itraconazole, terbinafine, and fluconazole have been found to be effective. Selenium sulfide shampoo may reduce the risk of spreading the infection in the early stages of therapy.
Pathophysiology
Tinea capitis is caused by keratinophilic fungal species (dermatophytes) from the genera Trichophyton and Microsporum. These fungi usually are present in nonliving cornified layers of skin and its appendages and sometimes are capable of invading the outermost layer of skin, stratum corneum, or other keratinized skin appendages derived from epidermis (eg, hair and nails).
Dermatophytes are among the most common infectious agents of humans, causing a variety of clinical conditions that are collectively referred to as dermatophytosis (or, in the plural, dermatophyses). From the site of inoculation, the fungal hyphae grow centrifugally in the stratum corneum. The fungus continues downward growth into the hair, invading keratin as it is formed. The zone of involvement extends upward at the rate at which hair grows, and it is visible above the skin surface by days 12-14. Infected hairs are brittle, and by week 3, broken hairs are evident.
Three types of in-vivo hair invasion are recognized, as follows:
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Ectothrix (inside the hair shaft)
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Endothrix (outside the hair shaft)
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Favus
Ectothrix invasion is characterized by the development of arthroconidia on the exterior of the hair shaft. The cuticle of the hair is destroyed, and infected hairs usually fluoresce a bright greenish-yellow color under a Wood lamp ultraviolet (UV) light. Common ectothrix-producing organisms include Microsporum canis, Microsporum gypseum, Trichophyton equinum, and Trichophyton verrucosum. [2]
Endothrix hair invasion is characterized by the development of arthroconidia within the hair shaft only. The cuticle of the hair remains intact, and infected hairs do not fluoresce under a Wood lamp UV light. All endothrix-producing organisms are anthropophilic (eg, Trichophyton tonsurans, Trichophyton violaceum). [3]
Favus, usually caused by Trichophyton schoenleinii, produces favuslike crusts or scutula and corresponding hair loss.
It has been suggested that predilection of tinea capitis for children (see Epidemiology) results from the presence of Malassezia furfur (Pityrosporum orbiculare or ovale), which is part of normal flora, and from the fungistatic properties of fatty acids of short and medium chains in postpubertal sebum.
Etiology
Infection of the scalp by dermatophytes usually is the result of person-to-person transmission. The organism remains viable on combs, brushes, couches, and sheets for long periods. Certain species of dermatophytes are endemic only in particular parts of the world. Zoophilic fungal infections of the scalp are rare.
In the United States, T tonsurans has replaced Microsporum audouinii and M canis as the most common cause of tinea capitis. T tonsurans also is the most common cause of the disease in Canada, Mexico, and Central America.
Historically, M audouinii was the classic causative agent in Europe and America, and Microsporum ferrugineum was most common in Asia. M audouinii and M canis remain prevalent in most parts of Europe, though T violaceum also is common in Romania, Italy, Portugal, Spain, and the former Union of Soviet Socialist Republics (USSR), as well as in Yugoslavia. In Africa, T violaceum, T schoenleinii, and M canis are commonly isolated. [4] T violaceum and M canis are prevalent in Asia. [5] T schoenleinii is common in Iran and Turkey, and M canis is common in Israel.
Epidermophyton floccosum and Trichophyton concentricum do not invade scalp hair. Trichophyton rubrum, which is the most common dermatophyte isolated worldwide, is not a common cause of tinea capitis.
The dermatophytic fungi that cause tinea capitis can be divided into two broad types, anthropophilic and zoophilic. Anthropophilic fungi grow preferentially on humans, and the most common type forms large conidia approximately 3-4 µm in diameter within the hair shaft. Zoophilic fungi are acquired through direct contact with infected animals. Smaller conidia approximately 1-3 µm in diameter are typically present, extending around the exterior of the hair shaft.
Common causes of endothrix infection include T tonsurans, characterized by chains of large spores, and T schoenleinii, characterized by hyphae with air spaces. Infected hairs break off sharply at the follicular orifice, leaving a conidia-filled stub or black dot. Suppuration and kerion formation (see the image below) commonly are associated with T tonsurans infection.

In ectothrix infection, fragmentation of the mycelium into spores occurs just beneath the cuticle. In contrast to endothrix infection, destruction of the cuticle occurs. This type of infection is caused by T verrucosum, Trichophyton mentagrophytes, and all Microsporum species.
Epidemiology
United States and international statistics
The occurrence of tinea capitis is no longer registered by public health agencies; therefore, the true incidence of this condition is unknown.
Tinea capitis is widespread in some urban areas, particularly in children of Afro-Caribbean extraction, in North America, Central America, and South America. It is common in parts of Africa and India. [6, 7, 8, 9] In rural southern Ethiopia, the incidence of tinea capitis was found to be 8.7% among children aged 4-14 years. [10] ; in Gondar, Ethiopia, the incideence in school-age children was found to be 29.4%. [11] In Southeast Asia, the rate of infection has reportedly decreased dramatically from 14% (average of male and female children) to 1.2% in the past 50 years because of improved general sanitary conditions and personal hygiene. In northern Europe, the disease is sporadic.
In a review of 48 international reports that included 5860 pediatric patients with mycologically confirmed tinea capitis, Gupta et al assessed the worldwide species distribution of the causative organisms during the period from 2020 to 2023. [12] Globally, M canis (52.39%) was the most common pathogen over this period, followed by T violaceum (14.74%), T tonsurans (10.24%), and T mentagrophytes (9.32%). The most common causative organisms in various areas of the world were as follows, in descending order of frequency:
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North America - T tonsurans, T violaceum, T soudanense, M canis
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South America - T tonsurans
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Europe - M audouinii, T tonsurans, M canis, T soudanense
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United Kingdom - M canis
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Africa - T rubrum, T violaceum, T tonsurans, T soudanense
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West Asia - M canis, T tonsurans, T violaceum, T mentagrophytes
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South and Central Asia - T violaceum, T mentagrophytes, T tonsurans, T verrucosum
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East Asia - M canis, T violaceum, T mentagrophytes, T tonsurans
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Southeast Asia - T mentagrophytes, M gypseum, T rubrum
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Australia - M canis, T tonsurans, M gypseum, T mentagrophytes
Age-related demographics
Tinea capitis occurs primarily in children: It is the most common pediatric dermatophyte infection worldwide, accounting for as many as 92.5% of dermatophytoses in children younger than 10 years. It is seen most commonly in children aged between 5 and 10 years [13] (mean age of onset, 6.9-8.1 y [14] ). The peak incidence has been reported to occur in school-aged Black male children, at rates of 12.9%. [13] In Northern California, the incidence among the pediatric population has been reported as 0.34%. [14]
Though considerably less common, tinea capitis in adults does occur, with an estimated frequency in the range of 3-11%. [15] Postmenopausal adult women (particularly Black women) are most often affected.
Sex-related demographics
The incidence of tinea capitis may vary by sex, depending on the causative fungal organism. M audouinii–related tinea capitis has been reported to be as much as five times more common in boys than in girls. After puberty, however, the reverse is true, possibly because of women having greater exposure to infected children and possibly because of hormonal factors. In infection by M canis, the ratio varies, but the infection rate usually is higher in boys. Girls and boys are affected equally by Trichophyton infections of the scalp, but adult women are infected more frequently than adult men are.
Prognosis
Tinea capitis carries a positive prognosis, with the vast majority of those treated obtaining resolution of the infection. Those who have maintained untreated or treatment-resistant tinea capitis are at risk for abscess development, referred to as a kerion. [16]
Continuous shedding of fungal spores may last several months despite active treatment; therefore, keeping patients with tinea capitis out of school is impractical. The causes of treatment failure include reinfection, relative insensitivity of the organism, suboptimal absorption of the medication, and lack of compliance with the long courses of treatment. T tonsurans and Microsporum species are typical offending agents in persistent positive cases. If fungi can still be isolated from the lesional skin at the completion of treatment, but clinical signs have improved, the recommendation is to continue the original regimen for another month.
Classification and severity of tinea capitis depend on the site of formation of their arthroconidia.
Ectothrix infection is defined as fragmentation of the mycelium into conidia around the hair shaft or just beneath the cuticle of the hair, with destruction of the cuticle. Inflammatory tinea related to exposure to a kitten or puppy usually is a fluorescent small-spore ectothrix. Some mild ringworm or prepubertal tinea capitis infections are of the ectothrix type, also termed the gray-patch type (microsporosis; see the image below). Some ectothrix infections involute during the normal course of disease without treatment. Depending on the extent of associated inflammation, lesions may heal with scarring.

Endothrix infections are noted in which arthrospores are present within the hair shaft in both anagen and telogen phases, contributing to the chronicity of the infections. Endothrix infections tend to progress and become chronic, and they may last into adult life. Lesions can be eradicated by systemic antifungal treatment. Because the organisms usually remain superficial, little potential for mortality exists. Disseminated systemic disease has been reported in patients who are severely immunocompromised.
Patient Education
Patient education is paramount in eradicating tinea capitis. According to the American Academy of Pediatrics, children with confirmed ringworm should start treatment before returning to school, and if treatment is started before the next day, exclusion is unnecessary. [17] Once appropriate treatment has been initiated, neither head shaving nor the wearing of a hat or cap is required. [12]
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Gray-patch ringworm (microsporosis) is ectothrix infection or prepubertal tinea capitis seen here in Black male child. "Gray patch" refers to scaling with lack of inflammation, as noted in this patient. Hairs in involved areas assume 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 lesional hair grew Microsporum canis.
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Typical lesions of kerion celsi on vertex scalp of young Chinese boy. Note numerous bright-yellow purulent areas on skin surface, surrounded by adjacent edematous, erythematous, alopecic areas. Culture from lesion grew Trichophyton mentagrophytes. Image from 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 vertex scalp of young Taiwanese boy. Image from 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 endoectothrix invasion of hair shaft by Microsporum audouinii. Intrapilary hyphae and spores around hair shaft are seen (hematoxylin and eosin stain with periodic acid-Schiff counterstain, magnification X250).
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Fungal hyphae and yeast cells of Trichophyton rubrum seen on stratum corneum of tinea capitis. Periodic acid-Schiff stain, magnification X250.
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Pronounced inflammatory tissue reaction with follicular pustule formation surrounding hair follicle seen in patient with clinical form of infection, termed kerion celsi. No fungal hyphae or spores were identified in lesion in either tissue sections or culture. Fluorescein-labeled Trichophyton mentagrophytes antiserum cross-reacted with antigens of dermatophyte in infected hairs within pustule (hematoxylin and eosin stain, magnification X75).
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Wood lamp examination of gray-patch area on the scalp. In Microsporum canis infection, scalp hairs emit diagnostic brilliant green fluorescence. Trichophyton tonsurans does not fluoresce with Wood lamp.
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Tinea capitis presenting as alopecia with scale in Black child.