Tinea Capitis

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.

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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:

• Ectothrix (inside the hair shaft)
• Endothrix (outside the hair shaft)
• 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.

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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.

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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 adjace....

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.

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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:

• North America - T tonsurans, T violaceum, T soudanense, M canis
• South America - T tonsurans
• Europe - M audouinii, T tonsurans, M canis, T soudanense
• United Kingdom - M canis
• Africa - T rubrum, T violaceum, T tonsurans, T soudanense
• West Asia - M canis, T tonsurans, T violaceum, T mentagrophytes
• South and Central Asia - T violaceum, T mentagrophytes, T tonsurans, T verrucosum
• East Asia - M canis, T violaceum, T mentagrophytes, T tonsurans
• Southeast Asia - T mentagrophytes, M gypseum, T rubrum
• 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.

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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.

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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 ....

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.

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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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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. The hairs appear discolored, lusterless, and brittle, and 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).

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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 adjace....

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; rarely, it occurs 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.

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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.^{[18, 19, 20]}

The infection may be widespread, and the clinical appearances can be subtle, especially in Black children with T 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 ruled out by mycologic 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. Because T tonsurans is an endothrix, its spores remain inside the hair shaft and do not fluoresce on Wood lamp examination. Thus, diagnosis should be made through mycologic analysis by scraping scale from the scalp and sending it to the laboratory for confirmation of the diagnosis. Given that M canis and M audouinii do exist in the United States, it is suggested to perform a Wood lamp examination to evaluate for an ectothrix infection of the hairs; if such infection is present, the hairs will fluoresce.^[16]

Pertinent physical findings are limited to the skin of scalp, eyebrows, and eyelashes.^[21]

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. The term black dot tinea capitis refers to an infection in which the hairs fracture, 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-eate" appearance.

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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 ....

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 T 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 erythema annulare 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.

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Complications

The causative fungal organisms of tinea capitis destroy hair and pilosebaceous structures, resulting in severe hair loss and scarring alopecia. 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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Laboratory Studies

Culture

Laboratory diagnosis of tinea capitis depends on examination and culture of skin rubbings, skin scrapings, or hair pluckings (epilated hair) from lesions.

Before specimen collection, any ointment or other local applications present should be removed with alcohol.

Infected hairs appearing as broken stubs are best for examination. They can be removed with forceps without undue trauma or collected by means of gentle rubbing with a moist gauze pad; broken, infected hairs adhere to the gauze. A toothbrush may be used in a similar fashion.^[22]

Alternatively, affected areas can be scraped with the end of a glass slide or with a blunt scalpel to harvest affected hairs, broken-off hair stubs, and scalp scale. This is preferable to plucking, which may remove uninvolved hairs. Scrapings may be transported in a folded square of paper. Skin specimens may be scraped directly onto special black cards, which make it easier to see how much material has been collected and provide ideal conditions for transportation to the laboratory; however, affected hairs are easier to see on white paper than on black paper.

Alternatively, a swab-culture technique has been proposed where a moistened cotton tip applicator from a bacterial culture swab is used to gather a sample and sent to the laboratory for culture growth.^[23]

Definitive diagnosis depends on an adequate amount of clinical material submitted for examination by direct microscopy and culture. The turn-around time for culture may take several weeks.

Selected hair samples are cultured or allowed to soften in 10-20% potassium hydroxide (KOH) before examination under the microscope. Examination of KOH preparations (KOH mount) usually determines the proper diagnosis if a tinea infection exists.

Conventional sampling of a kerion can be difficult. Negative results are not uncommon in these cases. The diagnosis and decision to treat lesions of kerion may need to be made clinically. A moistened standard bacteriologic swab taken from the pustular areas and inoculated onto the culture plate may yield a positive result.^[24]

Microscopic examination of the infected hairs may provide immediate confirmation of the diagnosis of ringworm and establish whether the fungus is small-spore or large-spore ectothrix or endothrix.

Culture provides precise identification of the species for epidemiologic purposes.^[25] Primary isolation is carried out at room temperature, usually on Sabouraud agar containing antibiotics (penicillin/streptomycin or chloramphenicol) and cycloheximide (Acti-Dione), which is an antifungal agent that suppresses the growth of environmental contaminant fungi. In cases of tender kerion, the agar plate can be inoculated directly by pressing it gently against the lesion.

Most dermatophytes can be identified within 2 weeks, although T verrucosum grows best at 37°C and may have formed only into small and granular colonies at this stage. Identification depends on gross colony and microscopic morphology. Specimens should be inoculated onto primary isolation media, such as Sabouraud dextrose, and incubated at 26-28°C for 4 weeks. The growth of any dermatophyte is significant.

In some cases, other tests involving nutritional requirements and hair penetration in vitro are necessary to confirm the identification.

Wood lamp examination

In 1925, Margarot and Deveze observed that infected hairs and some fungus cultures fluoresce in ultraviolet (UV) light. The black light commonly is termed Wood lamp. Light is filtered through a Wood nickel oxide glass (barium silicate with nickel oxide), which allows only the long UV rays to pass (peak at 365 nm). Wood lamp examination is useful for certain ectothrix infections (eg, those caused by M canis,M audouinii, and Microsporum rivalieri). In cases with endothrix infection, such as T tonsurans, however, negative Wood lamp examination findings are of no practical value for screening or monitoring infections.^[26]

Hairs infected by M canis, M audouinii, M rivalieri, and M ferrugineum fluoresce a bright green to yellow-green color (see the image below). Hairs infected by T schoenleinii may show a dull green or blue-white color, and hyphae regress leaving spaces within the hair shaft. T verrucosum exhibits a green fluorescence in cow hairs, but infected human hairs do not fluoresce. The fluorescent substance appears to be produced by the fungus only in actively growing infected hairs. Infected hairs remain fluorescent for many years after the arthroconidia have died.

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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. Trich....

When a diagnosis of ringworm is under consideration, the scalp is examined under a Wood lamp. If fluorescent infected hairs are present, hairs are removed for light microscopic examination and culture. Infections caused by Microsporum species fluoresce a typical green color. Unfortunately, most tinea capitis infections in North America are caused by T tonsurans and do not demonstrate fluorescence.^[27]  In favus, infected hairs appear yellow.

Serology

Serology  is not required for a diagnosis of dermatophytosis.

Dermoscopy and videodermatoscopy

Dermoscopy has been proposed as a way to make the diagnosis of tinea capitis and even to differentiate tinea capitis organisms.^{[28, 29]} T tonsurans has been described as having multiple comma-shaped hairs and M canis as having dystrophic and elbow-shaped hairs.^[30]

A small study in patients with tinea capitis from M canis found that comma hairs were a prominent and distinctive feature on videodermatoscopy; comma hairs were not seen in patients with alopecia areata.^[31]

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Histologic Findings

Skin biopsy, with a particular emphasis on examination of infected hairs with special histochemical stains, aids in the identification of the causative fungus, especially in cases of fungal folliculitis (Majocchi granuloma) and onychomycosis. Bullous tinea demonstrates subepidermal edema and reticular degeneration of the epidermis. Tinea corporis demonstrates subacute and chronic dermatitis with or without follicular inflammation and destruction. Suppurative folliculitis may be present. In the mildest form, hyperkeratosis, parakeratosis, spongiosis, slight vasodilatation, and a perivascular inflammatory infiltrate in the upper dermis are present.

Fungal hyphae can be demonstrated by using routine hematoxylin and eosin (H&E) stain, and identification can be facilitated by using special stains. Periodic acid–Schiff (PAS) stain with diastase digestion or counterstained with green dye facilitates identification of fungal elements. (See the image below.)

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Photomicrograph depicting endoectothrix invasion of hair shaft by Microsporum audouinii. Intrapilary hyphae and spores around hair shaft are seen (hem....

Fungi are seen sparsely in the stratum corneum (see the first image below). Hyphae extend down the hair follicle, growing on the surface of the hair shaft. Hyphae then invade the hair, penetrate the outermost layer of hair (ie, cuticle), and proliferate downward in the subcuticular portion of the cortex, gradually penetrating deep into the hair cortex. Pronounced inflammatory tissue reaction with follicular pustule formation surrounding hair follicles is seen in patients with the clinical form of infection termed kerion celsi (see the second image below).

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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, t....

In endothrix infection, spherical-to-boxlike spores are found within the hair shaft. This type of infection is caused by T tonsurans or T violaceum.

In ectothrix infection, organisms form a sheath around the hair shaft. In contrast to endothrix infection, destruction of the cuticle by hyphae and spores occurs.

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Medical Care

Choice of treatment for tinea capitis is determined by the species of fungus concerned, the degree of inflammation, and in some cases, by the immunologic and nutritional status of the patient.

After microscopic or culture confirmation, medical therapy should be initiated. Systemic administration of griseofulvin provided the first effective oral therapy for tinea capitis, and resistance to the medication has remained minimal.^{[32, 33, 34]} Dosing in the pediatric population is weight-based. Recommended dosing is 20-25 mg/kg/day in single or two divided doses for microsized griseofulvin or 15-20 mg/kg/day in single or two divided doses for ultramicrosized griseofulvin.^[35] The duration of treatment should be between 4 and 6 weeks.

Itraconazole, terbinafine, and fluconazole have been reported to be effective alternatives,^[32]  though possibly more expensive.^[36] Of these, itraconazole and terbinafine are used most commonly. There may be some advantage to giving itraconazole with whole milk to increase absorption.^[37]  Itraconazole and terbinafine appear to have the highest mycologic cure rates in children (79% and 81%, respectively), whereas griseofulvin and terbinafine have the highest complete cure rates (72% and 92%, respectively). Griseofulvin is more effective against Microsporum, whereas terbinafine and itraconazole are more effective against Trichophyton.^{[38, 39]}

Because itraconazole has been associated with heart failure, it is currently not favored as a first-line therapy for tinea. An exception may be serious M canis infections, which are relatively insensitive to terbinafine, or, according to some authors, if griseofulvin is not available.^[40]

Terbinafine acts on fungal cell membranes and is fungicidal. Adverse effects include gastrointestinal disturbances and rashes in 3-5% of cases.^[41]  

Fluconazole in tablet or oral suspension form is typically administered for 6 weeks. An extra week of therapy can be administered if clinically indicated at that time.

Oral ketoconazole is rarely an acceptable alternative to griseofulvin, because of the risk of hepatotoxicity and the higher cost.^[42]

In ectothrix infection (eg, M audouinii, M canis), a longer duration of therapy may be required.

Oral steroids may help reduce the risk for and extent of permanent alopecia in the treatment of kerion. Use of topical corticosteroids should be avoided during treatment of dermatophyte infections.

A national survey of pediatric dermatologists in the United States reported that in the treatment of tinea capitis in infants and children, practitioners tended to prefer fluconazole for patients younger than 2 months, griseofulvin for patients aged 2 months to 2 years, and terbinafine for patients aged 2 years or older.^[43] Significant interprovider variation in treatment approaches remains.

Topical treatment alone usually is ineffective and is not recommended for the management of tinea capitis. Selenium sulfide shampoo may reduce the risk of spreading the infection early in the course of therapy by reducing the number of viable spores that are shed.

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Prevention

Asymptomatic carriers, being the continuous source of infection, should be detected and treated. Siblings and playmates of patients should avoid close physical contact and sharing of toys or other personal objects, such as combs and hairbrushes; organisms can spread from one person to another, and infectious agents can be transported to different classrooms within the same or in different schools. Shared facilities and objects also may promote spread of disease, both within the home and in the classroom.

Those children receiving treatment should be allowed to return to school.^{[17, 44]}

Public health measures regarding the source of infection should be a concern for controlling tinea capitis.

The source of some zoophilic species often is difficult to trace. Outbreaks of M canis can be extensive. Patients' cats and dogs must be inspected under a Wood lamp and referred for treatment. At times, animal control agencies are contacted to round up stray dogs and cats. T mentagrophytes may follow known contact with rodents, but in many cases, no source can be identified.

In a study by Williams et al, as many as 14% of asymptomatic children were found to be carriers of causative dermatophyte for tinea capitis in a Philadelphia primary school.^[45] Without therapy, 4% developed symptoms of infection, 58% remained culture-positive, and 38% became culture-negative within an average follow-up period of 2.3 months.

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Long-Term Monitoring

Household contacts of tinea capitis patients should be screened for clinically silent fungal carriage on the scalp.^[46] Asymptomatic carriers, including adults and siblings in the family of patients with tinea capitis and patient caretakers and playmates, require active treatment because they may act as a continuing source of infection.^[47]

Shampoo and oral antimycotic therapy have been advocated for eradication of the carrier state. Studies have shown that most children who received griseofulvin plus biweekly shampooing with 2.5% selenium sulfide were negative for fungi on scalp culture after 2 weeks. Shampoos containing povidone-iodine are more effective in producing negative cultures than shampoos containing econazole and selenium sulfide or Johnson's Baby Shampoo. Therapeutic shampoos are applied twice weekly for 15 minutes for 4 consecutive weeks. Both povidone-iodine and selenium shampoos require further clinical study for the control of fungal spore loads in infected children and asymptomatic carriers.

Classrooms with young children (ie, kindergarten through second grade) must be evaluated for tinea capitis infection. These children are the ones most susceptible to such infection and have a greater risk of disease transmission.

Playmates in close physical contact with patients can spread tinea capitis organisms by sharing toys or personal objects, including combs and hairbrushes. These individuals must be evaluated for the presence of infection.

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Griseofulvin (Grifulvin V (DSC), Gris-PEG (DSC))

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Clinical Context: 

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Terbinafine (Lamisil)

• Dosing, Interactions, etc.

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Itraconazole (Onmel, Sporanox, Sporanox Oral Solution)

• Dosing, Interactions, etc.

Clinical Context: 

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Fluconazole (Diflucan)

• Dosing, Interactions, etc.

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Ketoconazole (Nizoral)

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