Tinea capitis

INTRODUCTION — Tinea capitis is a fungal infection of the scalp that most often presents with pruritic, scaling areas of hair loss. Trichophyton and Microsporum species of dermatophyte fungi are the major causes of tinea capitis. The infection is often contracted from another human or an animal through direct contact.

Tinea capitis primarily occurs in children. The most common clinical findings are single or multiple scaly patches with alopecia and patches of alopecia with black dots at follicular orifices that represent broken hairs (picture 1A-F). Other presentations include widespread scaling with subtle hair loss, a boggy edematous painful plaque called a kerion (picture 2), and favus, which characteristically exhibits multiple cup-shaped, yellow crusts (scutula) (picture 3).

Oral antifungal therapy is the primary treatment for tinea capitis. Patients usually respond well to treatment.

The clinical features, diagnosis, and management of tinea capitis will be reviewed here. Other dermatophyte infections are reviewed separately. (See "Dermatophyte (tinea) infections".)

EPIDEMIOLOGY — Tinea capitis is a common disorder. Children, particularly prepubertal children, are most likely to develop tinea capitis. Some studies have identified higher prevalences in male children than in female children [1-5]; however, other studies have not corroborated this finding [6]. Occasionally, adults develop tinea capitis [7-11].

Tinea capitis occurs worldwide with prevalences that vary geographically and demographically. Studies in the United States have revealed that tinea capitis is most common in African American children [1,12]. The reason for this is unknown. Theories to explain this observation have included effects of socioeconomic factors or differences in genetic susceptibility [1].

MICROBIOLOGY — Tinea capitis is a dermatophyte infection. Dermatophytes are filamentous fungi in the genera Trichophyton, Microsporum, and Epidermophyton that infect keratinized tissue of skin, hair, or nails. Organisms in the Trichophyton and Microsporum genera generally cause tinea capitis. Tinea capitis due to Epidermophyton species is rare [13].

Dermatophytes are divided into anthropophilic (human), zoophilic (animal), and geophilic (soil) fungi. Anthropophilic and zoophilic dermatophytes are the most common causes of tinea capitis. Examples of dermatophyte species associated with tinea capitis include:

●Anthropophilic:

•Trichophyton tonsurans

•Trichophyton mentagrophytes var. interdigitale

•Trichophyton violaceum

•Trichophyton soudanense

•Trichophyton schoenleinii

•Microsporum audouinii

•Epidermophyton floccosum (rare)

•Trichophyton rubrum (rare)

●Zoophilic:

•Microsporum canis

•Trichophyton verrucosum

•Trichophyton equinum

•Microsporum nanum

•Trichophyton species of Arthroderma benhamiae [14]

●Geophilic:

•Microsporum gypseum

•Microsporum fulvum

The likelihood that a particular dermatophyte is the cause of tinea capitis varies geographically and evolves over time. In the United States and the United Kingdom, T. tonsurans has replaced M. canis as the most common causative organism [1,15]. T. tonsurans is also the predominant cause of tinea capitis in Canada, Brazil, France, and Japan [16]. M. canis remains a primary cause of tinea capitis in central and southern Europe, Russia, Australia, and China; however, shifts in the predominating cause of tinea capitis to T. violaceum or other organisms have been noted in some areas [4,6,17]. M. audouinii and T. soudanense are primary causes of tinea capitis in West Africa [2,3]. T. verrucosum is a common cause of tinea capitis in Turkey [16].

Whether nondermatophyte fungi and yeasts may also cause tinea capitis is uncertain. (See 'Culture' below.)

PATHOGENESIS — Tinea capitis is acquired through contact of the scalp with the causative dermatophyte. Acquisition of the fungus may result from direct contact with an infected individual or animal or from contact with a contaminated object (eg, comb, brush, or hat). Contact with asymptomatic carriers of causative organisms is an additional mode of transmission that may play an important role in recurrences of tinea capitis and tinea corporis [18]. (See 'Management of close contacts' below and 'Treatment failure' below.)

Once the dermatophyte comes in contact with the stratum corneum on the scalp, the establishment of infection is mediated by a variety of factors. As an example, mannan glycoproteins in dermatophyte cell walls promote adherence of dermatophytes to keratin-containing host tissue [19]. In addition, production of proteolytic enzymes, such as keratinase, by the dermatophytes enables invasion of the cytokeratin-containing tissues of the skin and hair [19]. The infection progresses from the stratum corneum of the epidermis, extending down the follicle and to the hair. Biofilms can form, which may make therapy more difficult [20].

Dermatophyte infection of the hair may present in three forms, endothrix infection, ectothrix infection, and favus. In endothrix infections, arthroconidia (fungal spores) are found within the hair shaft on direct microscopic examination. Common examples include T. tonsurans, T. violaceum, and T. soudanense infections. In ectothrix infections, arthroconidia primarily surround the outside of the hair shaft. Dermatophytes often associated with ectothrix infections include T. verrucosum, M. canis, M. audouinii, M. nanum, and M. gypseum. Favus is a unique presentation in which hyphae and air spaces are found within hair shafts. (See 'Potassium hydroxide preparation' below.)

The innate immune system likely plays a significant role in host defense against dermatophyte infection. An in vitro study evaluating the role of inflammasomes, components of the innate immune system, found evidence to suggest that the NLRP3 inflammasome plays an important role in host defense against M. canis infection [21].

The reasons for the predominance of tinea capitis in children are not well understood. Proposed theories to explain the infrequency in adults include effects related to the fungistatic properties of short- and medium-chain fatty acids in postpubertal sebum and the colonization of adults by commensal yeasts, such as Pityrosporum, that may inhibit infection with dermatophytes [22].

CLINICAL MANIFESTATIONS — Tinea capitis may present with a variety of clinical features. There are five major clinical variants of tinea capitis as well as an asymptomatic carrier state. The causative organism and the host immune response to infection influence the clinical presentation.

Clinical variants — The most common clinical manifestations of tinea capitis are the development of scaly patches with alopecia and patches of alopecia with visible black dots. Diffuse scalp scaling with subtle hair loss, kerion, and favus are additional clinical variants. Pruritus is a common associated symptom in the various presentations of tinea capitis:

●Scaly patches with alopecia – Single or multiple scaly patches with hair loss are a common presentation of ectothrix infections (eg, M. canis) (picture 1A-E). Individual patches are often a few centimeters to several centimeters in diameter. The patches enlarge centrifugally over the course of weeks to months. Erythema may be present.

●Patches of alopecia with black dots – Endothrix infections may present with manifestations often referred to as "black dot tinea capitis." Multiple black dots, which represent the distal ends of hairs that have broken at the surface of the scalp, are present at follicular orifices within areas of alopecia (picture 1F). The broken hairs are a result of weakening of the hair shaft secondary to the endothrix infection. The alopecic areas may be single or multiple and typically range from a few centimeters to several centimeters in diameter.

●Widespread scaling with subtle hair loss – Tinea capitis may exhibit diffuse scaling on the scalp without clear areas of alopecia (picture 4). This presentation may closely resemble seborrheic dermatitis and may be due to unknown host factors leading to less hair loss.

●Kerion – Kerion is a severe manifestation of tinea capitis resulting from an intense immune response to the infection. Kerion is characterized by the development of an inflammatory plaque with pustules, thick crusting, and/or drainage (picture 2). A suppurative folliculitis may be the initial presentation [23]. Tenderness or pain is often present.

Kerions appear most commonly in children ages 5 to 10 and are rare in infancy [24]. Kerion is most often caused by a zoophilic dermatophyte; however, anthropophilic fungi can also cause a kerion. Persistent kerion can lead to scarring alopecia [25].

●Favus – Favus is a unique clinical presentation of tinea capitis resulting from infection with T. schoenleinii (and rarely other dermatophytes). In favus, perifollicular erythema progresses to the characteristic development of cup-shaped, yellow crusts called scutula (picture 3) [26]. The scutula contain fungi, neutrophils, dried serum, and epidermal cells. Scutula eventually coalesce to form adherent masses above areas of severe alopecia. There may be an associated unpleasant odor. The intense inflammation can result in permanent scarring. If untreated, favus may persist indefinitely [26].

Associated findings — Patients with tinea capitis may exhibit associated clinical findings:

●Cervical lymphadenopathy – Palpable cervical lymphadenopathy is a frequent finding in patients with tinea capitis, particularly when clinical signs of inflammation are present (picture 5).

●Dermatophytid reactions – Autoeczematization reactions (id reactions) are secondary dermatitic eruptions that occur in association with a localized inflammatory skin disorder. The term dermatophytid reaction is used to refer to autoeczematization reactions that occur in association with dermatophyte infections. The pathogenesis may involve an immune reaction to fungal antigens, such as a delayed-type hypersensitivity response.

Dermatophytid reactions often follow the onset of antifungal therapy, but may also precede treatment [27]. Patients develop a widespread pruritic eczematous eruption characterized by erythematous, scaly papules (picture 6). Involvement of the head, neck, trunk, or extremities is common. Dermatophytid reactions are managed with treatment of the underlying fungal infection as well as emollients, oral antihistamines, or topical corticosteroids as needed [27]. Oral corticosteroids are reserved for severe cases. (See "Dermatophyte (tinea) infections", section on 'Id reactions'.)

●Other – Infrequently, erythema nodosum occurs in association with kerion [28-30]. (See "Erythema nodosum".)

HISTOPATHOLOGY — Histopathologic features of tinea capitis include:

●Fungal elements (arthroconidia or hyphae) within or surrounding hair shafts

●Perifollicular mononuclear infiltrate in the dermis

●Multinucleated giant cells in the dermis (in cases where the hair follicle is disrupted)

The fungi can be highlighted with periodic acid-Schiff (PAS) or Grocott's methenamine silver (also called Gomori's methenamine silver or GMS) stains.

Biopsies of kerions will exhibit an inflammatory reaction with a neutrophilic, granulomatous, or mixed dermal infiltrate [23]. Fungi may be difficult to identify due to the intensity of the inflammatory reaction [31].

DIAGNOSIS — Tinea capitis should be strongly considered in children presenting with scale and hair loss on the scalp, particularly if cervical lymphadenopathy is present. Because the diagnosis is infrequent in adults, a higher index of suspicion is often necessary to recognize tinea capitis in the adult population. Immunocompromised states or immunosuppression may predispose adults to develop tinea capitis.

Tinea capitis often can be diagnosed based upon the physical examination if there are alopecic patches with scaling or black dots consistent with tinea capitis. A potassium hydroxide (KOH) preparation or fungal culture should be performed to confirm tinea capitis if the diagnosis is in question. These tests are often particularly useful for patients with widespread scalp scaling and subtle hair loss because of the close resemblance to seborrheic dermatitis. Biopsy of the scalp is not typically necessary. (See 'Potassium hydroxide preparation' below and 'Culture' below.)

Polymerase chain reaction (PCR) testing has emerged as an alternative diagnostic test but is not routinely utilized for tinea capitis. (See 'Other tests' below.)

Physical examination — The physical examination should include a careful examination of the hair and scalp to identify signs consistent with tinea capitis or suggestive of another disorder. Visualization of the characteristic "black dots" that can occur in endothrix tinea capitis or the classic scutula of favus are helpful signs that strongly suggest a diagnosis of tinea capitis. A localized inflamed, tender, boggy plaque on the scalp is suspicious for kerion. (See "Evaluation and diagnosis of hair loss", section on 'Physical examination'.)

Examination of the rest of the skin surface is also prudent to identify skin or nail findings suggestive of another condition. For example, psoriasis or seborrheic dermatitis often present with scalp disease associated with characteristic eruptions in other body areas. Cervical lymph nodes should be palpated because cervical lymphadenopathy is a common, though not ubiquitous finding in tinea capitis. (See 'Differential diagnosis' below.)

Examination of the affected area with a Wood's light can help identify tinea capitis in patients with some ectothrix infections and favus. Ectothrix infections secondary to M. canis often exhibit green-yellow fluorescence under Wood's light illumination [32]. Wood's light illumination of favus secondary to T. schoenleinii reveals faint blue fluorescence [26].

Dermoscopy — Dermoscopy of the hair and scalp (also known as trichoscopy) may be a useful adjunctive measure in the diagnosis of tinea capitis. Common dermoscopic findings in tinea capitis include broken hairs, dystrophic hairs, corkscrew hairs, comma hairs, and black dots (picture 7) [33-36]. The findings of a study of five children with tinea capitis suggest high magnification (x150) dermoscopy may identify additional features in tinea capitis, such as horizontal white bands in hair shafts (barcode-like hairs) and translucent, easily deformable hairs [37]. (See "Overview of dermoscopy".)

A review of 24 children with tinea capitis suggests that dermoscopic findings may vary based upon the type of infection [38]. In addition to broken hairs and black dots, children with endothrix infections (eg, T. tonsurans, T. soudanense) exhibited comma hairs and corkscrew hairs, whereas children with ectothrix infections (eg, M. canis, M. audouinii) exhibited barcode-like hairs and zigzag hairs. Additional study is necessary to confirm these findings.

Potassium hydroxide preparation — A potassium hydroxide (KOH) preparation is a rapid method for confirming the presence of a dermatophyte infection. Several hairs within the involved areas are plucked. The proximal ends of the hairs are then examined microscopically after application of potassium hydroxide to the slide. Arthroconidia (fungal spores) are found within the hair shaft in endothrix infections and predominantly outside of the hair shaft in ectothrix infections. KOH preparations of favus demonstrate hyphae and air spaces within hair shafts. Occasionally, KOH preparations fail to identify dermatophytes in patients with tinea capitis. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

Culture — Fungal cultures are performed to confirm tinea capitis when the diagnosis is uncertain. However, because culture results may not be available for several weeks, if there is high suspicion for tinea capitis based upon the physical examination, treatment is usually begun empirically. False-negative results are common when fungal cultures are taken from kerion, likely secondary to the intense inflammatory response. Cultures taken during antifungal treatment of tinea capitis also are often negative, making it difficult to confirm the accuracy of the diagnosis.

To obtain a sample for culture, a sterile toothbrush is rubbed over the affected area, or the site is swabbed with a moistened cotton swab [39-42]. Sending some hairs with the scraping may increase the yield. Infected hairs often break and thus come out most easily. Culture can also be performed from a tissue biopsy; however, this is rarely necessary.

Occasionally, nondermatophyte fungi and yeasts, including Alternaria, Aspergillus, Fusarium, Scopulariopsis, or Candida species, are cultured from patients with clinical findings suggestive of tinea capitis [43]. In immunocompetent patients, it can be difficult to determine if these common environmental contaminants are truly acting as pathogens. In immunocompromised patients, molds can be important pathogens. If the diagnosis of tinea capitis is unclear (eg, if other causes of scalp scaling, such as sebopsoriasis or eczematous dermatitis, are suspected), then performing a repeat culture to prove the presence of a nondermatophyte fungus can be helpful. Absence of the same organism on repeat culture suggests a contaminant.

Other tests — PCR techniques, molecular tests that can be utilized to detect fungal DNA, have emerged as an additional option for confirming the presence of dermatophyte infections [44]. An advantage of PCR is the potential for more rapid detection and speciation of causative fungi compared with fungal culture. Factors such as cost and availability are limiting factors for PCR testing [41]. (See "Onychomycosis: Epidemiology, clinical features, and diagnosis", section on 'Polymerase chain reaction'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of tinea capitis primarily consists of other scalp disorders that may present with scale, pustules, or hair loss. The differential diagnosis varies according to the clinical presentation. A careful physical examination often reveals features that distinguish other diseases from tinea capitis. Identification of dermatophytes on a potassium hydroxide (KOH) preparation or culture also distinguishes tinea capitis from other diseases.

The differential diagnoses for tinea capitis based upon the clinical findings are reviewed below:

●Scaly patches with alopecia:

•Psoriasis – Well-demarcated, erythematous plaques with coarse scale are characteristic findings of psoriasis (picture 8). Often patients have skin involvement in other areas, such as the elbows, knees, or intertriginous areas. Nail abnormalities, such as pitting, discoloration, onycholysis, and subungual hyperkeratosis may be present. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

●Patches of alopecia with black dots:

•Alopecia areata – Alopecia areata is an autoimmune form of hair loss that may occur in children and adults. Alopecia areata classically presents with discrete, often circular patches of alopecia (picture 9A-B). Scale is absent. Exclamation point hairs (short hairs up to a few millimeters in length with tapered proximal ends) are a common feature of alopecia areata that may be confused with broken hairs of tinea capitis (picture 10). (See "Alopecia areata: Clinical manifestations and diagnosis", section on 'Clinical features'.)

●Widespread scaling with subtle hair loss:

•Seborrheic dermatitis – Seborrheic dermatitis of the scalp presents with diffuse scaling often associated with erythema and pruritus (picture 11A-B). Alopecia is typically absent. Patients may have involvement in other areas, such as the eyebrows, nasolabial folds, and intertriginous areas. Seborrheic dermatitis usually occurs in infants, adolescents, and adults. Prepubertal children usually do not develop seborrheic dermatitis. (See "Seborrheic dermatitis in adolescents and adults" and "Cradle cap and seborrheic dermatitis in infants".)

●Kerion:

•Bacterial folliculitis – The suppurative folliculitis that may be an early manifestation of kerion should be distinguished from bacterial folliculitis (picture 12). A Gram stain or culture will reveal the causative bacteria. (See "Infectious folliculitis", section on 'Bacterial folliculitis'.)

•Folliculitis decalvans – Folliculitis decalvans is an uncommon form of cicatricial (scarring) alopecia that presents with one or more patches of alopecia with associated pustules. Follicular orifices typically are absent within the areas of alopecia, consistent with scarring. Tufted hairs (multiple hairs emerging from a single follicular orifice) are a common finding (picture 13). Unlike tinea capitis, folliculitis decalvans almost exclusively occurs in adults. Scalp biopsy confirms the diagnosis. (See "Folliculitis decalvans".)

•Dissecting cellulitis – Dissecting cellulitis is an uncommon form of cicatricial alopecia characterized by the development of follicular papules, pustules, fluctuant nodules, and abscesses on the scalp (picture 14). Young Black men are the most common population affected. Biopsy confirms the diagnosis. (See "Dissecting cellulitis of the scalp".)

Recognition of the characteristic cup-shaped scutula strongly suggests a diagnosis of favus. In less-classic cases, disorders such as psoriasis (picture 8), discoid lupus (picture 15), pityriasis amiantacea (picture 16), and the cradle-cap presentation of seborrheic dermatitis (picture 17) may enter the differential diagnosis.

Other disorders that may enter the differential diagnosis of tinea capitis are trichotillomania (trichotillosis) and pediculosis capitis. Trichotillomania is a condition in which the patient manipulates or pulls the hair, often resulting in unusual configurations of hair loss (picture 18). Scale and inflammation is absent. The pruritus associated with pediculosis capitis may lead to suspicion for tinea capitis. However, the visualization of lice or nits on physical examination confirms pediculosis capitis (picture 19). In contrast to tinea capitis, scale is minimal or absent. (See "Skin picking (excoriation) disorder and related disorders", section on 'Trichotillomania'.)

TREATMENT — Systemic antifungal treatment is the standard of care for children with tinea capitis. Special considerations for the treatment of kerion and infants and adults with tinea capitis are reviewed separately. (See 'Treatment of special populations' below.)

Overview of treatment — Treatment of tinea capitis begins once the diagnosis is made based upon the clinical evaluation and prior to the availability of culture results. If the diagnosis is likely tinea capitis, waiting until culture results have returned is not recommended because delaying treatment may increase risk for disease progression, permanent hair loss, and disease transmission.

Treatment should involve an oral antifungal agent that has demonstrated efficacy for tinea capitis. Topical antifungal therapy is unlikely to be effective because topical treatments have inadequate penetration of hair follicles and may miss sites of subclinical infection.

The systemic antifungal therapies for tinea capitis include griseofulvin, terbinafine, fluconazole, and itraconazole. Griseofulvin has a long history of use for childhood tinea capitis and is a well-accepted first-line therapy. Terbinafine has emerged as an alternative first-line agent that may offer the advantage of shorter treatment courses. Fluconazole and itraconazole are effective but less frequently used than griseofulvin and terbinafine. Only griseofulvin and terbinafine have formulations that are approved by the US Food and Drug Administration (FDA) for the treatment of tinea capitis. (See 'First-line therapy' below and 'Alternative therapies' below.)

In the past, ionizing radiation was used for the treatment of tinea capitis. Treatment of tinea capitis with ionizing radiation is no longer recommended due to the potential for long-term side effects [45].

Adjunctive interventions for tinea capitis include use of a shampoo with antifungal properties to reduce risk of spread of infection to other individuals. Many clinicians, including ourselves, also encourage household members to use an antifungal shampoo to reduce risk for reinfection from continued contact with asymptomatic carriers. (See 'Adjunctive interventions' below and 'Management of close contacts' below.)

Children treated for tinea capitis require clinical follow-up to determine whether oral antifungal treatment can be discontinued or whether additional treatment is needed. (See 'Prognosis and follow-up' below.)

First-line therapy — Oral griseofulvin and oral terbinafine are the most commonly used therapies for tinea capitis in children. Griseofulvin is a first-line therapy based upon the drug's efficacy in randomized trials and long history of use for this indication [46]. Terbinafine has emerged as an alternative first-line agent.  

Treatment selection — Most patients with tinea capitis have Trichophyton or Microsporum infections. Randomized trial data are helpful for guiding treatment selection in these patients:

●Trichophyton infections – Both griseofulvin and terbinafine are accepted first-line treatments for known or suspected Trichophyton tinea capitis. The use of terbinafine as an alternative first-line agent is a result of data demonstrating terbinafine is at least as effective as griseofulvin for Trichophyton infections, with shorter durations of treatment. In a meta-analysis of randomized trials, four weeks of terbinafine was as effective for achieving complete (clinical and mycologic) cure for Trichophyton infections as eight weeks of griseofulvin (risk ratio 1.06, 95% CI 0.98-1.15) [46].

There are data that suggest greater efficacy of terbinafine compared with griseofulvin for some Trichophyton infections when given for similar duration. Pooled data from two randomized trials that compared a six-week course of terbinafine granules (5 to 8 mg/kg per day) with a six-week course of griseofulvin microsize (10 to 20 mg/kg per day) found similar efficacy for tinea capitis overall but greater efficacy of terbinafine for the subgroup of children with T. tonsurans infections (complete cure rate 52.1 versus 35.4 percent, risk ratio 1.47, 95% CI 1.22-1.77) [47]. There was no difference in effect for T. violaceum infections.

●Microsporum infections – Griseofulvin appears to be more effective for Microsporum infections than terbinafine and is preferred over terbinafine for known or suspected Microsporum infections. A systematic review and meta-analysis of randomized trials found a lower cure rate for Microsporum infections for a six-week course of terbinafine than for a 6- to 12-week course of griseofulvin (34.7 versus 50.9 percent, risk ratio 0.68, 95% CI 0.53-0.86) [46].

Griseofulvin is first-line treatment for children in whom the cause of tinea capitis is unclear.

Griseofulvin

Administration — In the United States, griseofulvin is available in a microsize formulation as tablets or a suspension. In addition, an ultramicrosize formulation is available as tablets.

Typical treatment regimens for children are:

●Microsize formulation – 20 to 25 mg/kg per day for 6 to 12 weeks [48]. The typical initial dose is 20 mg/kg per day for six to eight weeks. If there is partial response, the dose can be increased to 25 mg/kg per day and/or the length of therapy extended up to 12 weeks. The maximum daily dose is 1000 mg per day.

●Ultramicrosize formulation – 10 to 15 mg/kg per day for 6 to 12 weeks [48]. The typical initial dose is 10 mg/kg per day for six to eight weeks. If there is partial response, the dose can be increased to 15 mg/kg per day and/or the length of therapy extended up to 12 weeks. The maximum daily dose is 750 mg per day.

Griseofulvin is absorbed more effectively when given with fatty food (eg, peanut butter, ice cream). Therapeutic failures are often due to lack of absorption.

Adverse effects and monitoring — Griseofulvin typically is well tolerated. Gastrointestinal distress, headache, and cutaneous eruptions are potential side effects. Uncommon serious side effects include hepatotoxicity, granulocytopenia, leukopenia, and severe cutaneous reactions.

Laboratory evaluation prior to griseofulvin treatment is not necessary. However, if therapy is continued beyond eight weeks or repeated courses of griseofulvin are given, liver function tests and a complete blood count should be obtained to evaluate for hepatic or hematologic toxicity.

Terbinafine

Administration — Terbinafine has very limited data for use in children under the age of four years.

Dosing for children is based upon weight. Typical pediatric dose regimens for terbinafine tablets are:

●10 to 20 kg – 62.5 mg daily for four to six weeks

●20 to 40 kg – 125 mg daily for four to six weeks

●Above 40 kg – 250 mg daily for four to six weeks

Terbinafine tablets can be taken without regard to meals.

An alternative formulation of terbinafine, terbinafine granules, is no longer available in the United States.

Adverse effects and monitoring — Terbinafine therapy is usually well tolerated. Headache, gastrointestinal distress, taste disturbances, cutaneous eruptions, and liver enzyme abnormalities are potential side effects. Uncommon severe side effects include drug hypersensitivity syndrome, drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome, serum sickness-like reaction, fulminant hepatic failure, drug-induced lupus, pancytopenia, and pancreatitis.

Liver function tests should be obtained prior to the start of terbinafine therapy. The tests should be repeated with the addition of a complete blood count if treatment extends beyond six weeks. Some clinicians do not obtain baseline liver function tests prior to treatment, given the rarity of preexisting liver disease in children and the typical short course of treatment with terbinafine.

Alternative therapies — Fluconazole and itraconazole are effective, less frequently used treatments for tinea capitis. Compared with griseofulvin and terbinafine, efficacy data for fluconazole and itraconazole are more limited.

Ketoconazole should not be used for the treatment of tinea capitis. The drug is associated with risk for severe liver injury and adrenal insufficiency.

Fluconazole — Oral fluconazole can be effective for tinea capitis [49,50]. Randomized trials performed in populations where Trichophyton infections predominated have demonstrated similar efficacy between regimens of fluconazole and griseofulvin [49,51,52]. In addition, a randomized trial that compared the efficacy of two to three weeks of treatment with fluconazole, itraconazole, or terbinafine and six weeks of treatment with griseofulvin for tinea capitis caused by Trichophyton species did not find significant differences in efficacy among these therapies.

Children can be treated with 6 mg/kg per day of fluconazole for three to six weeks [53]. The maximum daily dose is 400 mg. Data from a comparative study suggest that doses of 4 mg/kg may require longer durations of treatment than doses of 6 mg/kg [54]. Limited data suggest that once-weekly dosing of fluconazole also may be an effective treatment [50,55]. Children can be treated with a pulse dose of 6 mg/kg once weekly for 6 to 12 weeks. Some patients find the convenience of once-weekly dosing preferable despite the longer duration of treatment.

Fluconazole can lead to gastrointestinal distress, headache, cutaneous eruptions, and liver function test abnormalities. Uncommon serious side effects include hepatoxicity, severe drug hypersensitivity reactions (including Stevens-Johnson syndrome), anaphylaxis, Torsades de pointes, and prolongation of the QT interval.

Itraconazole — Relatively few randomized trials have evaluated itraconazole for tinea capitis [51,56,57]. These trials have reported similar efficacy of two-week courses of itraconazole and terbinafine in children with tinea capitis caused by Trichophyton species [57] as well as similar efficacy between six-week courses of itraconazole and griseofulvin in a trial population in which most patients had M. canis infections [56]. In addition, a randomized trial that compared the efficacy of two-week courses of itraconazole, fluconazole, or terbinafine (with an additional week of treatment as needed) and six-week courses of griseofulvin in children with tinea capitis caused by Trichophyton species did not find statistically significant differences in efficacy between the treatment groups [51].

The optimum regimen for itraconazole for tinea capitis is unclear. When used for tinea capitis in children, itraconazole is commonly prescribed at a dose of 3 to 5 mg/kg daily for four to six weeks. The maximum daily dose is 400 mg.

Pulse therapy also may be effective. Pulsed itraconazole is given at a dose of 5 mg/kg per day for one week each month for two to three months [48,58]. The suggested dose for pulse therapy with the oral solution of itraconazole is 3 mg/kg per day [48].

Potential side effects of itraconazole include gastrointestinal distress, skin eruptions, headache, sleepiness, dizziness, and liver function test abnormalities. Liver function tests are indicated prior to treatment in patients with pre-existing hepatic dysfunction. These tests also should be obtained in patients treated for longer than one month.

Adjunctive interventions — The management of tinea capitis should include measures to reduce spread of the infection and the likelihood of recurrence. We suggest that patients with tinea capitis use a shampoo with antifungal properties (eg, selenium sulfide 1 or 2.5%, ciclopirox 1%, or ketoconazole 2% shampoo) at least twice weekly to decrease shedding of fungal spores [59,60]. Use of antifungal shampoo by other household members may also decrease the risk for reinfection (see 'Management of close contacts' below). It is also recommended that combs and hair trimming equipment be cleaned mechanically and disinfected (eg, with household bleach) [61].

TREATMENT OF SPECIAL POPULATIONS

Kerion — Oral antifungal therapy is the mainstay of treatment for kerion. Treatment regimens are similar to treatment for other forms of tinea capitis. (See 'Treatment' above.)

Systemic glucocorticoids (eg, 0.5 to 1 mg/kg of prednisone for one week) are occasionally used in conjunction with antifungal therapy for patients with severe inflammation. However, it is unclear if the addition of a systemic glucocorticoid accelerates improvement or improves outcome [62,63].

Infants — Tinea capitis is uncommon in children under the age of one (picture 1D). Infants have been successfully treated with fluconazole, griseofulvin, and terbinafine [64-66]. We typically treat with fluconazole, given the extensive experience with oral fluconazole therapy in infants for other indications.

Effective treatment with topical agents has been reported in infants [64,66]. However, data are insufficient to recommend routine use of topical therapy [66].

Adults — The same medications are used for the treatment of children and adults with tinea capitis. The optimal treatment regimens for adults are unclear. Typical doses for adults are terbinafine 250 mg per day, itraconazole 5 mg/kg per day (maximum 400 mg per day), fluconazole 6 mg/kg per day, and griseofulvin ultramicrosize 10 to 15 mg/kg per day (maximum 750 mg per day) [67]. Treatment durations are similar to those used for children.

MANAGEMENT OF CLOSE CONTACTS — Household members of an individual diagnosed with tinea capitis should be physically examined for signs of tinea capitis and should be treated simultaneously if tinea capitis is detected.

Asymptomatic carriers of dermatophytes may serve as reservoirs for recurrent infection. Because of this possibility, we suggest use of an antifungal shampoo by all household members for two to four weeks [68]. Household members should begin to use the shampoo when the infected individual begins treatment for tinea capitis.

Children with tinea capitis should avoid sharing hair care tools and headwear (eg, helmets or hats) with other individuals. Pillowcases should not be shared. In addition, participation in sports with head-to-head contact should be avoided [69]. Bedding and towels used by the infected individual should be washed. Furniture that is frequently in direct contact with the affected individual or pet should be washed, if possible.

Cats or dogs (especially kittens and puppies) or other animals (such as cows, guinea pigs, and other animals) may be reservoirs for infection. The animals can have clinical signs of dermatophyte infection with scaling and hair loss, but can also be asymptomatic carriers. If there is an outbreak of tinea in a household, the pet (especially if new) should be evaluated by a veterinarian. The animal should also be evaluated if the patient or other household members experience recurrent dermatophyte infections [70].

PROGNOSIS AND FOLLOW-UP — The prognosis of tinea capitis is excellent, with complete clearance occurring in most patients after a course of treatment. Complete hair regrowth occurs in most children with hair loss. Patients with prolonged or severe infections (eg, kerion, favus) have the greatest risk for permanent alopecia. Still, the majority of lost hair often regrows.

There are rare reports of fungemia from dermatophyte infections in immunosuppressed patients. There is one report of culture-proven fungemia in an immunocompetent patient after surgical excision of a kerion due T. mentagrophytes [71].

Clinical follow-up to assess for clinical clearance should be performed at the end of therapy to assess for clinical cure. In patients who have experienced recurrent tinea capitis, we typically perform a fungal culture to confirm clearance after treatment. A fungal culture should also be performed in patients who appear to fail treatment. (See 'Treatment failure' below.)

Continuation of twice-weekly antifungal shampoo may help decrease the rate of reinfection.

TREATMENT FAILURE — Signs of ongoing infection include persistent erythema, scale, or drainage. Hair loss may remain after successful treatment of tinea capitis, particularly in patients with kerion or favus. A fungal culture should be performed when patients appear to fail treatment. (See 'Culture' above.)

If there is a poor response to treatment, adherence to the treatment regimen should be assessed. This includes review of the actual frequency of treatment and dose ingested, as well the method of drug administration. Griseofulvin is much more effectively absorbed when given with fatty foods, and terbinafine absorption is reduced when crushed or sprinkled into apple sauce or fruits. If the child has been unable to take the medication as prescribed, methods to improve adherence (eg, education or change in medication formulation) should be made to increase the likelihood of adequate treatment.

For patients initially treated with 20 mg/kg of griseofulvin per day and with good adherence to therapy, an inadequate response can be managed with an increase in dose to 25 mg/kg per day and extension of the treatment course to a total of 12 weeks. Alternatively, the patient can be switched to terbinafine. Increasing the dose and duration of griseofulvin is our preferred intervention for patients with M. canis infection. Occasionally, treatment for longer than 12 weeks is needed. If a patient has a poor response to initial treatment with terbinafine, then griseofulvin should be used, especially if the infection is with Microsporum species.

In addition to adherence to therapy, the possibility of reinfection from contact with an infected individual or pet, contaminated fomites, or an asymptomatic carrier of the dermatophyte should be considered when patients fail treatment. (See 'Management of close contacts' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dermatophyte infections".)

SUMMARY AND RECOMMENDATIONS

●Overview – Tinea capitis is a common fungal infection of the scalp and hair that most commonly occurs in children. Dermatophytes in the genera Trichophyton and Microsporum are responsible for almost all cases of tinea capitis. (See 'Epidemiology' above and 'Microbiology' above.)

●Forms of infection – Dermatophyte infection of the hair may present in three forms: endothrix infection, ectothrix infection, or favus. In endothrix infection, arthroconidia (fungal spores) are present within the hair shaft. Arthroconidia in ectothrix infections primarily surround the hair shaft. Favus is characterized by hyphae and air spaces within the hair shaft. (See 'Pathogenesis' above.)

●Clinical manifestations – Tinea capitis has multiple clinical presentations. The most common manifestations are scaly patches with alopecia and patches of alopecia with black dots at follicular orifices that represent broken hairs (picture 1A-F). Other manifestations include widespread scaling on the scalp with subtle hair loss (picture 4), kerion (an inflammatory, boggy plaque (picture 2)), and favus (picture 3). Scutula (cup-shaped, yellow crusts) are a characteristic finding in favus. (See 'Clinical manifestations' above.)

Cervical lymphadenopathy is common in patients with tinea capitis. Secondary dermatitic eruptions (dermatophytid reactions) may also occur (picture 6). (See 'Associated findings' above.)

●Diagnosis – The diagnosis of tinea capitis may be made based upon clinical findings. A potassium hydroxide (KOH) preparation or fungal culture should be performed to confirm tinea capitis if the diagnosis is in question. Examination with a Wood's lamp and dermoscopy may be helpful for diagnosis. (See 'Diagnosis' above.)

●Treatment:

•Antifungal therapy – Oral antifungal therapy is the mainstay of antifungal therapy. Therapeutic options include griseofulvin, terbinafine, fluconazole, and itraconazole:

-Microsporum tinea capitis – For patients with tinea capitis that is known or considered very likely to be secondary to Microsporum species, we recommend treatment with oral griseofulvin (Grade 1A). (See 'First-line therapy' above.)

-Trichophyton tinea capitis – For patients with tinea capitis that is known or very likely to be secondary to Trichophyton species, we suggest treatment with oral terbinafine based upon data indicating at least equivalent efficacy compared with griseofulvin with a shorter duration of treatment (Grade 2A). (See 'First-line therapy' above.)

•Adjunctive measures and management of close contacts – Adjunctive measures for tinea capitis that may be of benefit include use of antifungal shampoos by the patient and household members. Use by the patient may reduce spread of the infection to others. Use by household members may reduce risk for reinfection secondary to continued contact with asymptomatic carriers. (See 'Adjunctive interventions' above and 'Management of close contacts' above.)

●Follow-up and recognition of treatment failure – Clinical follow-up is necessary for patients treated for tinea capitis to ensure adequate treatment. Signs of treatment failure include persistent erythema, scale, or drainage. Common causes of treatment failure include inconsistent or improper treatment administration or reinfection. Patients with recurrent tinea capitis may benefit from a fungal culture after treatment to confirm clearance of the infection. (See 'Prognosis and follow-up' above and 'Treatment failure' above.)