- Tinea capitis
- Tinea capitis causes
- Tinea capitis classification
- Tinea capitis symptoms
- Tinea capitis diagnosis
- Tinea capitis treatment
- Tinea capitis treatment guidelines
- Tinea capitis prognosis
Tinea capitis or scalp ringworm, is a very common fungal infection of the scalp hair follicles and the surrounding skin with a dermatophyte fungus, usually species in the genera Microsporum and Trichophyton 1). Tinea capitis is not cause by a worm, despite its name. Tinea capitis is called “ringworm” as it can cause a ring-shaped, scaly, red rash. Tinea capitis rash forms a scaly, round patch that sometimes clears or improves in the middle, thus looking like a ring. Fungi are microscopic organisms that can live on the hair, nails, and outer skin layer. Tinea capitis occurs most commonly in children; however, it can also occur in adults. In the United States, tinea capitis most commonly affects children of African heritage between three and nine years of age 2). Ringworm can also occur on other parts of your body, but scalp ringworm is commonly seen in children. It is contagious and is acquired by contact with infected people, animals, or objects (such as towels, combs, and pillows). Scalp ringworm should be treated (by a prescription medicine your doctor can prescribe) because it is contagious and because, if left untreated, the affected area can develop hair loss and sometimes another, more serious, infection called a kerion.
The appearance of tinea captitis can vary depends somewhat on the type of tinea capitis and can resemble other skin conditions such as seborrheic dermatitis, atopic dermatitis, nonfungal alopecia areata, traction alopecia and trichotillomania, dandruff, discoid lupus erythematosus, lichen planus, eczema or psoriasis of the scalp 3), 4), 5), 6).
There are three types of tinea capitis: gray patch, black dot, and favus. Black dot, caused by Trichophyton tonsurans, is most common in the United States (Figure 2) 7). Early tinea captitis disease can be limited to itching and scaling, but the more classic tinea captitis presentation involves one or more scaly patches of alopecia with hairs broken at the skin line (black dots) and crusting 8). Tinea capitis may progress to kerion, which is characterized by boggy tender plaques and pustules. The child with tinea capitis will generally have neck and suboccipital (back of the head) enlarged lymph gland (lymphadenopathy), and your doctor may need to consider alternate diagnosis if enlarged lymph node (lymphadenopathy) is absent 9). However, lymphadenopathy can also occur in nonfungal scalp disease, and the absence of lymphadenopathy in an otherwise typical presentation should not delay aggressive treatment for tinea capitis 10).
If tinea capitis infection is not treated it could cause permanent scarring and hair loss. The inflammation of the skin caused by a fungal infection can also lead on to a ‘secondary’ bacterial skin infection.
Tinea capitis is usually treated oral antifungal medicines, including griseofulvin, terbinafine and itraconazole, because topical antifungal agents do not penetrate the hair shaft 11). At the same time as using oral medicines, treatment with 1% or 2.5% selenium sulfide (Selsun) shampoo or 2% ketoconazole shampoo should be used for the first two weeks because it may reduce transmission 12), 13). However, these medications are not always successful, and it may be necessary to try another agent. Intermittent treatment may also be prescribed such as once-weekly dosages.
For many years, the first-line treatment for tinea capitis has been griseofulvin because it is probably the most effective agent for infection with Microsporum canis and has a long track record of safety and effectiveness. However, recent randomized clinical trials have confirmed that newer agents, such as oral terbinafine or oral fluconazole (Diflucan) 4 to 6 weeks, have equal effectiveness and safety and shorter treatment courses 14), 15), 16), 17), 18), 19), 20). Terbinafine may be superior to griseofulvin for Trichophyton species, whereas griseofulvin may be superior to terbinafine for the less common Microsporum species 21), 22). Culture results are usually not available for two to six weeks, but 95% of tinea capitis cases in the United States are caused by Trichophyton, making terbinafine a reasonable first choice 23). However, kerion should be treated with griseofulvin unless Trichophyton has been documented as the pathogen 24), 25). Failure to treat kerion promptly can lead to scarring and permanent hair loss 26).
The child with tinea capitis should return for clinical assessment at the completion of therapy or sooner if indicated, but follow-up cultures are usually unnecessary if there is clinical improvement 27). Once treatment has started, the child may return to school, but for 14 days should not share combs, brushes, helmets, hats, or pillowcases, or participate in sports that involve head-to-head contact, such as wrestling 28). Household members should be clinically evaluated but not necessarily tested for tinea capitis 29). Many experts recommend treating all asymptomatic close contacts with a sporicidal shampoo, such as 2.5% selenium sulfide or 2% ketoconazole, for two to four weeks 30). If children do not improve, parents should be asked about adherence to the treatment regimen. The scalp should also be cultured to identify the organism and immunocompromise should be considered. A second treatment course with the same or a different agent is reasonable if the diagnosis is confirmed 31).
Figure 1. Tinea capitis scalp
Footnote: Tinea capitis clinical forms: alopecic microsporosis (A1 and A2); alopecic trichophytosis (B1 and B2); and kerion Celsi (C1 and C2) — arrow indicating reactional lymph node enlargement, typical of this presentation. Fungal culture of the main isolated agents: Microsporum canis macroculture showing white, cottony colonies with a bright-yellow reverse (D1) and microculture with hyaline septate hyphae and spindle-shaped macroconidia with more than 6 septa inside them (D2); Trichophyton tonsurans macroculture with powdery, brownish and cerebriform colonies (E1) and microculture with hyaline septate hyphae and interspersed microconidia (E2)[Source 32) ]
Is tinea capitis contagious?
Yes, tinea capitis is contagious. The infection is spread through close contact with an infected person, or by sharing combs, hairbrushes, hats, clothing, towels, beds and other furniture with someone who is infected. It’s also possible to catch ringworm from infected animals such as dogs, cats, horses or farm animals.The fungus can live for long periods of time in the environment and therefore infection can occur many months later.
Avoid sharing combs, hairbrushes, hats, towels, pillowcases, or helmets with other people. Fungus can live in combs, hairbrushes, and hair accessories, so clean them with simple bleach or purchase new ones. Do not visit the hairdressers or barbers until the infection is clear.Wash all bedding, towels and hats at 140 °F (60°C).
Who’s at risk of tinea capitis?
Anyone can get tinea capitis or scalp ringworm, though it is most commonly seen in children under the age of 10. In the United States, African American children are more likely to have tinea capitis or scalp ringworm than others. Boys are more commonly affected than girls.
Can tinea capitis be cured?
Yes. It can be cured if treated adequately as it is an infection. However, in order to prevent re-infection, other family members and close contacts may need to be checked to make sure they are not carrying the infection.
Tinea capitis causes
Tinea capitis is caused by an infection with a type of fungus called a dermatophyte. Dermatophytes are found in humans, animals and in the environment. Hair can be infected with Trichophyton (abbreviated as “T”.) and Microsporum (“M”.) fungi.
Microsporum canis is the usual dermatophyte fungus to cause tinea capitis. This fungus is zoophilic (having an attraction to or preference for animals) and grows naturally on an animal rather than a human. Microsporum canis tinea capitis is due to contact with an infected kitten or rarely an older cat or dog.
Other zoophilic fungi sometimes found to cause tinea capitis are:
- Trichophyton verrucosum (originating from cattle)
- Trichophyton mentagrophytes var. equinum (originating from horses)
- Microsporum nanum (originating from pigs)
- Microsporum distortum (a variant of Microsporum canis found in cats).
In the United States, Trichophyton tonsurans has also become a common cause of tinea capitis; this is passed on from one person to another as it naturally infects humans (i.e. it is anthropophilic). It frequently causes no symptoms and is commonly found in adult carriers.
Other anthropophilic (passed on from one person to another) fungi sometimes found to cause tinea capitis are:
- Trichophyton violaceum especially in African patients
- Microsporum audouinii
- Microsporum ferrugineum
- Trichophyton schoenleinii
- Trichophyton rubrum
- Trichophyton megninii
- Trichophyton soudanense
- Trichophyton yaoundei.
Dermatophyte fungi sometimes originate in the soil (geophilic organisms). These rarely cause tinea capitis:
- Nannizzia gypsea
- Microsporum fulvum.
Tinea capitis is most prevalent between three and seven years of age. It is slightly more common in boys than girls. Infection by Trichophyton tonsurans may occur in adults.
Anthropophilic infections such as Trichophyton tonsurans are more common in crowded living conditions. The fungus can contaminate hairbrushes, clothing, towels and the backs of seats. The spores are long-lived and can infect another individual months’ later.
Zoophilic infections are due to direct contact with an infected animal and are not generally passed from one person to another.
Geophilic infections usually arise when working in infected soil but are sometimes transferred from an infected animal.
How do I prevent further infection and stop spread of infection?
Inform your school teacher, parents of classmates and other playmates so children may be examined and treated if necessary. If more than two children in a school or nursery class are infected, the rest of the class may need to be tested (after parental consent). Children should be allowed to attend school or nursery once treatment with an oral antifungal medication and a medicated shampoo has been started.
In order to prevent further infection, other family members and pets should be examined by a doctor or vet respectively and treated with oral antifungal medication if infection is present. Sometimes it is best for the whole family to be treated with a medicated antifungal shampoo twice weekly for four weeks, whether or not fungal infection is proven.
Tinea capitis classification
Tinea capitis is classified according to how the fungus invades the hair shaft 33).
Small-spored, ectothrix hair invasion is due to infection with M. canis, M. audouinii, M. distortum, M. ferrugineum, N. gypseum, M. nanum, and T. verrucosum, typically produces characteristic fine scaling with patchy circular alopecia, dull grey in color due to arthrospores coating the affected hairs. The fungal branches (hyphae) and spores (arthroconidia) cover the outside of the hair. Inflammation may be minimal with anthropophilic fungi (e.g. M. audouinii, M. ferrugineum); however, zoophilic or geophilic species (e.g. M. canis, M. gypseum) typically demonstrate more intense inflammatory response.
Ectothrix infections can be identified by Woods light (long wave ultraviolet light) examination of the affected area the vet uses this to check your cat’s fur. The fur fluoresces green if infected with M. canis.
Black dot tinea capitis
Endothrix infection with Trichophyton species (e.g. T. tonsurans, T. violaceum, T. soudanense) produces relatively noninflammatory patches of alopecia with fine scale, classically studded with broken-off, swollen hair stubs, resulting in a ‘black dot’ appearance. The hair shaft is filled with fungal branches (hyphae) and spores (arthroconidia). Patches may be multiple. Endothrix infections do not fluoresce with a Wood light.
Figure 2. Black dot tinea capitis
In some cases, hair loss (alopecia) is minimal or absent and infection presents as generalized, diffuse scaling of the scalp, resembling dandruff.
In more inflammatory variants, a diffuse, patchy alopecia may coexist with scattered pustules or low-grade folliculitis. This may be associated with painful regional lymphadenopathy (enlarged lymph gland).
Kerion also known as ‘kerion celsi’, this is the term given to tinea capitis presenting as a painful, boggy, inflammatory tender mass with associated hair loss (alopecia) and lymphadenopathy (enlarged lymph node). Plaques may be solitary or multiple, studded with pustules and matted with thick crust. Regional lymphadenopathy is common. This variant represents a delayed host inflammatory response to the causative dermatophyte. Misdiagnosis as bacterial abscess is not uncommon; however, secondary bacterial infection should not be overlooked. Kerion is commonly seen with zoophilic, large-spore ectothrix species (e.g. Trichophyton Mentagrophytes, Trichophyton verrucosum); however, this has been superseded in recent years by endothrix infections with Trichophyton tonsurans, Trichophyton violaceum or Microsporum canis or Microsporum distortum (a variant of Microsporum canis found in cats), particularly in urban areas 34), 35), 36), 37).
Figure 3. Tinea capitis kerion
A chronic, inflammatory tinea capitis typically seen in T. schoenleinii infection, which results in honeycomb destruction of the hair shaft, is most commonly encountered in the Middle East and North Africa. Favus is characterized by yellow, crusted, cup-shaped lesions (‘scutula’) composed of hyphae and keratin debris, which develop around follicular openings. Favus may result in cicatricial alopecia. Favus infections fluoresce under Wood’s lamp.
Tinea capitis symptoms
Tinea capitis symptoms include itching, redness and dryness of the scalp. Sometimes bald patches can occur as infected hairs are brittle and break easily.
In more severe cases there can be pustules (white/yellow headed spots), yellow crusts and matted hair and, very rarely, a painful boggy swelling filled with pus and overlying hair loss called a kerion. In these cases, patients may have a fever or swollen, painful glands in the neck.
Tinea capitis may present in several ways:
- Dry scaling — like dandruff but usually with moth-eaten hair loss
- Black dots — the hairs are broken off at the scalp surface, which is scaly
- Smooth areas of hair loss
- Kerion — a very inflamed mass, like an abscess
- Favus — yellow crusts and matted hair
- Carrier state — no symptoms and only mild scaling (T. tonsurans).
Tinea capitis may result in swollen lymph glands at the sides of the back of the neck. Untreated kerion and favus may result in permanent scarring and bald areas.
Occasionally the body reacts to the fungus by causing an itchy rash at a site other than the scalp, such as the ear or the palms and soles. This is called an ‘id reaction’ also known as ‘dermatophytid’ and can appear when treatment is started. This “id reaction” can be treated with steroid creams.
A pruritic, papular “id eruption”, particularly around the outer helix of the ear, may accompany treatment initiation, but should not be confused with a drug reaction 38). These eruptions represent a cell mediated host response to the dermatophyte after effective therapy has been initiated and do not warrant cessation of systemic antifungal therapy. Topical (or occasionally, if very severe, oral) corticosteroids may provide symptomatic relief.
Tinea capitis diagnosis
Tinea capitis is suspected if there is a combination of a scaly scalp and hair loss, especially in children. Examination with Wood’s lamp where your doctor shines a black light in the ultraviolet spectrum with wavelength just shorter than the colour violet at the scalp, and certain types of dermatophyte fungus may appear as yellow-green fluorescent spots. Wood’s lamp glows violet in a dark environment because it also emits some light in the violet part of the electromagnetic spectrum. With Wood’s lamp, infected hairs by Microsporum canis, Microsporum audouinii, Microsporum rivalieri, and Microsporum ferrugineum will give a green to a yellow-green color 39). Infection with Trichophyton schoenleinii may show a blue color. It should be noted that tinea capitis caused by Trichophyton tonsurans usually does not show fluorescence 40).
The diagnosis can be confirmed by taking skin scales from the scalp or plucking hairs from the affected areas and sending them for testing in a laboratory. The samples are looked at under the microscope and cultured to confirm that a fungal infection is the cause. More definitive diagnosis is made by microscopy (branching hyphae and spores, the latter present within shortened hair stubs in the black dot type) and/or culture 41), 42). Fungus grows slowly therefore the culture results can take up to 6 weeks. Recently, molecular techniques such as polymerase chain reaction (PCR) have been used for dermatophyte identification in some laboratories 43).
Sometimes, diagnosis is made on skin biopsy showing characteristic histopathological features of tinea capitis.
Tinea capitis treatment
Tinea capitis needs to be treated with oral antifungal medication (which can only be obtained on prescription) AND a medicated antifungal shampoo (purchased over the counter from a pharmacy) to reduce spread of the fungus to other people. Treatment with 1% or 2.5% selenium sulfide (Selsun) shampoo or 2% ketoconazole shampoo should be used for the first two weeks because it may reduce transmission 44), 45).
It may be reasonable to start oral antifungal treatment immediately if your doctor has a strong suspicion that this is tinea capitis. However, the doctor may wish to wait for the test results to know the exact type of fungus causing the infection. This enables the correct antifungal medication to be given.
If you are started on oral treatment immediately and the test results then show this initial medication is not the most appropriate for the type of fungus you have, then your treatment can be changed.
The oral antifungal treatments used include:
- Griseofulvin. This is the only licensed oral antifungal for children. A 6 to 8 week course is needed. The tablets can be crushed, and mixed with a little water, if your children are unable to swallow them whole.
- Griseofulvin dose by body weight:
- < 50 kg: 15–20 mg per kg body weight per day (single or divided dose) for 6–8 weeks
- > 50 kg: 1 g per day (single or divided dose) for 6–8 weeks
- Doses up to 25 mg per kg body weight per day may be required in some cases
- Griseofulvin dose by body weight:
- Terbinafine. This is not licensed in children. This is because the manufacturer of this medication has not applied for a license for it to be used in children and has not conducted clinical trials to check its safety and effectiveness in children. It is licensed in adults. It is very effective and so is also very commonly used “off license” in children It is usually the first choice of treatment as it is accepted as the best treatment. A 2 to 4-week course is needed.
- Terbinafine dose by body weight:
- < 20 kg: 62.5 mg per day for 2–4 weeks
- 20 to 40 kg: 125 mg per day for 2–4 weeks
- > 40 kg: 250 mg per day for 2–4 weeks
- Terbinafine dose by body weight:
- Other antifungal treatments used include itraconazole and fluconazole. Itraconazole is safe, effective and has activity against both Trichophyton and Microsporum species. If itraconazole has been selected as first-line therapy, convert to terbinafine second line for Trichophyton infections or griseofulvin for Microsporum species, at standard dosing regimens.
- Itraconazole, 50–100 mg per day for 4 weeks or 5 mg per kg body weight per day for 2–4 weeks
- For cases refractory to the above regimens, other modalities to be considered in exceptional circumstances include fluconazole and voriconazole
Both griseofulvin and terbinafine have good evidence of efficacy and remain the most widely used first-line treatments. As a general rule, terbinafine is more efficacious against Trichophyton species (Trichophyton tonsurans, Trichophyton violaceum, Trichophyton soudanense), and griseofulvin more effective against Microsporum species (Microsporum canis, Microsporum audouinii). In the U.K., griseofulvin remains the only licensed treatment for tinea capitis in children, although the suspension formulation is no longer licensed for use. Terbinafine requires a shorter course of treatment, which may increase compliance.
Most oral antifungal treatment may increase liver enzymes, therefore, your doctor might check your liver enzymes before initiating, during, and after therapy. Side effects of oral antifungal can occasionally occur. These include diarrhea, abdominal pain, nausea, rash, and headache.
If you are a woman of childbearing age you should not become pregnant during and for one month after treatment with griseofulvin. Effective contraception is required during treatment. Men treated with griseofulvin should also use contraception during, and for six months after, treatment, as it can damage sperm which could possibly lead to abnormalities in the fetus
You should also buy an antifungal shampoo, such as 2% ketoconazole or 1% selenium sulphide. Use this twice weekly, to help stop the spread and recurrence of your infection.
Further samples of hair may be sent for testing after you have finished treatment to ensure it has worked. If this repeat test still shows fungus, then you will need a further course of medication.
Treatment of carriers
If the child has an anthropophilic infection (tinea capitis that is passed on from one person to another as it naturally infects humans), all family members should be examined for signs of infection. Brushings of scaly areas of the scalp should be taken for mycology. Sometimes it is best for the whole family to be treated whether or not the fungal infection is proven.
Children receiving appropriate therapy should be allowed to attend school or nursery.
It is advisable for parents of classmates and other playmates to be informed so their children may be examined and treated if necessary. In some countries, infected children are not allowed to attend school. Elsewhere children with tinea capitis can attend school providing they are receiving treatment.
Carriers may have no symptoms. Treatment of carriers is necessary to prevent the spread of infection. Antifungal shampoo twice weekly for four weeks may be sufficient, but if cultures remain positive, oral treatment is recommended.
Suitable shampoos include these ingredients:
- 2.5% selenium sulfide
- 1% to 2% zinc pyrithione
- 2% Ketoconazole.
Tinea capitis treatment guidelines
For the British Association of Dermatologists’ guidelines for the management of tinea capitis 2014 46), please download the guidelines here: http://www.bad.org.uk/library-media/documents/Tinea%20capitis%20guidelines%202014.pdf
Although a small percentage of patients may clear with topical agents 47), topical therapy alone is not recommended for the management of tinea capitis 48). However, topical agents are used to reduce transmission of spores 49) and povidone–iodine, ketoconazole 2% and selenium sulfide 1% shampoos have all shown efficacy in this context.
It is reasonable to begin treatment on the basis of one or more cardinal signs 50), while awaiting confirmatory mycology. Clear evidence has now emerged to show that the optimal treatment regimen varies according to the dermatophyte involved (Table 1) 51). Treatment protocols should therefore reflect local epidemiology and be based on the most likely culprit organism 52). A prolonged course or a change of agent may be required in cases of treatment failures or if an unexpected fungus is identified on culture.
Although in the U.K., griseofulvin remains the only licensed treatment for tinea capitis in children, cumulative evidence now demonstrates that newer antifungal agents have higher response rates, and are safe and more cost‐effective 53). This is reflected in recent changes to the licensing and availability of antifungal therapies in parts of Europe and the U.S.A.
Table 1. Choice of drug according to organism isolated
|Tinea capitis organism||Antifungal drug|
|Trichophyton violaceum, soudanense||Terbinafine|
|Microsporum canis||Griseofulvin or itraconazole|
|Microsporum audouinii||Griseofulvin or itraconazole|
Table 2. Antifungal treatment (U.K. 2014)
|Griseofulvin||200–300 mg per day||8 weeks|
|Terbinafine||125 mg per day||4 weeks|
|Itraconazole||100 mg per day||4 weeks|
|Fluconazole (suspension)||180 mg||4 weeks|
Footnote: a) Based on treatment of a 20‐kg child. b) Based on halving a conventional tablet.[Source 55) ]
Griseofulvin is a fungistatic drug that inhibits nucleic acid synthesis, arrests cell division at metaphase and impairs synthesis of the cell wall. There is over 50 years of experience in the use of the drug, and it remains the only licensed product for use in the treatment of tinea capitis in children in the U.K. It is available in several forms (micronized, ultramicronized and suspension), but recently the suspension has become increasingly expensive and not so widely available 56). The suspension is no longer a licensed formulation in the U.K., and griseofulvin tablets are no longer available in some European countries, having been superseded by other agents 57).
The standard licensed treatment protocol for those aged > 1 month is 1 g in children weighing > 50 kg, or 15–20 mg/kg daily in single or divided doses for 6–8 weeks if < 50 kg. Taking the drug with fatty food may increase absorption and improve bioavailability. Dosage recommendations vary according to the type of formulation used and how easily it is absorbed. It may be necessary to use doses up to 25 mg/kg daily for more prolonged periods in resistant cases.
A meta‐analysis of seven studies28 showed that response rates are highly variable depending on the species involved: 88 ± 5% for Microsporum species compared with 67·7 ± 9% for Trichophyton species. A recent meta‐analysis of randomized controlled trials (RCTs) suggests that 8 weeks of griseofulvin treatment is significantly more effective than 4 weeks of terbinafine in confirmed Microsporum infection 58). There is no evidence of resistance to griseofulvin in vitro, but accumulated evidence suggests that the drug is less effective against Trichophyton species in the clinical setting 59) and higher doses for longer periods (12–18 weeks) may be required in Trichophyton infections 60).
Side‐effects occur in 20% of cases, mostly gastrointestinal upset, in particular diarrhoea, rashes and headache 61). The drug is contraindicated in pregnancy and men are cautioned against fathering a child for 6 months after treatment.
Advantages: licensed for use in children in the U.K.; extensive experience; suspension more palatable to children and allows more accurate dosage adjustments.
Disadvantages: increasingly expensive; prolonged treatment required with potential to affect compliance.
Contraindications: lupus erythematosus, porphyria, severe liver disease.
Drug interactions: include warfarin, ciclosporin and the oral contraceptive pill.
Terbinafine is an allylamine that acts on the cell membrane and is fungicidal. It shows activity against all dermatophytes 62), but has much higher efficacy against Trichophyton species than Microsporum 63). At higher doses, terbinafine is more effective against M. canis but confers no advantage over griseofulvin 64) and prolonging treatment does not improve efficacy 65). In part, this is because for M. canis infection, the minimum inhibitory concentration for terbinafine (and to some extent itraconazole) can exceed the maximum concentration reported in hair, contributing to treatment failures 66). Additionally, terbinafine is not excreted in the sweat or sebum of prepubertal children, and cannot be incorporated into the hair shaft in children, so does not effectively reach the scalp surface where the arthroconidia are located in Microsporum infections, accounting for its relative inefficacy 67).
In contrast, meta‐analysis of randomized controlled trials shows that 2–4 weeks of terbinafine is at least as effective as 6–8 weeks of griseofulvin in T. tonsurans infections 68). Terbinafine may now be considered the optimal choice, when cost‐efficiency and compliance are taken into account 69). Although shorter treatment protocols increase compliance 70) and terbinafine has a clear cost advantage (Table 2) 71), it remains unlicensed for use in children in the U.K. However, its widespread use is reflected in the publication of weight‐related dosage schedules in recent editions of the British National Formulary for Children.
Although not available in liquid form in the U.K., a new granule formulation of terbinafine (available in 125‐mg or 187·5‐mg packets to be sprinkled on food) has been licensed for use in children > 4 years of age in the U.S.A. 72) and offers significantly higher cure rates than standard griseofulvin suspension, even at higher dosage schedules 73). However, it is not currently available or licensed in the U.K.
Pharmacokinetic studies of terbinafine show that children require significantly weight‐normalized doses to approximate the equivalent drug levels needed for efficacy in adults. However, there is no suggestion of any altered safety profile in children compared with adults 74).
Overall, terbinafine appears well tolerated in children 75). Side‐effects include gastrointestinal disturbances and rashes in < 8%, and very few (0·8%) are required to discontinue treatment 76).
Advantages: fungicidal; shorter treatment regimens, so potential to improve compliance; cost; safety.
Disadvantages: no suspension formulation (but in U.S.A., granules provide a palatable alternative); not licensed for treatment of children in the U.K.
Drug interactions: plasma concentration is decreased by rifampicin and increased by cimetidine.
Itraconazole exhibits both fungicidal and fungistatic activity depending on the tissue concentration of the drug, but, like other azoles, its primary mode of action is fungistatic, through depletion of cell‐membrane ergosterols, which interferes with membrane permeability. Doses of 50–100 mg daily for 4 weeks 77) or 5 mg/kg daily for 2–4 weeks have comparable efficacy with griseofulvin or terbinafine 78).
Itraconazole is now the preferred agent in the majority of European countries33 and has activity against both Microsporum 79) and Trichophyton species 80). The drug is well tolerated 81) and has been shown to be safe for use in the first year of life 82). Intermittent dosing regimens are effective and may be preferred 83).
Although licensed in Europe, the drug is not currently licensed for the treatment of tinea capitis in children in the U.K. aged 12 years and under.
Advantages: pulsed regimes; shorter treatment protocols; available in liquid form; has licence for use in children aged > 12 years.
Disadvantages: not licensed in the U.K. for children aged ≤ 12 years with tinea capitis.
Drug interactions: enhanced toxicity of warfarin, some antihistamines (specifically terfenadine, astemizole), antipsychotics (sertindole), anxiolytics (midazolam), digoxin, cisapride, ciclosporin and simvastatin (increased risk of myopathy); decreased efficacy with concomitant H2 blockers, phenytoin and rifampicin.
Fluconazole has been used in the treatment of tinea capitis 84) and has been advocated as an alternative to terbinafine 85), but its use has been relatively limited because of side‐effects and because it confers no cost advantage. Comparative efficacy with griseofulvin in a multicentre study of mixed pathogens 86) and superior activity in eradication of T. violaceum, T. verrucosum and M. canis has been shown with fluconazole 87), but due its cost and limited availability, griseofulvin remains the treatment of choice in many parts of the world.
Fluconazole is not licensed for the treatment of tinea in children aged < 10 years in the U.K.; however, it is licensed for use in all children for mucosal candidiasis. Furthermore, the drug is licensed for treatment of tinea in children aged > 1 year in Germany 88). Once‐weekly dosing regimens have been used and appear well tolerated 89).
Voriconazole is more potent against dermatophyte isolates than griseofulvin or fluconazole 90), but cost, licensing restrictions and availability limit its current usage.
Although the efficacy of ketoconazole in tinea capitis at doses of 3·3–6·6 mg/kg daily has been demonstrated in the past, and it has shown comparability with griseofulvin 91), resolution of symptoms appears slower and the side‐effect profile is sufficiently poor (especially the risk of hepatotoxicity) that oral ketoconazole was withdrawn from use in U.K. and Europe in 2013.
Exclusion from school
Although the potential risk of transmission of infection to unaffected classmates has led some authorities to recommend exclusion from school 92), most experts consider this impractical and suggest that children receiving appropriate systemic and adjunctive topical therapy should be allowed to attend school or nursery 93).
Index cases due to the anthropophilic T. tonsurans are highly infectious 94). More than 50% of family members (including adults) may be affected, often with occult disease 95). Failure to treat the whole family will result in high recurrence rates. Therefore we recommend screening of all family members and treating those found positive.
Cleansing of fomites
Viable spores have been isolated from hairbrushes and combs. For all anthropophilic species, these should be cleansed with disinfectant 96). This has particular implications for barbers, who need to ensure that appropriate measures are taken to disinfect multiuser equipment. Proprietary phenolic disinfectants are no longer available, but simple bleach or a 2% aqueous solution of sodium hypochlorite containing 16·5% salt are suitable alternatives.
The use of corticosteroids (both oral and topical) for inflammatory varieties of tinea capitis (e.g. kerion and severe id reactions) may reduce itching and general discomfort, but is controversial. Historically, oral steroids were thought to reduce scarring, but studies show that, compared with oral antifungal therapy alone, they do not reduce the time to clearance, and therefore confer no long‐term advantage 97), so are not recommended. Scarring is rare in T. tonsurans infection, and hair usually fully regrows after effective oral antifungal therapy alone.
Some individuals are not clear at follow‐up. The reasons for this include (i) lack of compliance – especially in long treatment courses; (ii) suboptimal absorption of drug; (iii) relative insensitivity of the organism; and (iv) reinfection.
If fungi can still be isolated at the end of treatment, but the clinical signs have improved, it is reasonable to continue therapy for a further 2–4 weeks. However, if there has been no clinical response, it is imperative to ensure that the antifungal therapy is appropriate for the causal organism identified on culture. If so, the options then are (i) to increase the dose or duration of the original drug; or (ii) to change to an alternative agent, for example griseofulvin → itraconazole (for M. canis); terbinafine → itraconazole (for T. tonsurans); or itraconazole → terbinafine (for T. tonsurans).
The optimal management of asymptomatic carriers (i.e. those individuals without overt clinical infection who are culture positive) is unclear, but current management practice depends on the spore load 98). Asymptomatic carriage is highest in contacts of individuals with T. tonsurans infection 99), but can occur in M. audouinii outbreaks as well 100).
In asymptomatic carriers with a high spore load, oral therapy is usually justified 101). If the spore load is low, carriage may be eradicated with topical treatment alone, but close follow‐up is needed, with repeat mycology, to ensure that treatment has been effective. Ideally, the eradication of asymptomatic carriers requires the support and involvement of community healthcare workers, including school nurses, to be comprehensive and effective 102). However, although guidelines have been issued, tinea capitis is not considered a public health priority in the U.K. at present, so enforcement is hampered and widely variable 103).
The definitive end point for adequate treatment must be mycological cure, rather than clinical response. Therefore, follow‐up with repeat mycology sampling is recommended at the end of the standard treatment period and then monthly until mycological clearance is documented. Treatment should therefore be tailored to each individual patient according to response.
Tinea capitis prognosis
Tinea capitis has a good prognosis with treatment 104). Tinea capitis usually has a good prognosis when treated early and appropriately. However, those who remain untreated are at risk for the development of an abscess, also known as a kerion. The fungi can shed spores for many months leading to spread. A common cause of treatment failure is a lack of medication compliance.
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