OVERVIEW: What every practitioner needs to know
Are you sure your patient has tinea capitis? What are the typical findings for this disease?
Tinea capitis is the most common type of superficial dermatophytosis in children, affecting the skin and hair of the scalp. The disease occurs most often in prepubertal children and is characterized by scaling and hair loss of the scalp. The most common dermatophytes that cause tinea capitis include Trichophyton tonsurans (most prevalent in the United States), T. violaceum, Microsporum canis and M. audouinii (most prevalent in the world outside the United States).
The most common clinical findings include the following:
Alopecia +/- scale (localized or generalized)
Posterior cervical and/or posterior auricular lymphadenopathy
Hairs broken near the scalp (“black dots”) – only with T. tonsurans infection
Diffuse scale – This can mimic seborrheic dermatitis, with widespread scale throughout the scalp. Seen more commonly in African Americans.
Different clinical presentations arise from various causative organisms based on the pattern of hair invasion (endothrix, ectothrix, versus favus); and associated inflammatory responses (seborrheic dermatitis-like, papular-pustular, versus kerion). The hair in the affected individual usually returns. However if the infection persists, alopecia could become permanent. On the other hand, secondary bacterial infection may also lead to permanent scarring alopecia.
Less common presentations
1. Kerion: This is a boggy plaque or multiple plaques with purulent drainage caused by an intense inflammatory response to the fungal infection. There is usually associated cervical lymphadenopathy. If treatment is delayed, scarring alopecia can develop. It occurs more often with M. canis and T. tonsurans infection.
2. Diffuse pustules and papules: This can mimic folliculitis, with widespread pustules, but does not respond to systemic antibiotics. There may be associated lymphadenopathy.
3. Favus: Favus is caused by Trichophyton schoenleinii and is uncommon in the United States. Clinically, there are scutula, or disc-like scales (consisting of hyphae and keratin debris) covering hair follicles. These scales can coalesce and cover a large area of the scalp. Favus may lead to scarring alopecia.
What other disease/condition shares some of these symptoms?
There are many scalp and hair disorders that may resemble the clinical presentations of tinea capitis. The diagnosis of tinea capitis should always be considered, but other conditions that may resemble tinea capitis include:
1. Seborrheic dermatitis
2. Bacterial folliculitis
5. Alopecia areata
6. Discoid lupus erythematosus
What caused this disease to develop at this time?
Fungal infections in humans can be superficial, deep, or systemic. The superficial infections are those that are limited to the epidermis, nails, hair, and mucosa without hematogenous spread or extension to other organ systems. The three common types of superficial fungal infections are dermatophytosis, tinea versicolor and candidiasis.
Infections caused by dermatophytes, a group of related fungi that live in soil, on animals or humans, are named tinea, dermatophytosis, or ringworm because of the annular appearance of the lesions. There are three genera of pathogenic dermatophytes that are comparable in their abilities to digest keratin and invade the skin, hair, and nails to produce clinical diseases. They are Microsporum, Trichophyton, and Epidermophyton, with only the first two genera being the causative pathogens associated with tinea capitis. Transmission of dermatophytes to humans occurs via three sources, including human (anthropophilic), animals (zoophilic) and soil (geophilic).
Tinea capitis is a fungal infection of the scalp, caused most commonly by fungi in the genera Microsporum and Trichophyton.
Microsporum is a zoophillic organism, which means it is caused by exposure to infected animals, and is more prevalent worldwide.
Trichophyton can be zoophilic or anthropophilic, which is a fungus spread via infected persons or fomites, and is most prevalent in the United States and Europe.
Prepubertal children most commonly develop tinea capitis. This susceptibility is thought to be due to lack of fungistatic fatty acids in the sebum on the scalp.
Immunosuppression does not increase incidence, but increases severity of infection.
Predisposing factors include large family size, crowded living conditions, and low socioeconomic status. In addition, spread from fomites (hairbrushes, combs, hats, and contaminated grooming instruments) are also well known. Hair care practices (styling, frequency of washing, use of oils and grease, etc.) traditionally are believed to play a role in the acquisition of tinea capitis.
Asymptomatic carriers of dermatophytes in a community have also been attributed to disease prevalence. This occurs most often with T. tonsurans and T. violaceum in African American, Afro-Caribbean, or black children in Africa.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Microscopic exam with potassium hydroxide (KOH) or chlorazol black:
The examination yields rapid results, but also requires considerable experience. The potassium hydroxide solution contains dimethylsulfoxide (DMSO), and the slides should not be heated because heating may dissolve fungi as well as epidermal cells.
A scraping from the scale on the scalp with either a #15 blade or the side of a glass slide should be collected, and a drop of agent (potassium hydroxide or chlorazol black) placed over the scale, then a coverslip. If hyphae or spores are visualized, the presence of fungus is confirmed. Ectothrix infections (dermatophyte is surrounding, but has not penetrated, the hairshaft) show arthroconidia surrounding the hair, whereas endothrix infections show spores within the hair shaft. Fungi can be difficult to recover if there is a brisk inflammatory response.
The change in epidemiology of dermatophytosis in the United States has made the Wood’s light examination irrelevant in most cases in the US. The fluorescence is the result of a substance emitted when the fungus invades the hair shaft; therefore, the lights are usually not visible in the skin. M. canis and M. audouinii fluoresce bright green, T. schoenleinii fluoresces pale green, and T. tonsurans has no fluorescence. Sources of error in Wood’s light examination include an insufficiently dark room, or false positive with lint, scale, serum or ointment-containing petrolatum, which fluoresces blue or purple.
Fungal culture is useful in confirming the carrier state and in demonstrating mycologic cure when clinical symptoms have resolved. Dermatophyte identification may also provide epidemiologic information (i.e., human-to-human versus animal-to- human transmission) and guide the choice of antifungal therapy.
There are several types of fungal culture media, including Sabouraud’s dextrose agar, MycoselTM (Mycobiotic), or Dermatophyte Test Medium. The antibiotics contained in these media will inhibit the growth of bacteria and saprophytic fungi.
A cotton-tipped applicator can be moistened with tap water, then rubbed vigorously over the affected area of the scalp, before being placed into Dermatophyte Test Medium. The specimen should be kept for 2 to 3 weeks, and most fungi will grow in 2 weeks. The inoculated area will turn red, indicating the presence of fungus. Any other color indicates a contaminant. Alternatively, a cotton swab or a travel toothbrush can be rubbed over the scalp, then be placed in a sterile cup and sent to the laboratory for plating and culture.
Would imaging studies be helpful? If so, which ones?
Imaging studies are not necessary for diagnosis.
Confirming the diagnosis
Microscopic exam is the most common tool for diagnosis. Fungal culture is used concurrently when clinical suspicion is high but microscopic test is negative. The other advantage to culture is speciation.
If you are able to confirm that the patient has tinea capitis, what treatment should be initiated?
Because treatment must penetrate the hair follicle to be effective, systemic therapy is required. In addition, preventative measures are also important in the management of tinea capitis. For recalcitrant cases, screening and appropriate treatment of close contacts may be necessary.
Griseofulvin is the initial treatment of choice. A dose of 20-25 mg/kg/d for 6 to 8 weeks is required, and absorption is enhanced by a fatty meal. The dose of microsize griseofulvin is 10-15 mg/kg/d. It is less expensive than alternative oral antifungals, but requires longer treatment courses. Efficacy is superior to terbinafine for Microsporum species. Treatment beyond 12 weeks may uncommonly be required.
The following are additional therapeutic options for treatment. All have similar efficacy for infections from Trichophyton.
Terbinafine is dosed at 62.5 mg/day for children weighing 10-20 kg, 125 mg/day for children weighing 20-40 kg, and 250 mg/day for children weighing >40 kg. Length of treatment for Trichophyton infection is 2-4 weeks, and for Microsporum infection it is 8-12 weeks. The advantage of terbinafine treatment for Trichophyton infection is that the length of treatment is shorter than griseofulvin. A recent industry-sponsored study found that terbinafine was more efficacious than griseofulvin in treating tinea capitis due to Trichophyton, but not in Microsporum infection. A very recent meta-analysis (April 2011) comparing terbinafine with griseofulvin also showed that terbinafine was more efficacious in treating tinea capitis due to
Trichophyton, and griseofulvin was more efficacious than terbinafine in treating tinea capitis due to Microsporum. Since the cost of terbinafine has decreased significantly, there is increased use of this medication as first-line treatment in the United States.
Itraconazole has similar efficacy to terbinafine for infections from
Trichophytonand is dosed at 5 mg/kg/d for the capsules and 3 mg/kg/d for the oral solution for 2-6 weeks. A disadvantage is that it may be more expensive than griseofulvin and has drug interactions. An advantage is shorter treatment duration.
Fluconazole also has similar efficacy to terbinafine for infections from
Trichophytonand is dosed at 5-6 mg/kg/day for 3-6 weeks. It also may be more expensive than griseofulvin and has drug interactions. An advantage is shorter treatment duration.
Adjunctive topical treatment with selenium sulfide or ketoconazole shampoo decreases carriage and shedding of spores, which are responsible for contagiousness. Either shampoo can be used 2-3x/week for 2-4 weeks or until cure.
We recommend clinical evaluation every 4 weeks, with fungal culture, to determine need for continued treatment.
When a patient fails to respond to 2 months of griseofulvin, other therapy, such as changing to terbinafine, is recommended.
Treatment of a kerion, due to profound inflammation, should include oral prednisone dosed at 0.5 – 1 mg/kg/day for 2-4 weeks and consider treating for concurrent bacterial infection if warranted.
Cost of Treatment
Cost of treatment according to drugstore.com at the time of this writing (May 30, 2011):
Griseofulfin microsize 125 mg/5mL (120 mL bottle): $42.99
Griseofulfin cost for a 30 kg child at 20 mg/kg/day for 8 weeks = $103
Terbinafine 250 mg tablets X 30 tablets: $51.99
Terbinafine tablets for a 30 kg child at 125 mg/day for 4 weeks = $25
Terbinafine 187.5 mg granule packets X 14 packets: $150
Terbinafine granules for a 30 kg child dosed at 187.5 mg/day for 4 weeks = $300
Itraconazole 100 mg capsules X 30 capsules: $245.99
Itraconazole cost for a 30 kg child at 5 mg/kg/day for 4 weeks = $369
Itraconazole 10 mg/mL solution (450 mL bottle): $631
Itraconazole solution cost for a 30 kg child at 5 mg/kg/day for 4 weeks = $631
Fluconazole 40 mg/mL suspension (35 mL bottle): $109.98
Fluconzole cost for a 30 kg child at 5 mg/kg/day for 4 weeks = $330
Fluconazole 200 mg tablets X 24 tablets: $198
Fluconazole tablets cost for a 30 kg child at 5 mg/kg/day for 4 weeks = $198
What are the adverse effects associated with each treatment option?
All oral antifungals used to treat tinea capitis are well tolerated.
Both griseofulvin and terbinafine (>4 yo) are FDA approved for the treatment of tinea capitis.
The most common adverse effects of griseofulvin and terbinafine are gastrointestinal effects and headache. The incidence of vomiting, abdominal pain, diarrhea, and nausea are all <2%, and the incidence of headache is also <2%, with both griseofulvin and terbinafine. Pancytopenias and liver dysfunction are rare. Labs do not need to be checked routinely. If terbinafine is used >4 weeks, we recommend checking a CBC and liver function at 4 weeks.
Drug interaction with terbinafine is rare, but may occur with cimetidine and cyclosporine, among others.
Griseofulvin can also cause photosensitivity and a morbilliform eruption, and also interacts with warfarin and barbiturates, among others. A disulfiram-like reaction can occur with alcohol ingestion.
Itraconazole also causes GI upset and headache uncommonly. It is contraindicated in patients with ventricular dysfunction and has many drug interactions, including drugs metabolized by CYP3A4. Liver toxicity is rare. Routine blood work to check liver function is not required, unless there are signs and symptoms of liver dysfunction or a history of liver disease.
Fluconazole most commonly causes nausea and vomiting. It has many drug interactions as well and rarely causes liver toxicity. Routine blood work is not required. It rarely causes torsades de pointes.
What are the possible outcomes of tinea capitis?
Tinea capitis usually resolves with treatment, and alopecia is not typically scarring or irreversible;
however, it can take several months for hair to appear normal after successful treatment for tinea capitis.
Inflammatory types of tinea capitis, such as kerion and favus, can lead to scarring alopecia, which is irreversible.
There can also be chronic infection, if the dermatophyte is resistant to treatment, or if there is reinfection from infected family members, friends, classmates or fomites.
Recurrence is not uncommon.
What causes this disease and how frequent is it?
The prevalence of tinea capitis in the United States ranges from 3%-13%. African American children have the highest incidence in the United States.
It is most common in children ages 3-7 years old.
Incidence is lowest (<1%) in Spain and Palestine and highest (~50%) in Ethiopia.
Trichophyton tonsurans is the most common cause of tinea capitis in North America and the United Kingdom.
Microsporum canis is the most common pathogen in central Europe, South America, and Africa.
Trichophyton violaceum is the most common pathogen in western and southern Asia and Australia.
Exposure to animals can be a cause of transmission.
How do these pathogens/genes/exposures cause the disease?
The fungi responsible for tinea capitis are able to invade keratin in hair.
T. tonsurans causes an endothrix infection, in which the fungi invade the hair shaft, which can lead clinically to broken hairs and the “black dot” appearance. Endothrix infections do not fluoresce with Wood’s lamp examination.
Microsporum causes an ectothrix infection, in which the fungi coat the outside of the hair.
What complications might you expect from the disease or treatment of the disease?
Besides side effects and complications discussed above, an “Id” reaction can occur, which consists of a widespread, papular or papulovesicular eruption that is prominently on the extremities. It can be seen prior to or after initiating therapy. It must be differentiated from a drug eruption. It is best treated with topical corticosteroids and systemic antihistamines.
Are additional laboratory studies available; even some that are not widely available?
Currently no additional laboratory tests are recommended. However, in the event that the patient needs to be treated with systemic anti-fungal medication other than griseofulvin for more than one month, metabolic panels should be obtained to assure normal liver functions.
How can tinea capitis be prevented?
Tinea capitis can be prevented by treating contacts and by avoiding sharing hats, hair care products, and combs.
What is the evidence?
Grading and Strength of Evidence for the Treatment of Tinea Capitis
Kakourou, T, Uksal, U. “Guidelines for the management of tinea capitis in children”. Pediatr Dermatol. vol. 27. 2010. pp. 226-8. Treatment with terbinafine – Grading of recommendation A; strength of evidence Ia
Treatment with griseofulvin is superior to terbinafine for cases caused by
Microsporum – Grading of recommendation A; strength of evidence Ia
Treatment with itraconazole or fluconazole is similar in efficacy and duration required, compared to terbinafine – Grading of recommendation A; strength of evidence 1a
Adjunctive treatment with topical selenium sulfide – Grading of recommendation B; strength of evidence IIa
Adjunctive treatment with topical ketoconazole- Grading of recommendation B; strength of evidence III
Selenium sulfide or ketoconazole shampoo should be used for 5 min twice weekly for 2-4 weeks or three times weekly until clinical and mycologic cure – Grading of recommendation C; strength of evidence IV
Ia: Evidence obtained from meta-analysis of randomized controlled trials.
Ib: Evidence obtained from at least one randomized controlled trial.
IIa: Evidence obtained from at least one well-designed controlled study without randomization.
IIb: Evidence obtained from at least one other type of well-designed quasi-experimental study.
III: Evidence obtained from well-designed non-experimental descriptive studies such as comparative studies, correlation studies, and case control studies
IV: Evidence obtained from expert committee reports or opinions or clinical experience of respected authorities.
A: Requires at least one randomized controlled trial as part of the body of literature of overall good quality and consistency addressing the specific recommendation.
B: Requires availability of well-conducted clinical studies but no randomized clinical trials on the topic of recommendation.
C: Requires evidence from expert committee reports or opinions and/or clinical experience of respected authorities. Indicates absence of directly applicable studies of good quality.
Gupta, A, Adam, P, Dlova, N. “Therapeutic options for the treatment of tinea capitis caused by Trichophyton species: griseofulvin versus the new oral antifungal agents, terbinafine, itraconazole and fluconazole”. Pediatr Dermatol. vol. 8. 2001. pp. 433-8.
Ginter-Hanselmayer, G, Smolle, J, Gupta, A. “Itraconazole in the treatment of tinea capitis caused by Microsporum canis: experience in a large cohort”. Pediatr Dermatol. vol. 21. 2004. pp. 499-502.
Sethi, A, Antaya, R. “Systemic antifungal therapy for cutaneous infections in children”. Pediatr Infect Dis J. vol. 25. 2006. pp. 643-4.
Abdel-Rahman, SM, Farrand, N, Schuenemann, E. “The prevalence of infections with Trichophyton tonsurans in schoolchildren: the CAPITIS study”. Pediatrics. vol. 125. 2010. pp. 966-73.
Andrews, MD, Burns, M. “Common tinea infections in children”. Am Fam Physician. vol. 77. 2008. pp. 1415-20.
Isa-Isa, R, Arenas, R, Isa, M. “Inflammatory tinea capitis: kerion, dermatophytic granuloma, and mycetoma”. Clin Dermatol. vol. 28. 2010. pp. 133-6.
Elewki, BE, Cáceres, HW, DeLeon, L. “Terbinafine hydrochloride oral granules versus oral griseofulvin suspension in children with tinea capitis: results of two randomized, investigator-blinded, multicenter, international, controlled trails”. J Am Acad Dermatol. vol. 59. 2008. pp. 41-54.
Tey, HL, Tan, AS, Chan, YC. “Meta-analysis of randomized, controlled trials comparing griseofulvin and terbinafine in the treatment of tinea capitis”. J Am Acad Dermatol. vol. 64. 2011. pp. 633-70.
Ongoing controversies regarding etiology, diagnosis, treatment
Because of its long-term safety record, dosing flexibility, and lower cost compared to terbinafine granules, griseofulvin is the first-line treatment for tinea capitis. It is well-tolerated. With the reduced cost of terbinafine tablets and short treatment course recommended, the medication is more often being used as first-line treatment now. Furthermore, recent studies have shown that terbinafine is at least as efficacious in infections due to Trichophyton, with shorter treatment times.
While the patient is being treated with griseofulvin, we advocate 1 month follow-up. If there is still evidence (scale, little improvement of alopecia) of continued infection, treat for an additional 4 weeks. At 2 months, if infection is still present, we advocate switching to terbinafine. Because it can take several weeks for a follow-up culture to grow, the need for additional treatment is based on clinical impression; however, treatment endpoint is when a negative culture is obtained. The recurrence rate is lower when mycotic clearance is achieved.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has tinea capitis? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- Confirming the diagnosis
- If you are able to confirm that the patient has tinea capitis, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of tinea capitis?
- What causes this disease and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- What complications might you expect from the disease or treatment of the disease?
- Are additional laboratory studies available; even some that are not widely available?
- How can tinea capitis be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment