eMedicine Specialties > Dermatology > Fungal Infections
Tinea Capitis: Treatment & Medication
Updated: Sep 11, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Choice of treatment for tinea capitis is determined by the species of fungus concerned, the degree of inflammation, and in some cases, by the immunologic and nutritional status of the patient.
- Systemic administration of griseofulvin provided the first effective oral therapy for tinea capitis.
- Topical treatment alone usually is ineffective and is not recommended for the management of tinea capitis.
- Newer antifungal medications, such as ketoconazole, itraconazole, terbinafine, and fluconazole, have been reported as effective alternative therapeutic agents for tinea capitis. Of these agents, itraconazole and terbinafine are used most commonly.
- Selenium sulfide shampoo may reduce the risk of spreading the infection early in the course of therapy by reducing the number of viable spores that are shed.
Medication
Griseofulvin has been the treatment of choice in all ringworm infections of the scalp. A 2008 meta-analysis found that griseofulvin remains an effective therapy for tinea capitis.8 Most specialists recommend a griseofulvin dosage of 20-25 mg/kg/d for 6-8 weeks. Griseofulvin accumulates in keratin of the horny layer, hair, and nails, rendering them resistant to invasion by the fungus. Treatment must continue long enough for infected keratin to be replaced by resistant keratin, usually 4-6 weeks. In inflammatory lesions, compresses often are required to remove pus and infected scale. Therapeutic progress is monitored by regular clinical examination with the aid of a Wood lamp for fluorescent species such as M audouinii and M canis. Adverse effects include nausea and rashes in 8-15%. The drug is contraindicated in pregnancy, and the manufacturers caution against men fathering a child for 6 months following treatment.9
Several newer antimycotic agents, including itraconazole, terbinafine, and fluconazole, have been reported as effective and safe. A review found that these agents may be similar to griseofulvin for treatment in children with tinea capitis caused by Trichophyton species and have the advantage of shorter treatment durations; however, they may be more expensive.10
Gupta et al11 reported the following alternative effective and safe treatment regimens for tinea capitis with endothrix species infection including T tonsurans: itraconazole continuous regimen (3-5 mg/kg/d with a full meal for 4-6 wk), itraconazole pulse regimen with capsules (5 mg/kg/d for 1 wk times 3 pulses 3 wk apart), and itraconazole pulse regimen with oral solution (3 mg/kg/d for 1 wk times 3 pulses, ie, 1 wk per mo). The oral solution contains cyclodextrin, which may cause diarrhea in children. The pharmacokinetics of the liquid formulation are not well established in children. In some children (weighing 20-40 kg), a single 100-mg capsule daily for 4-6 weeks has been used successfully.
Because itraconazole has been associated with heart failure, it is currently not favored as a first-line therapy for tinea. An exception may be serious M canis infections, which are relatively insensitive to terbinafine, or, according to some authors, if griseofulvin is not available.12
Terbinafine tablets at doses of 3-6 mg/kg/d for approximately 2-4 weeks have been used successfully for T tonsurans infections.13,14 An international study found that terbinafine has potent activity against dermatophyte isolates obtained from patients with tinea capitis worldwide.15 A pediatric study found terbinafine produced significantly better cure rates than griseofulvin for tinea capitis caused by T tonsurans but not for disease caused by M canis.16 M canis is relatively resistant to terbinafine but has been treated effectively with higher doses and longer courses of therapy. General guidelines for tinea capitis are treatment for 2-4 weeks, with dosage determined by body weight, as follows:
- 10-20 kg - 62.5 mg/d
- 20-40 kg - 125 mg/d
- Greater than 40 kg - 250 mg/d
Terbinafine acts on fungal cell membranes and is fungicidal. Adverse effects include gastrointestinal disturbances and rashes in 3-5% of cases.17
Fluconazole tablets or oral suspension (3-6 mg/kg/d) are administered for 6 weeks. In 1 trial, a dose of 6 mg/kg/d for 20 days was effective. An extra week of therapy (6 mg/kg/d) can be administered if clinically indicated at that time.
In ectothrix infection (eg, M audouinii, M canis), a longer duration of therapy may be required.
Although oral ketoconazole also is an acceptable alternative to griseofulvin, it is not considered a treatment of choice because of the risk of hepatotoxic effect and higher cost. Treatment for the deep folliculitis seen in Majocchi granuloma is systemic oral antifungal therapy.
Oral steroids may help reduce the risk for and extent of permanent alopecia in the treatment of kerion. Avoid using topical corticosteroids during treatment of dermatophyte infections.
Antifungal agents
Mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.
Griseofulvin (Fulvicin)
Antibiotic derived from a Penicillium species that is deposited in the keratin precursor cells that are replaced gradually by noninfected tissue. As a result, new keratin becomes highly resistant to fungal invasions. Active against dermatophytes but not against yeasts or bacteria. Resistant strains of dermatophytes are rare. In its fine particle form, is absorbed readily from gut, and absorption is enhanced when fatty food is taken simultaneously. Accumulates in keratin of the stratum corneum, hair, and nails. Has a long record of safety, but newer regimens may prove more cost effective.
Adult
500 mg to 1 g microsize (330-375 mg ultramicrosize) PO in single or divided daily doses
Pediatric
20-25 mg microsize/kg/d (5 mg/lb/d) PO or 7.3 mg ultramicrosize/kg/d (3.3 mg/lb/d) for 6-8 wk
Lower doses may be effective in some patients
May decrease hypoprothrombinemic activity of warfarin (adjust dose); coadministration decreases contraceptive effects, resulting in breakthrough bleeding, amenorrhea, or unintended pregnancy; may reduce effects of cyclosporine and salicylates; barbiturates may decrease griseofulvin effects; concurrent administration with ethanol may cause disulfiram-like reaction
Documented hypersensitivity; porphyria; hepatocellular failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Oral form found to be embryotoxic and teratogenic to pregnant rats; therefore, do not prescribe for women contemplating pregnancy (wait at least one month following completion of griseofulvin therapy before becoming pregnant); men should wait at least 6 months following completion of griseofulvin therapy before fathering a child
Patients are encouraged to take medication after fatty meal to increase absorption from the alimentary tract
Proven to be nontoxic but adverse effects are reported occasionally, including headache, nausea, fatigue, abdominal discomfort, or transient rash; less common adverse reactions include urticaria, diarrhea, and photosensitivity; may precipitate acute intermittent porphyria and systemic lupus erythematosus in predisposed individuals
Hepatotoxicity has been rarely noted following therapeutic doses
Itraconazole (Sporanox)
One of 2 triazole antimycotic medications with potential for treatment of superficial dermatophyte infections in pediatric population. Since it is poorly water soluble, should be taken with fatty meal to improve absorption. Most of absorbed itraconazole is bound to plasma albumin. Because of lipophilic property, it is found in highest concentrations in fat, omentum, skin, nails, and vaginal and cervical tissues. Antimycotically significant concentrations may remain in skin up to 4 wk after cessation of medication.
Hydroxyitraconazole is 1 of 30 metabolites active pharmacologically. Terminal elimination half-life of itraconazole is 20-60 h, which indicates that steady-state concentrations are reached only after at least 2 wk of daily administration. Large biliary excretion of itraconazole and its metabolites occurs because of their large molecular sizes and high molecular weights. They are excreted 65% in feces and 35% in urine. No indication exists for dosage adjustment for impaired hepatic and renal functions. Has significantly greater selectivity for inhibiting fungal enzymes than does ketoconazole.
Results of several clinical trials indicated that itraconazole is a safe and effective alternative to griseofulvin-failed cases. Itraconazole has slightly higher cure rate in children with tinea capitis infection caused by T violaceum, compared to treatment with terbinafine. Treatment duration is 2 wk. In children with T tonsurans infection treated with 1-3 pulses of itraconazole, a 100% cure rate has been reported by Gupta et al in a small series. The pulse schedule was itraconazole 5 mg/kg/d for 1 wk, then 2 wk with no drug, followed by 1 wk with medication. When a third pulse was required, 3 wk elapsed between second and third drug treatments.
Adult
200 mg PO qd; not to exceed 400 mg/d
Increase in 100-mg increments if no improvement (administer >200 mg/d in divided doses)
200 mg IV bid for 4 doses, followed by 200 mg/d
Pediatric
3-5 mg/kg/d PO for 4-6 wk
Antacids may reduce absorption of itraconazole; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; may increase tacrolimus and cyclosporine plasma concentrations when high doses are used; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (lovastatin or simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death; may increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce itraconazole levels (phenytoin metabolism may be altered)
Documented hypersensitivity; concomitant administration with HMG-CoA reductase inhibitors (eg, lovastatin, simvastatin), astemizole (recalled from US market), cisapride, midazolam, triazolam, or terfenadine (recalled from US market) dofetilide, pimozide, levacetylmethadol (levomethadyl), quinidine, ergot alkaloids metabolized by CYP3A4, such as dihydroergotamine, ergometrine (ergonovine), ergotamine, and methylergometrine (methylergonovine) are contraindicated
Coadministration with cisapride, dofetilide, oral midazolam, pimozide, levacetylmethadol (levomethadyl), quinidine, lovastatin, simvastatin, or triazolam
Coadministration with ergot alkaloids metabolized by CYP3A4, such as dihydroergotamine, ergometrine (ergonovine), ergotamine and methylergometrine (methylergonovine)
Congestive heart failure or history of congestive heart failure (itraconazole cap for treatment of onychomycosis)
Pregnant women or women contemplating pregnancy (itraconazole cap for treatment of onychomycosis)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Serious adverse effects include congestive heart failure, hepatotoxicity, neutropenic disorder, and Stevens-Johnson syndrome; may cause hepatotoxicity; oral sol and oral cap not for use interchangeably
Caution in patients with risk factors for congestive heart failure such as ischemic and valvular cardiac disease, significant pulmonary disease, renal failure and other edematous disorders; do not use itraconazole injection in patients with CrCl <30 mL/min; caution in patients with CrCl of 30-80 mL/min; hypokalemia and hypomagnesemia in patients receiving intravenous itraconazole
Hypertriglyceridemia reported in patients treated with oral itraconazole 400 mg qd for systemic mycoses
Ketoconazole (Nizoral)
Many safer alternatives are available. Usually not used to treat tinea capitis. Is a broad-spectrum synthetic antifungal compound of the azole group. When orally administered, is active against anthropophilic dermatophytes. Is hydrophilic and high concentrations of the drug develop within skin, making it potentially beneficial for treating superficial dermatophytosis. Delivery of this drug to the skin is accomplished through normal blood circulation and sweat. Some excretion occurs into sebum and epidermal basal layer. In the presence of normal gastric acidity, is well absorbed, and peak plasma concentrations are achieved in 3-4 d. Of the drug, 99% is bound to plasma proteins.
Extensively metabolized through oxidation and degradation of imidazole ring, O-dealkylation, oxidative degradation of piperazine ring, and aromatic hydroxylation. Untransformed ketoconazole is the only active antifungal compound. None of the metabolites possesses therapeutic activity.
Despite active metabolism, ketoconazole is excreted in bile and eliminated unchanged. Dosage adjustment is not required in patients with impaired renal function in view of the rapid metabolism and active biliary excretion.
Adult
Initial: 200 mg/d in single tab
In serious infections, may increase to 400 mg/d
Pediatric
Not established
Potent inhibitor of cytochrome P450 3A4 enzyme system; therefore, coadministration of ketoconazole and drugs primarily metabolized by enzyme system may result in increased plasma concentrations of drugs (eg, cyclosporine, warfarin, terfenadine, astemizole); rifampin and phenytoin may decrease ketoconazole levels
Since hepatic toxicity is noted in adult patients treated with ketoconazole, is not considered appropriate therapy for pediatric tinea capitis; furthermore, no data are available concerning biodisposition and metabolism of ketoconazole in infants and children; coadministration of ketoconazole with terfenadine (recalled from US market), astemizole (recalled from US market), cisapride, or triazolam is contraindicated
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Significant incidence of idiosyncratic hepatic toxicity (primarily hepatocellular type) in 1 in 15,000; rare fatalities have occurred from severe hepatic necrosis; reversible transient mild elevations of liver enzymes can occur
Fluconazole (Diflucan)
Triazole compound that is relatively water soluble and well absorbed upon ingestion. Peak plasma concentration is achieved within 1-2 h after oral administration. Drug is distributed widely to body tissues, and fluids free without binding to plasma proteins. Drug has a long half-life of 22-30 h in adults, and steady-state levels are reached within 6-10 d after initiation of treatment. Most of the drug is excreted unchanged in urine with little hepatic metabolism. Eliminated slower from skin than from plasma, which contributes therapeutic benefit against superficial dermatophytosis, even after dosage has been discontinued. Dosage adjustment is required for patients with renal impairment, since drug is eliminated primarily by the kidneys.
More dosing regimen studies are needed. Available in orange flavor oral suspension as 10-40 mg/mL.
Adult
6 mg/kg PO for 20 d (reported effective) or 3-6 mg/kg PO for 6 wk (offers excellent antifungal results)
Pediatric
<6 months: Not established
>6 months: 5 mg/kg/d PO for 4-6 wk or 6 mg/kg/d PO for 20 d
Levels may increase with hydrochlorothiazides; fluconazole levels may decrease with chronic coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adverse reaction in approximately 16% of patients who received more than 7 d of medication; reaction is mild and reversible when drug is discontinued; most common adverse effects include nausea, vomiting, and abnormal liver function tests
Terbinafine (Lamisil)
Allylamine with antifungal properties. Well absorbed upon oral administration. Peak plasma concentration is reached in approximately 2 h. Drug has strong plasma protein binding. Has large lymphatic distribution and is associated with chylomicrons. Preferential uptake into fat resulted in relatively high concentration in the skin. Concentration within the stratum corneum reaches 75 times that of plasma concentration during first 2 wk of therapy. Antifungal activity remains in the skin for 2 mo after plasma concentration has depleted, following cessation of medication. Fifteen inactive metabolites following ingestion have been identified. Metabolized through N -demethylation and aromatic ring oxidation. Most metabolites are eliminated by kidneys; therefore, dosage adjustment is indicated in patients with renal or hepatic dysfunction.
Compared to itraconazole, terbinafine has slightly lower cure rate; 4 wk of treatment with terbinafine is reported as effective as 8 wk of griseofulvin therapy.
High cure rates of fungal infections in children are reported.
Adult
250 mg/d PO
Pediatric
Weight-based dosing (PO):
10-20 kg: 62.5 mg/d for 2-4 wk
20-40 kg: 125 mg/d for 2-4 wk
>40 kg: Administer as in adults
May decrease cyclosporine effects; toxicity of terbinafine may increase with rifampin and cimetidine
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue if chemical irritation or signs of hepatobiliary dysfunction develop; agranulocytosis, leukopenia, neutropenia and thrombocytopenia reported; caution in renal impairment (CrCl <50 mL/min); associated with cutaneous eruptions; adverse effects include acute generalized exanthematous pustulosis, alopecia, bullous pemphigoid, erythema multiforme, psoriasiform drug eruption, Stevens-Johnson syndrome, toxic epidermal necrolysis, and partial or complete loss of taste, but generally reversible upon discontinuation
More on Tinea Capitis |
| Overview: Tinea Capitis |
| Differential Diagnoses & Workup: Tinea Capitis |
 Treatment & Medication: Tinea Capitis |
| Follow-up: Tinea Capitis |
| Multimedia: Tinea Capitis |
| References |
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References
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Further Reading
Keywords
tinea capitis, ringworm of the scalp, tinea tonsurans, herpes tonsurans, superficial fungal infection of skin of scalp, superficial fungal infection of skin of eyebrows, superficial fungal infection of skin of eyelashes, superficial mycosis, dermatophytosis, scaly noninflamed dermatosis, scaly erythematous lesions, hair loss, alopecia, kerion, kerion celsi, parasitic infestation of skin, dermatophyte infection
Pityrosporum ovale, keratinophilic fungi, ectothrix infection, arthroconidia, endothrix infections, favus, tinea favosa, Trichophytonschoenleinii, Trichophyton violaceum, scutula, black dot tinea capitis, dermatophyte idiosyncratic reactions, id reactions
acute vesicular dermatitis, annular erythema, erythema nodosum, intradermal trichophytin, Trichophyton concentricum, anthropophilic fungi
