Tinea appears to be common, so this piece will dwell on Tinea capitis. I will draw on materials from “Management of tinea capitis in childhood” by Bennassar et al published in Clinical, Cosmetic and Investigational Dermatology 12 July 2010 and Medscape.
Tinea capitis (TC) is a dermatophyte infection of the scalp hair follicles and intervening skin. It affects primarily prepubertal children. The causative pathogens belong to only two genera: Trichophyton and Microsporum. Although there is a great local variation in the epidemiology of TC worldwide, T. tonsurans is currently the most common cause of TC with M. canis the second. The most important dermatophyte carriers are stray cats and dogs, pet puppies, kittens and rabbits.These dermatophytosis are most frequently incurred by contact with an infected child, either directly or via objects/materials such as clothes, furniture.It has been recently reported that an asymptomatic adult carrier may provide a source for continued reinfection in children.The asymptomatic carrier state refers to a clinical situation where a person shows no signs or symptoms of TC, yet a dermatophyte positive scalp culture is obtained. Although the asymptomatic carriage typically occurs in adults who have been exposed to children, it may also affect children. Asymptomatic carriers at home or at school shed the fungus and are potentially important sources of disease transmission.
Tinea capitis is the most common fungal infection in children. Patients typically present with scaling of the scalp or circumscribed alopecia with broken hair at the scalp
TC always requires systemic treatment because topical antifungal agents do not penetrate down to the hair follicle root. Topical treatment is only used as adjuvant therapy to systemic antifungals. Factors that may influence the choice between equally effective therapies include tolerability, safety, compliance, availability of liquid formulation and cost.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.
Since the late 1950s, Griseofulvin has been the gold standard for systemic therapy of TC. It is active against dermatophytes and has a long-term safety profile. The main disadvantage of griseofulvin is the long duration of treatment required (6–12 weeks or longer) which may lead to reduced compliance. Griseofulvin is fungistatic and inhibits the mitosis of dermatophytes by interacting with microtubules and disrupting the mitotic spindle; therefore it works best on actively-growing dermatophytes. Two types of preparation are available: microsize and ultramicrosize, either in tablets or in oral suspension. The pediatric dose authorized for treating TC is 15–25 mg/kg/day using the microsize formulation. When the ultramicrosize formulation is used a dose of 10–15 mg is recommended because it is better-absorbed than the microzise form. Griseofulvin produces a sustained blood level so it should be given in a single or in divided doses daily. Absorption varies from person to person: individual patients attain consistently high or low levels of drug. Taking the drug with fatty meals (eg, creamy yoghurt, chocolate or whole milk) may enhance absorption. The recommended duration of therapy for TC is 6–12 weeks or until the patient tests negative for fungi (light microscopy and culture).
Terbinafine belongs to the allyamine class of drugs, a new generation of antifungal agents. It is fungicidal to dermatophytes since it inhibits squalene epoxidase, a membrane-bound enzyme in the biosynthetic pathway of sterol synthesis of the fungal cell membrane. It is well absorbed and binds strongly and nonspecifically to plasma proteins.The absorption characteristics are not altered when terbinafine is taken with food. Its clearance in children is 40% higher than in adults. Since terbinafine is highly lipophilic and keratophilic, it is distributed throughout adipose tissue, dermis, epidermis, nails, and hair and persists in these tissues for weeks. Terbinafine is delivered to the stratum corneum via the sebum and, to a lesser extent, through incorporation into the basal keratinocytes and diffusion through the dermis-epidermis. Terbinafine is not found in eccrine sweat. It remains in skin at concentrations above the mean inhibitory concentration (MIC) for most dermatophytes for 2 to 3 weeks after discontinuation of long-term oral therapy. After 6 and 12 weeks of oral therapy, terbinafine has been detected in the nail plate for 30 and 36 weeks, respectively, at a concentration well above the MIC for most dermatophytes. Terbinafine is metabolized in the liver, and dose adjustments may be needed in patients with liver or renal dysfunction.
It is available as 250 mg tablets. The standard pediatric single daily dose is 62.5 mg (10–20 kg); 125 mg (20–40 kg) and 250 mg (≥40 kg). Some suggest a weight-based dose of 4 to 5 mg/kg per day as an alternative. Terbinafine is concentrated in the hair and may remain present at fungicidal concentrations for several weeks after a course of treatment has been completed. The duration of treatment is generally 4 weeks, although shorter durations (2 weeks) have also been reported to be effective
Itraconazole is a triazole antifungal agent against Trichophyton and Microsporum spp. It exhibits both fungistatic and fungicidal activity depending on its concentration in the tissues, though its primary mode of action is fungistatic by inhibiting the cytochrome P-450-dependent enzymes, blocking the synthesis of ergosterol, the principal component of fungal cell membranes. Itraconazole is lipophilic and has a high affinity for keratinizing tissues. It adheres to the lipophilic cytoplasm of keratinocytes in the nail plate, allowing progressive buildup and persistence in the nail plate. The drug reaches high levels in the nails that persist for at least 6 months after discontinuation of 3 months of therapy and during pulsed cycles. The concentration in the stratum corneum remains detectable for 4 weeks after therapy. Itraconazole levels in sebum are 5 times higher than those in plasma and remain high for as long as 1 week after therapy. The drug has an affinity for mammalian cytochrome P-450 enzymes, as well as for fungal P-450-dependent enzyme, and thus has the potential for clinically-important drug interactions with rifampicin, oral contraceptives, H2 receptor antagonists, Proton Pump inhibitors (PPIs), warfarin and cyclosporine.It is available as capsules or an oral solution. Itraconazole capsule formulation should be ingested with a meal whereas the oral solution should be taken in the fasting state for optimum bioavailability. The recommended pediatric dose is 5 mg/kg/day given continuously or by repeat pulsing. Where the oral solution is used, dosage is reduced to 3 mg/kg/day.Using the continuous regimen, the duration of treatment for Trichophyton spp. and Microsporum spp. tinea capitis is 2 and 6 weeks with cure rates of 85.7% and 88% respectively.
Fluconazole is primarily a fungistatic triazole, preventing the conversion of lanosterol to ergosterol, an essential component of the fungal cytoplasmic membrane. It is distinguished from the other azoles by its water solubility that results in excellent bioavailability by the oral route. Because fluconazole is highly soluble in water it is transported to the skin through sweat and concentrated by evaporation. It achieves high concentrations in the epidermis and nails and persists up to 3 months.It is available as a tablet or oral suspension. Doses of 5–6 mg/kg/ per day for 4–6 weeks can effectively treat TC.
For Terbinafine, Itraconazole, Fluconazole, the pulse therapy can be used in Tinea capitis (TC) as seen in Tinea unguium (Onychomycosis).
Adjunctive topical therapies such as Selenium sulphide, Zinc pyrithione, Povidoneiodine or Ketoconazole shampoos as well as fungicidal creams or lotions have been shown to decrease the carriage of viable spores responsible for the disease contagion and reinfection and may shorten the cure rate with oral antifungal.
Asymptomatic carriers should be detected and treated, since they are the continuous source of infection. Siblings and playmates of patients should avoid close physical contact and sharing of toys or other personal objects, such as combs and hairbrushes, since organisms can spread from one person to another and infectious agents can be transported to different classrooms within the same or in different schools. Shared facilities and objects also may promote spread of disease, both within the home and the classroom.
By Edward O. Amporful