Tinea Capitis Caused by Trichophyton Tonsurans

Tinea capitis is the most common dermatophyte infection among children worldwide, and though the epidemiology varies according to geographical region, population, and socioeconomic conditions,^1,2 T tonsurans is responsible for 90% of fungal scalp infections in North and Central America, with Microsporum canis, M audouinii, and T mentagrophytes causing the remaining 10%.² The infection occurs most frequently in African-American children ages 3 to 9 years, making this case in a 2-year-old Caucasian child unusual.^3,4

T tonsurans is commonly found on humans and is, therefore, most commonly spread person-to-person. However, the organism remains viable on combs and hairbrushes and since carriers of the fungus may be either symptomatic or asymptomatic, transmission may occur by sharing hair care products or co-bedding.^5,6 Animal-to-human transmission of T tonsurans by canine dermatophytosis has also been reported.⁷ In this case, there is no known history of close contacts with similar symptoms; although the family pet is a possible carrier, scalp cultures from close contacts within the home may be helpful.

Skin lesions of tinea capitis vary depending upon the etiologic organism. T tonsurans is an endothrix hair invasion manifesting with arthroconidia that develop on the shaft of the hair causing the hair to break off close to the follicle, creating the typical black-dot lesion. Other lesions that are specifically associated with T tonsurans infection are a scaly patch and alopecia.⁸

Current literature reveals that the newer fungicidal agent, terbinafine, is more effective against dermatophytosis caused by endothrix organisms such as T tonsurans when compared to ectothrix organisms such as M canis.^2,9 Oral griseofulvin for a 4- to 6-week course has historically been the first-line pharmacologic agent for the treatment of tinea capitis; however, tinea capitis periodically undergoes demographic shifts in its therapeutic response to oral antifungals and though response rates to griseofulvin remain similar to those of the 1970s, a cure now requires higher dosing and increased length of treatment.³ Numerous studies now report that terbinafine is not only a good choice for first-line treatment but is often effective after griseofulvin failure.^3,9 Additionally, the short duration of terbinafine treatment increases patient compliance and is considerably more cost-effective.^3,9

This child was treated with a 2-week course of once-daily terbinafine, and follow-up verified complete resolution of the scalp lesion. Studies report that there are likely to be asymptomatic dermatophyte carriers among household contacts of index cases that may continue to be a reservoir for infection of other household members and even reinfection of the index case.⁶ Asymptomatic dermatophyte infection is also likely to progress to active disease at some time. Early treatment of symptomatic cases is indicated and the examination of siblings and other household members is appropriate. Household members should be instructed not to share hairbrushes, combs, hair ties, or ribbons. Antifungal shampoos should be considered for possible household asymptomatic carriers.⁸

References:

1. Bhanusali D, Coley M, Silverberg JI, Alexis A, Silverberg NB. Treatment outcomes for tinea capitis in a skin of color population. J Drugs Dermatol. 2012;11(7):852-856.

2. Vena GA, Chieco P, Posa F, Garofalo A, Bosco A, Cassano N. Epidemiology of derrmatophytoses: retrospective analysis from 2005 to 2010 and comparison with previous data from 1975. New Microbiol. 2012;35(2):207-213.

3. Grover C, Arora P, Manchanda V. Comparative evaluation of griseofulvin, terbinafine and 
fluconazole in the treatment of tinea capitis. Int J Dermatol. 2012;51(4):455-458.

4. Chapman JC, Daniel CR 3rd, Daniel JG, et al. Tinea capitis caused by dermatophytes: a 15-year retrospective study from a Mississippi Dermatology Clinic. Cutis. 2011;88(5):230-233.

5. Hryncewicz-Gwóz´dz´ A, Beck-Jendroschek V, Brasch J, Kalinowska K, Jagielski T. Tinea capitis and tinea corporis with a severe inflammatory response due to Trichophyton tonsurans. Acta Derm Venereol. 2011;91(6):708-710.

6. Pomeranz AJ, Sabnis SS, McGrath GJ, Esterly NB. Asymptomatic dermatophyte carriers in the households of children with tinea capitis. Arch Pediatr Adolesc Med. 1999;153(5):483-486.

7. Brilhante RS, Cordeinro RA, Gomes JM, Sidrim JJ, Rocha MF. Canine dermatophytosis caused by an antropophilic species: molecular and phenotypical characterization of Trichophyton tonsurans. J Med Microbiol. 2006;55(Pt 11):1583-1586.

8. American Academy of Pediatrics. Tinea capitis (ringworm of the scalp). In: Pickering LK, ed. 
Red Book: 2003 Report of the Committee on Infectious Diseases. 26th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2003:617-618.

9. Bennassar A, Grimalt R. Management of tinea capitis in childhood. Clin Cosmet Investig Dermatol. 2010;3:89-98.