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The image depicts a patient with a kerion. This condition begins as Tinea capitis (scalp ringworm) that undergoes a delayed-type hypersensitivity reaction to the causative fungus. This inflammation causes the initial erythematous, scaly plaque of Tinea capitis to become boggy with inflamed, purulent nodules and plaques. The hair follicle is frequently destroyed by the inflammatory process in a kerion, leading to scarring alopecia. Treatment includes long-term systemic therapy, usually with oral griseofulvin and the addition of an antibiotic to treat any secondary bacterial infection. In addition, oral corticosteroids are administered to treat the severe inflammation.
Tinea capitis is a dermatophyte (B) infection most commonly caused by Trichophyton tonsurans that is transmitted from person to person via fomites, such as a barber’s razor. Treatment with topical agents (C) is inadequate and patients require systemic therapy. The initial infection of Tinea capitis is usually painless (D) with intense pruritus at times. However, with progressive inflammation and the development of a kerion, the lesion becomes painful.
Hardin JM: Cutaneous Conditions, in Knoop KJ, Stack LB, Storrow AB, Thurman RJ (eds): The Atlas of Emergency Medicine, ed 3. New York, The McGraw-Hill Company, 2010, (Ch) 13:p 388-389.
Trovato MJ, Schwartz RA, Janniger CK. Tinea capitis: current concepts in clinical practice. Cutis. Feb 2006;77(2):93-9.
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