Tinea capitis is also known as scalp ringworm. It is an infection caused by dermatophyte species of fungi, most often those of the genera Trichophyton and Microsporum. Some of the most common causative species in the United States are Trichophyton tonsurans, Microsporum audouinii, and Microsporum canis. The condition manifests as numerous scaly lesions and patches of broken hair on the scalp. Lesions may suppurate and evolve into kerions. Two patterns of infections are recognized: ectothrix and endothrix. An ectothrix infection involves the outside of the hair shaft, while an endothrix infection involves the inside. Tinea capitis is most commonly encountered in children, but it is also seen in adults. Contact with animals or immunosuppression (HIV, corticosteroid therapy, renal transplantation) may predispose adults to infection. Some adults have tinea capitis that went untreated in childhood.

Majocchi-like granulomas, deep ulcerated fungal infections, severe tinea capitis and corporis, and fungal nail involvement are characteristic of an inherited deficiency of CARD9 (caspase recruitment domain-containing protein 9), an inflammatory cascade-associated protein. The disorder is autosomal recessive and is most common in North Africa countries including Algeria, Morocco, and Tunisia. The infections usually begin in childhood and are caused by Trichophyton rubrum and Trichophyton violaceum. Lymphadenopathy, high IgE antibody levels, and eosinophilia are common, and the disorder can be fatal.