| • | M. audouinii (the classic “non-inflammatory” tinea capitis has been replaced by T. tonsurans as the most common cause of tinea capitis in the U.S.) |
| • | endothrix: T. tonsurans (“black dot” ringworm) |
| • | ectothrix: M. canis (“gray patch” alopecia) |
| • | some species of microsporum fluoresce yellow-green on Wood’s lamp |
inflammatory type of t. capitis
| • | ranging from a pustular folliculitis (e.g. tinea barbae) to a kerion |
| • | most commonly caused by : |
| • | zoophilic dermatophytes – M. canus |
| • | ddx: bacterial pyodermas (furunculosis, impetigo), folliculitis decalvans, perifolliculitis capitis abscedens et suffodiens |
| • | treatment – PO steroids (may reduce incidence of scarring; data show no difference in cure rates, but goal is symptom relief; dose = 1 mg/kg/day QAM for first 10-15 days of therapy) |
| • | two subtypes may result in permanent hair loss: |
Kerion:
| • | inflammatory boggy mass with pustules; |
| • | represent an exaggerated host response to fungal elements; felt to be a delayed-type hypersensitivity reaction |
| • | most commonly caused by zoophilic or geophilic dermatophyte (T. tonsurans and M. canus; in rural areas – T. verrucosum); |
Favus:
| • | a severe chronic form of tinea capitis; rarely seen in the U.S |
| • | seen in rural areas and associated with poor hygiene, poor nutrition |
| • | cup shaped yellow crusts that may progress to patches of scarring alopecia |
| • | usually Trichophyton schoenlinii |
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