Tinea and fungal skin infection — structured clinical encounter

Station 1 — recognition and confirmation

Asked for my first impression, I would recognise this as tinea capitis. The broken hair stubs and the black dots flush with the scalp are hair broken off at the surface, the endothrix pattern typical of Trichophyton tonsurans, and the enlarged occipital node favours a fungal scalp infection over a non-infectious dermatosis such as alopecia areata, which is smooth and non-scaly with exclamation-mark hairs and no nodes. I would confirm with potassium hydroxide microscopy of a plucked hair looking for branching septate hyphae and arthroconidia, and send fungal culture to identify the species. [1]

Station 2 — the oral-therapy principle

Asked how I would treat it, I would state that tinea capitis always needs an oral antifungal because the fungus lives inside the hair shaft and a topical cream cannot penetrate the follicle. A topical alone would fail, the hair loss would continue, and the child would keep spreading spores. I would therefore start an oral agent — griseofulvin or terbinafine, guided by the species — rather than a cream. [2]

Station 3 — the species-guided drug choice

Asked which drug for a confirmed Trichophyton tonsurans in a 22 kg child, I would choose terbinafine. The meta-analyses show terbinafine is superior for Trichophyton species and griseofulvin is superior for Microsporum species. Using the weight bands of 62.5 mg daily under 20 kg, 125 mg daily for 20 to 40 kg and 250 mg daily over 40 kg, a 22 kg child takes 125 mg daily for 4 weeks. If the organism were Microsporum I would switch to griseofulvin at 10 mg/kg/day microsize for 6 to 8 weeks, because griseofulvin is superior for that genus. [4] [5]

Station 4 — household carrier screening

Asked how I would prevent recurrence, I would explain that recurrence after an adequate oral course almost always reflects an untreated reservoir: asymptomatic scalp carriage in household contacts and an untreated pet. I would screen and treat the family contacts, use an antifungal shampoo such as ketoconazole to reduce spore shedding, and have a veterinarian examine any pets. For a zoophilic organism I would specifically ask about kittens and puppies as the source, because an untreated animal will reinfect the treated child within weeks. [10]

Station 5 — the kerion and the steroid pitfall

Finally I describe how I would handle a four-year-old with a painful, boggy, purulent, inflamed scalp mass two weeks after the family acquired a kitten. I would recognise this as a kerion, an intense delayed hypersensitivity reaction to a zoophilic dermatophyte, most likely Microsporum canis. I would start an oral antifungal immediately and add a short tapering course of oral corticosteroid to reduce the inflammation and the risk of permanent scarring alopecia, and I would explicitly avoid incision and drainage because the pus is inflammatory rather than a drainable bacterial abscess. I would also warn against using a topical corticosteroid on any unrecognised scaly annular lesion, because it produces tinea incognito: it suppresses the border and itch while allowing unchecked fungal spread, leaving an atrophic, pustular lesion that is harder to recognise and to treat. [1] [2] [6]