Tinea capitis

Peak age 3–7 years. In the US:

• >90% of cases caused by Trichophyton tonsurans, an anthropophilic (human-to-human) dermatophyte.
• Disproportionately affects Black children (attack rates reported 10–30× higher than White children in urban US cohorts).
• Asymptomatic carriage is common (5–30% of children in some communities).
• Microsporum canis is the second most common cause globally and remains common in zoophilic (kittens, puppies) exposures.
• Adults (particularly post-menopausal women and immunosuppressed) can present with atypical tinea capitis.

Dermatophytes invade the hair shaft and follicular epithelium. Invasion patterns:

• Endothrix (inside hair shaft): T. tonsurans, T. violaceum. Hair shaft weakens → breaks at scalp level → 'black dots'. Wood's lamp negative.
• Ectothrix (outside hair shaft): M. canis, M. audouinii, T. verrucosum, T. mentagrophytes. Fluoresces green-yellow under Wood's lamp.
• Favus (historical, rare): T. schoenleinii with scutula (yellow cup-shaped crusts).

Host immune response drives inflammation (kerion). Highly inflammatory organisms (zoophilic M. canis) produce more kerion; anthropophilic T. tonsurans often produces subtler disease.

Four classic patterns (overlap common):

• Black dot (most common in US, T. tonsurans): non-inflammatory alopecia with tiny dots at the scalp where hair shafts have broken. Mild scale. Can look almost like alopecia areata but with scale and/or dots on closer inspection.
• Grey patch / seborrheic (M. canis classic): round scaly patches with hair loss/breakage; fluoresces under Wood's lamp.
• Kerion: boggy, exquisitely tender, pustular/crusted mass with scarring alopecia risk. Cervical/occipital lymphadenopathy common. Often febrile in children.
• Favus (rare in US): yellow cup-shaped crusts (scutula) with hair loss; chronic, scarring.

Associated: posterior cervical and occipital lymphadenopathy (a helpful clinical clue — scalp process without nodal reaction is less likely tinea capitis).

Critical content. This is one of the highest-yield SoC pediatric dermatoses.

• Presume tinea capitis in any Black child (US) with scalp alopecia, scale, or a scalp mass until proven otherwise.
• Textured hair makes examination harder — part the hair systematically with a comb, use bright light, look at the scalp closely. Scale can be trapped between braids/locs.
• Black dot sign: broken hair shafts visible at the scalp as tiny dots. Diagnostic when seen.
• Dermoscopy (trichoscopy) — high-yield, SoC-friendly: comma hairs, corkscrew hairs, zigzag hairs, morse code hairs, black dots. Can confirm diagnosis at the bedside without KOH.
• Post-inflammatory hyperpigmentation after kerion is common and long-lasting.
• Culturally appropriate hair care during treatment: gentle cleansing, no tight styles on inflamed scalp, communicate that the infection is not caused by hair practices.
• Asymptomatic carriers are disproportionately Black children in US community studies — screen household contacts with brush samples (sterile toothbrush swept through hair) for fungal culture.

• Black dot (endothrix, T. tonsurans): most common in US.
• Grey patch (ectothrix, Microsporum): classic Wood's lamp–positive.
• Seborrheic pattern: diffuse scale, may be subtle.
• Kerion: inflammatory, boggy, often misdiagnosed.
• Favus: rare, chronic, scutula.
• Agminate / carrier state: asymptomatic fungal culture positivity in scalp of contacts.

• Seborrheic dermatitis — greasy scale, no alopecia, no lymphadenopathy, bilateral diffuse distribution. Can coexist with tinea.
• Alopecia areata — smooth well-demarcated patch, no scale, exclamation point hairs on dermoscopy; no lymphadenopathy.
• Trichotillomania — irregular patches with hairs of varied length, no scale, normal scalp.
• Traction alopecia — marginal (hairline/temporal), styling history, can be itchy but typically no scale.
• Bacterial folliculitis / abscess — often mistaken for kerion in a Black child. Consider tinea first; obtain fungal culture before I&D.
• Scalp psoriasis — thicker silvery scale, often extends beyond hairline to forehead; bilateral.
• Atopic dermatitis (scalp) — eczematous, pruritic, no black dots.

Confirm before starting systemic antifungals — therapy is weeks long with monitoring needs.

• Fungal culture (Sabouraud agar or DTM): gold standard. Brush sample (sterile toothbrush swept through affected scalp; also for asymptomatic contacts). Results in 2–4 weeks — start empirical therapy concurrently when suspicion is high.
• KOH preparation: lower yield in tinea capitis than glabrous tinea; hyphae are inside the hair shaft. Still obtain when possible.
• Dermoscopy: bedside rule-in (comma hairs, corkscrew hairs, black dots).
• Wood's lamp: green-yellow fluorescence suggests Microsporum; T. tonsurans is non-fluorescent, so a negative Wood's lamp does NOT rule out tinea capitis.
• PCR (multiplex dermatophyte PCR): increasingly available; fast turnaround.
• Pre-treatment labs: CBC and LFTs for terbinafine; generally safe in healthy children, but obtain baseline if any concern or for courses >4 weeks.

Systemic therapy required. Topical antifungals alone do not cure tinea capitis.

• T. tonsurans (most US cases) → terbinafine 6 weeks, weight-based: <20 kg 62.5 mg/day; 20–40 kg 125 mg/day; >40 kg 250 mg/day. Well-tolerated; take with food; check baseline LFTs.
• M. canis / Microsporum → griseofulvin 20–25 mg/kg/day (ultramicrosize; use higher 25 mg/kg for microsize) x 6–8 weeks minimum; take with fatty food for absorption. Terbinafine less effective against Microsporum.
• Adjunct: selenium sulfide 2.5% shampoo or ketoconazole 2% shampoo 2–3×/week, used by patient AND household contacts, for at least 2 weeks — reduces spore shedding, limits transmission.
• Household contact management: examine and brush-culture all household children. Treat confirmed cases with oral therapy; treat asymptomatic carriers and close contacts with sporicidal shampoo.
• Re-culture at completion to document cure in children with recurrence history or poor response.

• Itraconazole 3–5 mg/kg/day x 2–4 weeks (pulse or continuous) — alternative for terbinafine-intolerant or Microsporum infections. Drug interactions common (CYP3A4).
• Fluconazole 6 mg/kg/day x 3–6 weeks — less effective than terbinafine/griseofulvin but useful in specific scenarios.
• Kerion: add prednisolone 1 mg/kg/day x 1–2 weeks (short taper) to reduce scarring risk in severely inflammatory lesions. Continue antifungal throughout.
• Treatment failure / recurrence: re-culture for susceptibility, address adherence, screen household contacts again, extend duration, consider switching agents.

Excellent for uncomplicated cases with adequate systemic therapy. Kerion may leave scarring alopecia if treatment is delayed. Recurrence occurs when household contacts are undertreated — hence the emphasis on environmental + familial decontamination. Post-inflammatory hyperpigmentation after kerion resolves over months.

• Presume tinea capitis in a Black child with scalp scale, hair loss, or mass. Biopsy + culture before I&D.
• Kerion ≠ bacterial abscess. Do not drain. Systemic antifungal ± short steroid taper.
• Wood's lamp negative ≠ not tinea. T. tonsurans (most US cases) is non-fluorescent.
• Posterior cervical / occipital lymphadenopathy is a helpful clinical clue.
• Treat the family, not just the index case. Shampoos for all household children; culture siblings.
• Terbinafine covers Trichophyton beautifully, Microsporum poorly. Match drug to organism when known.
• Id reaction during treatment: don't stop therapy; treat the id with topical steroid and continue antifungal.
• Brush culture is non-invasive and high-yield — use it liberally for contact tracing.

Your child has a fungal infection of the scalp. It is common and treatable, but requires oral medication for 6–8 weeks — shampoos alone are not enough. You (the parents) and other children in the household should use an antifungal shampoo like selenium sulfide or ketoconazole 2–3 times weekly for 2 weeks to avoid re-infection. Wash combs, brushes, hats, and pillowcases. The child can attend school once oral treatment is started. Hair loss from areas of infection typically regrows unless there was a severe kerion — in that case some scarring may remain. This infection is not caused by hair-care practices or hygiene. Return if you notice a boggy or painful mass on the scalp (may need additional anti-inflammatory treatment), or if the rash spreads.