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Fungal skin infection - scalp

SNOMED: 402798004748 words•Updated 03/03/2026
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Exam Tips

  • In a child with patchy alopecia plus scaling, think tinea capitis first; oral treatment is required because topical monotherapy does not penetrate infected hair shafts.
  • Black dots (broken hairs), posterior cervical/post-auricular nodes, and contact history strongly support the diagnosis.
  • Kerion is an urgent dermatology referral because delayed treatment risks irreversible scarring alopecia.
  • Take scalp/hair samples before or at treatment start and use species result to refine choice (Trichophyton often terbinafine-responsive; Microsporum often griseofulvin-responsive).
  • Always assess and manage household transmission (siblings, asymptomatic carriers, shared fomites, pets) to reduce recurrence.
  • Trichoscopy clues (comma/corkscrew hairs) are high-yield image-based exam findings; see figure of dermoscopic signs in your dermatology revision text.

Definition

Tinea capitis is a dermatophyte infection of scalp hair shafts, follicles, and surrounding skin, seen mainly in prepubertal children in the UK. It is usually caused by Trichophyton tonsurans (human-to-human spread) or Microsporum canis (often animal-associated), and presents as scaly scalp disease with patchy alopecia that may become inflammatory (kerion) and scar if treatment is delayed.

Pathophysiology

Infective spores are transmitted by direct contact, shared fomites (for example hats/brushes), or animal exposure, then colonize stratum corneum and invade hair shafts. Hyphae proliferate within or around hair (endothrix invasion is typical of Trichophyton and contributes to 'black dot' broken hairs; ectothrix invasion is more typical of Microsporum and may fluoresce under Wood's light). Host inflammatory response determines phenotype: mild scaling/non-inflammatory disease versus intense delayed hypersensitivity with pustules and boggy kerion. Untreated inflammation can damage follicles permanently, causing cicatricial alopecia.

Risk Factors

  • Age 3-7 years (prepubertal child)
  • Close contact with infected children in household/school
  • Asymptomatic carrier in family (especially siblings)
  • Sharing combs, brushes, hats, pillows, hair accessories
  • Contact with infected cats/dogs or other animals (zoophilic dermatophytes)
  • Afro-Caribbean ethnicity in UK epidemiology
  • Overcrowded settings and humid environments
  • Immunosuppression (including atypical or persistent infection)

Clinical Features

Symptoms

  • Itchy scalp
  • Scalp tenderness or pain in inflammatory disease
  • Parental concern about patchy hair loss
  • Occasionally asymptomatic (carrier state)

Signs

  • Diffuse or patchy scalp scaling
  • Single or multiple asymmetrical alopecic patches
  • Black dot alopecia from broken hair stubs
  • Erythema, pustules, crusting
  • Kerion: boggy, painful inflammatory plaque/mass with crust
  • Post-auricular or cervical lymphadenopathy
  • Possible eyebrow/eyelash involvement
  • Associated dermatophyte lesions on trunk/limbs

Investigations

Scalp scrapings and epilated/broken hairs for microscopy (KOH) and fungal culture:Microscopy may show hyphae/arthrospores in 1-2 days; culture identifies species (for example T. tonsurans or M. canis) in about 2-3 weeks and guides oral drug choice
Toothbrush/cytobrush sampling (if child cannot tolerate scraping or for carrier screening):Culture-positive dermatophyte in asymptomatic contacts/carriers; microscopy not usually possible from brush sample
Wood's light (selective use, not routine in primary care):Some Microsporum infections fluoresce yellow-green; Trichophyton tonsurans typically does not fluoresce
Dermoscopy/trichoscopy (where trained operator available):Comma hairs, corkscrew hairs, broken hairs, and black dots support diagnosis and can help monitor response (see figure in dermatology text showing trichoscopic signs of tinea capitis)

Management

Lifestyle Modifications

  • Start treatment promptly and advise that scalp ringworm is contagious until adequately treated
  • Do not share combs, brushes, hats, bedding, or hair tools; wash textiles and clean hair equipment
  • Screen household members/close contacts for symptoms and consider sampling for carriers
  • Check pets (especially cats/dogs) for dermatophyte infection and arrange veterinary assessment if suspected
  • Explain that topical creams alone are insufficient for scalp infection because hair shaft penetration requires systemic therapy

Pharmacological Treatment

Systemic antifungal (first-line options in children)

  • Terbinafine oral once daily by weight: 10-20 kg 62.5 mg, 20-40 kg 125 mg, over 40 kg 250 mg (commonly 4 weeks for Trichophyton, longer if needed)
  • Griseofulvin oral (licensed in children): typically 10 mg/kg once daily (can be increased up to 20 mg/kg daily in severe/refractory disease; max 1 g/day), usually 6-8 weeks or until mycological cure

Choose agent according to likely/confirmed species: terbinafine generally better for Trichophyton; griseofulvin often preferred for Microsporum. Send mycology before treatment where possible. Contraindications/warnings: terbinafine—avoid in chronic or active liver disease; counsel re hepatotoxicity symptoms and serious rash. Griseofulvin—avoid in pregnancy, porphyria, severe liver failure; enzyme induction can reduce efficacy of combined hormonal contraception.

Alternative systemic antifungal (specialist or if first-line unsuitable/fails)

  • Itraconazole oral (child dosing often 5 mg/kg/day; specialist regimen)
  • Fluconazole oral (child dosing often 6 mg/kg/day; specialist/off-label context)

Use when organism, tolerance, comorbidity, or response necessitates alternative therapy. Important safety: itraconazole has major CYP3A4 drug interactions and is contraindicated in heart failure risk; both agents require interaction checks and liver safety consideration.

Adjunctive topical reduction of spore shedding

  • Ketoconazole 2% shampoo twice weekly for 2-4 weeks (patient and often close contacts/carriers)

Adjunct only; does not cure scalp hair infection on its own. Useful to reduce transmission while systemic treatment takes effect.

Surgical / Interventional

  • No routine surgical treatment; incision and drainage of kerion is not indicated

Complications

  • Secondary bacterial infection (including impetiginization/cellulitis)
  • Kerion with pain and marked inflammation
  • Scarring alopecia and permanent hair loss
  • Post-inflammatory pigment change
  • Dermatophytid (id) reaction with itchy papules/vesicles (often ear helix, trunk, limbs)
  • Rare erythema nodosum

Prognosis

With timely diagnosis and appropriate oral antifungal treatment, prognosis is usually excellent and hair regrowth is expected. Delayed treatment, severe inflammatory kerion, poor adherence, untreated contacts/carriers, or immunosuppression increase risk of persistence, recurrence, and permanent alopecia.

Sources & References

đź’ŠBNF Drug References(4)

âś…NICE Guidelines(1)

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