{
 "topic": "Tinea Capitis",
 "slug": "tinea-capitis",
 "category_id": 15088,
 "summary": "Tinea capitis: T. tonsurans vs M. canis epidemiology, endothrix/ectothrix pathophysiology, kerion recognition, and why systemic (not topical) antifungal therapy is required.",
 "written_by": "claude-sonnet",
 "references": [
  {
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 ],
 "short": [
  {
   "title": "In short",
   "content": "- Tinea capitis is a dermatophyte infection of the scalp and hair shafts, the most common cutaneous mycosis in children, occurring worldwide with a prevalence estimated at 3-13% in the pediatric population.\n- Peak age is 3-7 years; it mainly affects prepubertal children and is uncommon in infants under 6 months and postpubertal adolescents.\n- Trichophyton tonsurans causes up to 95% of US cases and is anthropophilic (human-to-human spread via infected hairs, hats, combs, theater seats, and other fomites); Microsporum canis causes under 5% of US cases and is zoophilic, almost always from contact with infected kittens or puppies.\n- Black children have the highest infection rates, for unclear reasons; boys and girls are affected equally in T. tonsurans epidemics, while M. canis affects boys more often.\n- Up to 60% of affected children are asymptomatic carriers, and asymptomatic carriage (including in adult family members) perpetuates spread and reinfection.\n- Presentations include diffuse scaling, patchy alopecia with broken-off hairs, the \"black dot\" pattern (short hairs broken at the scalp surface), and kerion - a boggy, edematous, inflammatory plaque that can scar; posterior cervical/suboccipital lymphadenopathy is common.\n- T. tonsurans causes endothrix infection (spores within the hair shaft, persisting into telogen phase, more chronic) while Microsporum species typically cause ectothrix infection (spores sheathing the hair shaft, limited to anagen phase).\n- Topical therapy is not effective because topical agents cannot penetrate the hair shaft; first-line treatment is oral griseofulvin for at least 8 weeks (some sources say 4-8 weeks) in children over 2 years, absorption improved when taken with fatty food, or terbinafine for 2-6 weeks in children over 4 years; oral fluconazole can be used under age 2.\n"
  }
 ],
 "long": [
  {
   "title": "Definition",
   "content": "Tinea capitis is a dermatophyte (mold-like fungus) infection of the scalp and hair shafts, sometimes called ringworm of the scalp.\n"
  },
  {
   "title": "Epidemiology",
   "content": "Tinea capitis is the most common cutaneous mycosis in children, occurring worldwide in all age groups, though it is largely a disease of prepubertal children, with peak occurrence at 3-7 years of age and less involvement of infants under 6 months and postpubertal adolescents. Estimated prevalence in the pediatric population is 3-13%. Black children have the highest infection rates, and Hispanic children also show higher incidence, though the reasons for these disparities are unclear. Boys and girls are affected equally in epidemics caused by T. tonsurans, whereas M. canis infection is more common in boys. As many as 60% of affected children are asymptomatic carriers.\n"
  },
  {
   "title": "Etiology",
   "content": "In the United States, Trichophyton tonsurans is responsible for up to 95% of cases; it is an anthropophilic (human-to-human) organism acquired through direct contact with an infected person, or via contaminated fomites such as hairbrushes, combs, hats, clothing, theater seats, and other furniture, and can also be airborne within the immediate environment - high carriage rates have been found among noninfected schoolmates. Microsporum canis, a zoophilic organism, accounts for under 5% of US cases and is acquired almost entirely through contact with infected pets, especially kittens and puppies; school or child-care outbreaks have followed visits from infected animals. Microsporum audouinii, once a leading cause in the US, is now rarely implicated, while Trichophyton violaceum is the dominant organism in eastern Europe and South Asia and is seen more often in immigrant populations in the US. Susceptibility is increased by poor hygiene, prolonged skin moisture, and minor scalp injury. Asymptomatic carriage, particularly among adult family members of infected children, is an important reservoir for reinfection and further spread.\n"
  },
  {
   "title": "Pathophysiology",
   "content": "Dermatophyte spores infect the hair shaft in one of two patterns. T. tonsurans produces an endothrix infection, with spores located within the hair shaft; this infection can persist past the anagen (growth) phase into telogen, making it more chronic. Microsporum species and some Trichophyton species instead produce an ectothrix infection, with spores distributed in a sheath around the outside of the hair shaft; ectothrix infections persist only during the anagen phase, making them comparatively self-limited.\n"
  },
  {
   "title": "Clinical Features",
   "content": "Presentation is variable and can include diffuse scaling with little alopecia, diffuse pustule formation, patchy hair loss with scaling, the \"black dot\" pattern (well-demarcated alopecia with hairs broken off at the scalp surface, especially characteristic of T. tonsurans), or a kerion - a boggy, edematous, inflammatory plaque that can be tender, and which risks scarring alopecia if untreated. Posterior cervical and suboccipital lymphadenopathy is a common accompanying finding and is a useful clue favoring tinea capitis over other causes of alopecia.\n"
  },
  {
   "title": "Diagnostics",
   "content": "Tinea capitis should be considered whenever a child has patchy alopecia or stubby, broken hair growth, even without visible crusting, scaling, redness, or other inflammatory signs, and especially when accompanied by regional lymphadenopathy. Mycologic examination should be performed, looking particularly for T. tonsurans; lesions are often more elevated than other forms of tinea and may show the black-dot pattern. Diagnosis can be difficult clinically alone given the range of presentations.\n"
  },
  {
   "title": "Differential Diagnosis",
   "content": "The main alternatives to consider in a child with scalp hair loss are seborrheic dermatitis and atopic dermatitis (both more common than tinea capitis in children), alopecia areata (in which crusting, scaling, or redness are absent since inflammation is not typical), and psoriasis.\n"
  },
  {
   "title": "Treatment",
   "content": "Topical antifungal therapy is not effective for tinea capitis because topical medications cannot adequately penetrate the hair shaft to reach the fungus; systemic therapy is required. First-line treatment is oral griseofulvin, given for at least 8 weeks (one source specifies 4-8 weeks) in children over 2 years of age, with absorption improved when taken with fatty foods. Oral terbinafine for 2-6 weeks is an alternative in children over 4 years of age. In children under 2 years, oral fluconazole can be used; topical azole (e.g., clotrimazole) or allylamine (e.g., terbinafine) therapy may be effective in this age group only if the hairs affected are fine. Because asymptomatic carriers (including affected family members) can cause reinfection and continued spread, carrier screening and consideration of treatment is warranted, particularly among adults exposed to an infected child.\n"
  },
  {
   "title": "Complications",
   "content": "Untreated or inflammatory (kerion-type) infection can progress to scarring alopecia. Tinea capitis is among the most common causes of acquired hair loss in children.\n"
  }
 ],
 "clinical": [
  {
   "title": "Recognizing and Confirming Tinea Capitis",
   "content": "Suspect tinea capitis in a school-age child (peak 3-7 years) with patchy alopecia, broken or stubby hairs, scalp scaling, or a boggy inflammatory plaque (kerion), particularly when accompanied by posterior cervical or suboccipital lymphadenopathy - consider it even when classic crusting or redness is absent. Perform a mycologic examination looking for T. tonsurans, the cause of up to 95% of US cases; ask about contact with kittens or puppies if M. canis (zoophilic) is suspected, and about contact with other affected children, shared combs/hats/hairbrushes, or affected family members for T. tonsurans (anthropophilic) exposure. Because up to 60% of children with tinea capitis are asymptomatic carriers, and adult family members can also be asymptomatic carriers who perpetuate reinfection, consider screening close contacts when a child has recurrent infection.\n"
  },
  {
   "title": "Treating Tinea Capitis",
   "content": "Do not use topical antifungals alone - they cannot penetrate the hair shaft and will not clear the infection. Start oral griseofulvin (first-line) for at least 8 weeks in children over 2 years of age, advising administration with fatty food to improve absorption; oral terbinafine for 2-6 weeks is an alternative in children over 4 years. In children under 2 years, use oral fluconazole; topical azole (e.g., clotrimazole) or allylamine (e.g., terbinafine) therapy is an option in this youngest age group only when the affected hairs are fine. Manage a kerion with the same systemic antifungal therapy - most patients, including those with a boggy, fluctuant-appearing kerion and tender regional adenopathy, respond well to griseofulvin without needing incision or drainage. Counsel families about hygiene measures and shared-object precautions (combs, hats, brushes, bedding) to reduce spread to other household members and contacts.\n"
  }
 ]
}