Tinea Kapitis

01Pathophysiology

Tinea capitis is a superficial dermatophyte infection of the scalp, hair follicles, and hair shafts. The causative organisms are keratinophilic fungi that produce keratinases, enzymes that digest keratin in the stratum corneum and the hair shaft itself. This is why the infection targets keratinized structures rather than deeper tissues.

Once the dermatophyte reaches the hair follicle, it invades the hair shaft in one of two patterns. In endothrix invasion (characteristic of Trichophyton tonsurans), the arthroconidia proliferate inside the hair shaft, replacing its internal structure. This weakens the hair so severely that it fractures at or just below the scalp surface, leaving behind the "black dot" stumps that are visible on examination. In ectothrix invasion (characteristic of Microsporum species), the arthroconidia coat the outside of the hair shaft, destroying the cuticle. These hairs typically break a few millimeters above the scalp, producing the classic "grey patch" appearance with visible short stubs.

The kerion is a frequently tested complication and represents a type IV delayed-type hypersensitivity reaction to fungal antigens, not a bacterial abscess. The vigorous immune response causes a boggy, erythematous, tender mass studded with pustules and sometimes draining sinuses. The pustules contain sterile material, not pus from a bacterial infection. This distinction is critical because the management of a kerion is antifungal therapy, not incision and drainage. If the kerion is left untreated or mismanaged, scarring alopecia can result from destruction of the hair follicles by the inflammatory response.

The reason posterior cervical lymphadenopathy is so commonly associated with tinea capitis is the immune system's response to the fungal antigens draining from the scalp. This finding, combined with alopecia and scaling in a child, should immediately raise suspicion for this diagnosis.

A related concept is the dermatophytid reaction (also called an "id reaction"), which is a secondary hypersensitivity eruption at a site distant from the primary infection. The patient develops a pruritic, vesicular rash (often on the hands or trunk) that is fungus-free on KOH prep. This occurs because circulating fungal antigens trigger an immune response elsewhere. The treatment is to treat the primary tinea infection, not the secondary eruption.

02Classification and Clinical Manifestation

03Diagnostic Workup

The diagnostic approach begins with KOH preparation because it is fast, cheap, and provides an immediate answer at the bedside. The technique requires collecting the right specimen: pluck broken or abnormal-looking hairs (do not cut them) and scrape the scales from the active, advancing border of the lesion. Dissolving these specimens in 10 to 20% KOH and examining under light microscopy reveals hyphae and spores. A positive KOH is sufficient to start treatment.

Fungal culture is ordered simultaneously because it identifies the exact organism, which can guide treatment selection (griseofulvin for Microsporum, terbinafine for Trichophyton) and help with contact tracing. The culture takes 2 to 4 weeks. Dermatophyte test medium (DTM) is a rapid alternative that turns red in the presence of dermatophytes, though it does not speciate as reliably.

The Wood's lamp is useful as a quick screening tool, but students must remember its limitation: it only detects Microsporum infections (which produce pteridine, the fluorescent metabolite). Since T. tonsurans accounts for the majority of cases in North America and does not fluoresce, a negative Wood's lamp is a common finding and should never be used to exclude tinea capitis. This is one of the most tested points on this topic.

04Management and Treatment

The single most important concept to understand about tinea capitis management is that topical antifungal therapy alone is never sufficient. The infection resides within the hair follicle and hair shaft, which topical agents cannot penetrate adequately. Systemic therapy is required in every case. Topical antifungal shampoos are used only as adjuncts to reduce fungal burden on the scalp surface and limit transmission to close contacts.

Griseofulvin has historically been the standard first-line agent and remains the drug of choice for Microsporum infections. It works by inhibiting fungal mitosis through disruption of the mitotic spindle. A critical teaching point is that griseofulvin is lipophilic and requires fatty food for adequate gastrointestinal absorption. Exam questions may present a child who is "not improving" on griseofulvin, and the answer often involves asking about whether the medication is being taken with meals. The treatment course is 6 to 8 weeks, and it should be continued for 2 weeks beyond clinical resolution to prevent relapse.

Terbinafine is now preferred for Trichophyton infections because clinical trials demonstrate higher cure rates and shorter treatment duration compared to griseofulvin for this genus. It works by inhibiting squalene epoxidase, an enzyme in the ergosterol synthesis pathway. It does not require fatty food for absorption. Baseline liver function tests should be obtained before starting either griseofulvin or terbinafine, with repeat testing if the course exceeds 8 weeks or if the patient develops symptoms of hepatotoxicity (nausea, jaundice, fatigue).

For the kerion, the management is straightforward but frequently tested: treat with systemic antifungals, not surgery. A short course of oral corticosteroids (prednisone 1 to 2 mg/kg/day tapered over 1 to 2 weeks) may be added to decrease inflammation and reduce the risk of permanent scarring alopecia. If there is concern for secondary bacterial superinfection (spreading cellulitis, worsening despite antifungal therapy), antibiotics can be added, but incision and drainage is never indicated.

Household contacts should be examined, and asymptomatic carriers (common in families of affected children) can be treated with antifungal shampoo alone. Fomites such as combs, brushes, hats, and pillowcases should be cleaned or discarded.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on tinea capitis questions falls into three categories.

First, the kerion trap. A vignette will describe a child with a boggy, purulent scalp mass and will tempt the student to select "incision and drainage" or "oral antibiotics" as the next best step. The correct answer is systemic antifungal therapy. The pustules of a kerion are sterile (the result of an immune reaction), and surgical drainage worsens the condition and increases scarring risk. Recognize the boggy, non-fluctuant quality and the history of preceding scalp scaling or alopecia as the discriminating features.

Second, the Wood's lamp trap. A question may present a child with classic tinea capitis and state that the Wood's lamp examination is negative. Students may incorrectly rule out the diagnosis. Remember that T. tonsurans, the most common organism, does not fluoresce. A negative Wood's lamp is expected and does not exclude tinea capitis.

Third, the topical-only trap. A vignette may describe a child started on topical clotrimazole or ketoconazole cream who is not improving after several weeks. The answer is to switch to or add systemic antifungal therapy. Topical monotherapy cannot reach the fungal organisms within the hair shaft and follicle. Every case of tinea capitis requires oral treatment.

The core competency being tested across all tinea capitis questions is pattern recognition in pediatric alopecia: the combination of patchy hair loss + scalp scaling + broken hairs + posterior cervical lymphadenopathy in a prepubertal child should trigger this diagnosis. From there, the exam tests whether you know that systemic therapy is mandatory, that the kerion is not an abscess, and that a negative Wood's lamp does not change the diagnosis.