Dermatology · PANCE / PANRE

Tinea Infections (corporis, capitis, pedis, cruris, versicolor)

Superficial dermatophyte (and Malassezia) infections of skin, hair, and nails with site-specific presentations.

Also known as: tinea, ringworm, dermatophytosis, athlete's foot, jock itch, tinea versicolor, pityriasis versicolor

Overview

Superficial fungal infections of keratinized tissue. Dermatophyte tineas (Trichophyton, Microsporum, Epidermophyton) cause classic ringworm of body (corporis), scalp (capitis), feet (pedis), groin (cruris), hands (manuum), and nails (unguium/onychomycosis). Tinea versicolor (pityriasis versicolor) is caused by Malassezia furfur — a yeast, not a true dermatophyte.

Epidemiology

Tinea pedis is the most common dermatophytosis worldwide (~10% point prevalence). Tinea capitis predominantly affects prepubertal children, especially Black children in the US (Trichophyton tonsurans). Tinea versicolor is common in adolescents and young adults in humid climates.

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Question 1DermatologyEasy
A 7-year-old child has a circular scaly erythematous lesion with central clearing on his arm. KOH preparation of skin scraping shows septate hyphae. Which of the following is the most likely diagnosis?
  • AAtopic dermatitis
  • BPityriasis rosea
  • CTinea corporis
  • DNummular eczema
Reveal answer & full explanation
Correct answer: C — Tinea corporis
  • AAtopic dermatitis
  • BPityriasis rosea
  • CTinea corporis
  • DNummular eczema

Why Tinea corporis is correct

  • Tinea corporis (ringworm): dermatophyte infection caused by Trichophyton, Microsporum, or Epidermophyton species
  • Presents as an annular plaque with central clearing, raised scaly border, and occasionally pustules
  • KOH preparation showing septate, branching hyphae is the key diagnostic finding
  • Treatment: topical antifungal for 2–4 weeks (clotrimazole, terbinafine, ketoconazole)

Why the others are wrong

  • Atopic dermatitis — pruritic flexural eczema; does not present as a ring-shaped lesion with central clearing; KOH negative
  • Pityriasis rosea — begins with a herald patch, then a Christmas-tree distribution on the trunk; KOH negative
  • Nummular eczema — coin-shaped pruritic plaques but without central clearing; KOH negative

Additional high-yield points

  • Tinea capitis (children): scaly scalp, hair loss, kerion (boggy inflammatory mass); requires systemic treatment with griseofulvin or terbinafine for 6–8 weeks
  • Tinea pedis: athlete's foot
  • Tinea cruris: jock itch
  • Tinea unguium (onychomycosis): nail infection requiring systemic terbinafine for 6–12 weeks
Question 2DermatologyMedium
A 36-year-old woman has annular plaques with central clearing on the thigh. KOH preparation shows branching septate hyphae. Which of the following is the most appropriate treatment?
  • ATopical permethrin cream
  • BTopical terbinafine cream
  • COral acyclovir capsules
  • DTopical mupirocin ointment
Reveal answer & full explanation
Correct answer: B — Topical terbinafine cream
  • ATopical permethrin cream
  • BTopical terbinafine cream
  • COral acyclovir capsules
  • DTopical mupirocin ointment

Why Topical terbinafine cream is correct

  • Annular plaques with central clearing plus septate branching hyphae on KOH confirm tinea corporis.
  • Terbinafine is fungicidal against dermatophytes and is first-line for localized disease.
  • A topical agent suffices when only limited, non-hair-bearing skin is involved.

Why the others are wrong

  • Topical mupirocin ointment — Mupirocin targets gram-positive bacteria for impetigo and has no antifungal action; a rash-treatment trap.
  • Oral acyclovir capsules — Acyclovir treats herpesvirus, which causes grouped vesicles, not KOH-positive plaques.
  • Topical permethrin cream — Permethrin kills scabies mites and lice, not dermatophytes.
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Risk factors

  • Warm humid climates, occlusive footwear, sweating
  • Communal showers, gyms, pools, wrestling/martial arts ('tinea gladiatorum')
  • Diabetes mellitus, obesity, immunosuppression
  • Topical corticosteroid use (tinea incognito — masked inflammation, spreading edge)
  • Animal exposure (Microsporum canis — kittens, puppies; zoonotic kerion)
  • Family member with tinea capitis (shared combs, hats)

Pathophysiology

Dermatophytes secrete keratinases that allow invasion of stratum corneum, hair, and nail. Inflammation results from host immune response; minimal inflammation in immunosuppressed → 'tinea incognito' under steroids. Malassezia is a lipophilic yeast colonizing sebaceous skin; conversion from yeast to mycelial form produces clinical pityriasis versicolor; azelaic acid produced by the organism inhibits melanocytes (hypopigmentation).

Clinical presentation

Symptoms

  • Pruritus (mild to moderate)
  • Scalp scaling, hair loss (capitis)
  • Burning, fissuring between toes (pedis)
  • Cosmetic concerns (versicolor)

Signs / physical exam

  • Tinea corporis: annular erythematous plaque with raised scaly active border and central clearing; satellite lesions if extensive
  • Tinea capitis: scaly patches with broken hairs ('black dot' pattern from endothrix T. tonsurans); kerion = boggy inflammatory mass with pustules and lymphadenopathy; favus = yellow scutula crusts
  • Tinea pedis: interdigital maceration and fissuring (most common); moccasin pattern (chronic hyperkeratosis covering plantar/lateral foot); vesiculobullous (acute inflammatory)
  • Tinea cruris: erythematous scaly plaques in inguinal folds extending to medial thighs, SCROTUM SPARED (vs candida — scrotum involved)
  • Tinea manuum: 'two feet-one hand' syndrome — dry hyperkeratotic palm
  • Onychomycosis: yellow/white nail discoloration, subungual hyperkeratosis, onycholysis, dystrophy (distal subungual most common)
  • Tinea versicolor: hypo- or hyperpigmented finely scaling macules and patches on upper trunk, neck, shoulders; 'fawn-colored' or pink in untanned skin

Classic findings

Active raised scaly border with central clearing (corporis); KOH 'spaghetti and meatballs' (versicolor); Wood's lamp yellow-green fluorescence (Microsporum tinea capitis).

Differential diagnosis

  • Nummular eczema — Coin-shaped, no central clearing, KOH negative
  • Psoriasis — Silvery scale, extensor surfaces, nail pitting
  • Seborrheic dermatitis — Greasy scale in seborrheic distribution
  • Pityriasis rosea — Herald patch + Christmas-tree truncal eruption
  • Erythrasma (groin/folds) — Coral-red Wood's lamp fluorescence (Corynebacterium minutissimum); thin brown patches; treat with erythromycin/clindamycin
  • Granuloma annulare — Smooth annular skin-colored to violaceous papules without scale; KOH negative
  • Alopecia areata (vs tinea capitis) — Smooth bald patches without scale, exclamation point hairs, no broken hairs at scalp; KOH/culture negative
  • Vitiligo (vs tinea versicolor) — Complete depigmentation, no scale, Wood's lamp bright milky white fluorescence

Diagnostic workup

Diagnostic criteria

KOH and/or culture positivity in characteristic clinical setting.

Labs

  • KOH preparation of scale or hair: branching septate hyphae (dermatophyte) or short hyphae + spores ('spaghetti and meatballs') for versicolor
  • Fungal culture (Sabouraud or DTM agar) — confirms species, especially for capitis and onychomycosis before systemic therapy
  • Wood's lamp: blue-green fluorescence with Microsporum tinea capitis (T. tonsurans is non-fluorescent); pale yellow with versicolor; coral-red with erythrasma
  • PAS-stained nail clipping or PCR for onychomycosis diagnosis
  • Baseline LFTs before oral terbinafine or itraconazole

Imaging

  • Not indicated

Diagnostic algorithm

VariantSite / LesionPreferred Therapy
Corporis (ringworm)Annular plaque, raised scaly border, central clearingTopical azole or terbinafine 2-4 wks
CapitisScaly scalp, broken hairs, ± kerionOral terbinafine or griseofulvin × 4-8 wks + antifungal shampoo
PedisInterdigital maceration; moccasin hyperkeratosisTopical terbinafine; oral if moccasin/extensive
CrurisInguinal scaly plaques sparing scrotumTopical azole or terbinafine
OnychomycosisYellow nail, subungual debris, onycholysisOral terbinafine 6 wks (fingers) / 12 wks (toes)
VersicolorHypo/hyperpigmented finely scaling macules on trunkSelenium sulfide or ketoconazole shampoo; oral itraconazole if extensive
Tinea variants and first-line therapy.

Treatment

First-line

  • Tinea corporis / cruris / pedis (limited): topical antifungal — clotrimazole 1% BID, ketoconazole 2% BID, terbinafine 1% BID, ciclopirox 0.77% BID — continue 1-2 weeks beyond clinical resolution (typically 2-4 weeks)
  • Tinea pedis (moccasin or extensive): oral terbinafine 250 mg daily × 2 weeks OR oral itraconazole 200 mg BID × 1 week pulse
  • Tinea capitis (REQUIRES SYSTEMIC): oral griseofulvin (microsize) 20-25 mg/kg/day × 6-8 weeks (preferred for Microsporum) OR oral terbinafine 3-6 mg/kg/day × 4-6 weeks (preferred for Trichophyton tonsurans, more common in US); adjunctive selenium sulfide or ketoconazole shampoo 2-3x/wk reduces shedding and transmission
  • Onychomycosis: oral terbinafine 250 mg daily × 6 weeks (fingernails) or 12 weeks (toenails) — most effective; alternatives: itraconazole pulse, fluconazole weekly; topical efinaconazole or tavaborole if oral contraindicated
  • Tinea versicolor: topical selenium sulfide 2.5% lotion, ketoconazole 2% shampoo, or clotrimazole — lather, leave 10 min, rinse — daily × 1-2 weeks; or oral itraconazole 200 mg/day × 5-7 days for widespread/refractory (avoid oral fluconazole single-dose regimens that were once popular — relapse common)

Kerion (inflammatory tinea capitis)

  • Oral antifungal (terbinafine or griseofulvin) PLUS short course oral prednisone 0.5-1 mg/kg/day × 5-10 days to reduce scarring alopecia
  • Antibiotic only if bacterial superinfection — DO NOT drain kerion (sterile inflammation)

Tinea incognito (steroid-modified)

  • Discontinue topical corticosteroid
  • Treat with appropriate antifungal — often requires systemic therapy because of extensive subclinical spread

Second-line / adjunct

  • Avoid systemic ketoconazole due to hepatotoxicity and adrenal suppression risk (FDA boxed warning)
  • Recheck culture and consider drug resistance (e.g., Trichophyton indotineae — emerging terbinafine-resistant species)
  • Counsel on hygiene: clean and dry skin folds, antifungal foot powder, change socks, treat shoes with antifungal spray

Complications

  • Scarring alopecia from untreated kerion
  • Bacterial superinfection (impetigo, cellulitis), especially with maceration
  • Onychomycosis: chronic relapsing course, gateway for cellulitis in diabetics
  • Id reaction (autoeczematization): vesicular dermatitis on hands during active tinea pedis — sterile, immune-mediated
  • Terbinafine adverse effects: hepatotoxicity, taste disturbance, drug interactions (CYP2D6)
  • Itraconazole adverse effects: heart failure exacerbation, drug interactions (potent CYP3A4 inhibitor)

PANCE pearls

  • Tinea cruris spares the scrotum; candida intertrigo involves the scrotum with satellite pustules — quick distinguishing feature.
  • Pruritic annular plaque with central clearing and active border = tinea corporis until proven otherwise — KOH first, treat empirically only if KOH unavailable.
  • NEVER use topical betamethasone/clotrimazole combination (Lotrisone) — the steroid potency is too high for the skin folds where it is commonly used; causes atrophy and tinea incognito.
  • Tinea capitis is the only superficial fungal infection that REQUIRES systemic therapy — topicals will not penetrate hair shaft.
  • Tinea versicolor responds to therapy but pigment changes can take months to fade — counsel patients to avoid attributing relapse to treatment failure.

References

  • AAD 2014 — Guidelines of Care for Superficial Mycotic Infections of the Skin: Tinea Corporis, Tinea Cruris, Tinea Pedis (Drake et al.; updated standards)
  • Cochrane 2016 — Systemic Antifungal Therapy for Tinea Capitis in Children (Chen et al., Cochrane Database Syst Rev 2016)
  • AAFP 2014 — Diagnosis and Management of Tinea Infections (Ely, Rosenfeld, Stone, Am Fam Physician 2014)

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