Dermatophyte tinea infections

Overview

• Definition: dermatophyte (tinea) infections are superficial fungal infections confined to keratinized tissue, skin, hair, and nails, caused by species in the genera Trichophyton (the most common), Microsporum, and Epidermophyton.
• One template, many sites: the same organism family produces regional variants named for their location, corporis (body), pedis (feet), cruris (groin), capitis (scalp), and unguium (nails), so the morphology repeats even though the address changes.
• Signature look: red, annular, scaly patches and plaques, sometimes studded with pustules, with an actively advancing, raised, scaly leading edge and a clearer center.
• Why it matters: the site dictates the route of therapy, because topical drugs cannot penetrate hair follicles or the nail plate, and a topical steroid applied to an unrecognized tinea suppresses inflammation without killing the organism, producing a relapsing, atypical "incognito" plaque.

Epidemiology

• Most common dermatophytosis: tinea pedis is the most frequent presentation and follows a recognizable "two feet, one hand" distribution, bilateral on the feet but often unilateral on the hand from scratching and touching the feet.
• Reservoir for spread: untreated tinea pedis seeds onychomycosis and tinea cruris and is also a portal for bacterial cellulitis.
• Autoinoculation: a common cause of recurrent infection is spread from a tinea infection at another body site.
• Childhood exposure: tinea corporis in children commonly follows contact with an infected pet.

Risk factors

• Diabetes mellitus: an established risk factor for dermatophyte infection.
• Reduced peripheral circulation: impairs clearance and predisposes to chronic infection.
• Immune compromise: raises susceptibility to extensive or recalcitrant disease.
• Chronic maceration of skin: for example from athletic activity, promotes tinea pedis and cruris.
• Concomitant tinea pedis: a recognized risk factor for tinea cruris and onychomycosis through autoinoculation.

Pathophysiology

• Keratin-restricted growth: dermatophytes are confined to keratinized tissue, the stratum corneum, hair shaft, and nail plate, and do not invade living tissue.
• Centrifugal expansion: the organism advances outward at the rim of the lesion and leaves cleared skin behind, producing the raised, erythematous, scaly leading edge where the live organism concentrates and where a scraping should be taken.
• Steroid-suppressed relapse (tinea incognito): a topical corticosteroid calms the inflammation (redness and itch) without killing the fungus, so the rash quiets while on the steroid, then rebounds once it is stopped, and the ring blurs into an atypical, less-scaly plaque.
• Inflammatory host response (kerion): in tinea capitis, a vigorous inflammatory reaction to the organism produces a boggy, pustular, inflamed mass with regional adenopathy rather than the quiet scaly patch typical elsewhere.

Clinical features

• Tinea corporis, the reference pattern: an annular ("ringworm") plaque with central clearing and a raised, erythematous, scaly, actively advancing border; the border, not the quiet center, is where the organism lives.
• Tinea pedis: interdigital scale and maceration in the web spaces, plus scale and erythema on the soles and sides of the foot in a "moccasin" distribution, classically bilateral on the feet with unilateral hand involvement.
• Tinea cruris: arciform, polycyclic erythematous or hyperpigmented plaques over the thighs, perineum, and buttocks with a partially raised, sharply demarcated, centrifugally expanding border, typically sparing the scrotum, mildly pruritic, and often accompanied by tinea pedis.
• Tinea capitis: scaly scalp patches with "black-dot" broken hairs and occipital or posterior-cervical adenopathy, mainly in children; a boggy, pustular, inflamed mass is a kerion.
• Tinea incognito: a steroid-modified plaque that improves on a topical steroid and recurs once it is stopped, with a blurred, less scaly, atypical ring in place of the classic active border.
• Tinea unguium (onychomycosis): brittle, thickened, discolored nails from nail-plate invasion, requiring oral rather than topical therapy.

Differential diagnosis

• Plaque psoriasis: silvery-white scale over extensor surfaces, scalp, and the gluteal cleft, with pinpoint bleeding on scraping the scale (Auspitz sign), and the plaque does not clear centrally, unlike the active-bordered, centrally clearing ring of tinea.
• Granuloma annulare: an annular plaque with peripheral papules and central clearing, but scale is absent, unlike the scaly advancing border of tinea corporis, and a KOH preparation is negative.
• Nummular eczema: a filled-in "coin" of eczematous plaque without the central clearing or advancing scaly rim that defines tinea.
• Erythrasma: red-brown intertriginous patches with fine or absent scale that fluoresce coral-red under a Wood's lamp, a fluorescence dermatophyte infection does not show, and tinea cruris typically has an active scaling border, a feature uncommon in erythrasma.
• Inverse psoriasis: well-demarcated, shiny plaques confined to flexures with minimal to no scale, unlike the scaly, centrifugally expanding plaque of tinea cruris.
• Candidal intertrigo: beefy-red plaques with satellite papules and pustules that typically involve the scrotum, unlike tinea cruris, which spares the scrotum.
• Allergic contact dermatitis: dermatitis that extends beyond the intertriginous fold with an asymmetric or linear pattern tied to a specific exposure, rather than the confined, advancing annular border of tinea.
• Atopic or nummular dermatitis mimicking tinea incognito: these improve and stay improved on a topical steroid, without the off-drug rebound that marks tinea incognito.
• Alopecia areata (for tinea capitis): smooth, non-scaly patches of hair loss without the black-dot broken hairs or occipital adenopathy that accompany tinea capitis.

Diagnosis

• Clinical diagnosis, confirmed by potassium hydroxide (KOH) preparation: the annular plaque with an active scaly border establishes the clinical impression; a KOH preparation of a scraping from the active edge showing hyphae is the best initial confirmatory test.
• First, scrape the active border, not the quiet center, because the organism concentrates at the advancing rim.
• Then obtain the most accurate test if confirmation is needed: fungal culture, which is more accurate than KOH but slower to result.
• For suspected Microsporum infection, a Wood's lamp examination can support the diagnosis.
• If a plaque improved on a topical steroid and recurred once it was stopped, recognize tinea incognito and re-scrape for KOH rather than resuming steroid.

Clinical pearl. A scaly plaque that quiets on a topical steroid and rebounds once it is stopped is not resistant eczema, it is tinea incognito: the steroid muted the inflammation without killing the organism, so confirm with a KOH prep of the active edge and treat with an antifungal, never a combined antifungal-steroid cream.

Management

• First-line for limited, non-hair-bearing skin, topical antifungal: for tinea corporis or cruris, terbinafine 1% cream applied once daily for 1 week; for interdigital tinea pedis, terbinafine 1% cream applied twice daily for 1 week; for plantar or lateral-foot tinea pedis, terbinafine 1% cream applied twice daily for 2 weeks.
• If disease is hair-bearing (capitis or beard), involves the nails, or is extensive, escalate to an oral antifungal because topical drugs cannot reach the organism down the follicle or under the nail plate: griseofulvin microsize 10 mg/kg PO once daily for a representative 4 to 6 weeks for tinea capitis, continued until clinical or mycologic eradication.
• For onychomycosis confirmed by nail specimen, terbinafine 250 mg PO once daily for 6 weeks for fingernails or 12 weeks for toenails.
• Avoid two classic traps: combined antifungal-steroid creams, which breed tinea incognito by suppressing inflammation while the fungus burrows deeper, and oral ketoconazole, which is avoided for hepatotoxicity and liver failure risk.
• If a kerion is present, treat with the same oral antifungal course as tinea capitis; the boggy inflammatory mass is a host reaction to the organism, not a bacterial abscess requiring incision.

Complications

• Tinea incognito: an atypical, steroid-modified relapsing plaque from inappropriate topical steroid or combination antifungal-steroid use.
• Kerion: a boggy, pustular, inflamed mass with scarring alopecia and regional adenopathy from a vigorous inflammatory response to tinea capitis.
• Autoinoculation and spread: untreated tinea pedis reseeds tinea cruris and onychomycosis and can serve as a portal for secondary bacterial cellulitis.
• Nail destruction: onychomycosis left untreated causes progressive nail thickening, brittleness, and discoloration.

Prognosis

• Favorable with site-appropriate therapy: limited glabrous-skin infections generally clear with a short course of topical antifungal.
• Slower resolution for hair-bearing and nail disease: capitis, beard, and nail infections need weeks of oral therapy because the organism sits down the follicle or under the nail plate where topicals cannot follow.
• Prone to relapse when mismanaged: treatment with a combined antifungal-steroid cream or premature discontinuation invites tinea incognito or recurrence.

Prevention

• Treat tinea pedis promptly to remove the reservoir that seeds tinea cruris, onychomycosis, and, through skin breakdown, bacterial cellulitis.
• Avoid combined antifungal-steroid creams for any suspected tinea, since they suppress the signs of infection while letting the organism persist.
• Confirm nail or scalp infection with a specimen before starting a multi-week oral course, since griseofulvin for tinea capitis runs 4 to 6 weeks and terbinafine for onychomycosis runs 6 to 12 weeks.
• Screen for autoinoculation by examining the feet, groin, and nails whenever tinea corporis or cruris is diagnosed at one site.

Key points

• Dermatophyte infections are keratin-restricted fungal infections (Trichophyton, Microsporum, Epidermophyton) producing an annular plaque with an active, scaly advancing border and central clearing.
• The best initial test is a KOH prep of the active edge showing hyphae; fungal culture is the most accurate test.
• Treat limited glabrous skin with a topical antifungal for 1 to 2 weeks; hair-bearing skin and nails need oral terbinafine or griseofulvin for weeks because topicals cannot penetrate.
• Never use a combined antifungal-steroid cream, the classic cause of tinea incognito, and avoid oral ketoconazole for hepatotoxicity risk.
• "Two feet, one hand" tinea pedis and scrotal sparing in tinea cruris are the pattern clues that separate dermatophyte infection from its mimics.
• A kerion in tinea capitis is a host inflammatory reaction, treated with the same oral antifungal course, not incision and drainage.