Dermatophyte infection by body site

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Name disease by site because depth and drug delivery change. Examine scalp, hair, nails, palms, soles, groins and other plaques rather than treating the reported spot in isolation. In darker skin, erythema may be brown, violaceous or grey and central hyperpigmentation can conceal the active border; scale, edge elevation, broken hair and distribution remain reliable.

Mycology is most important before systemic treatment, when appearance is altered by steroid, when diagnosis is uncertain or when a result changes contact investigation. Clean the site, stop topical antifungal briefly if clinically safe, and sample abundant keratin from the advancing edge. A negative result does not exclude fungus if sampling is poor or treatment preceded it; repeat from a better site rather than assuming resistance.

Local glabrous skin often responds to topical terbinafine or an azole. Hair and usually nail disease require systemic therapy based on species, age, interactions and organ safety. Griseofulvin remains useful for some Microsporum scalp infections, while terbinafine is effective for many Trichophyton infections. Follow current local dermatology and microbiology advice rather than guessing from appearance alone.

Key points

Tinea corporis is annular with an advancing scaly edge; cruris affects groin folds, pedis affects toe webs or sole, and manuum often produces one dry scaly palm with two affected feet.
Tinea capitis causes scale, broken hairs, black dots or alopecia and always needs systemic treatment; topical cream alone cannot reach infected hair shafts.
A boggy pustular kerion risks permanent scarring and needs urgent systemic treatment, bacterial assessment and dermatology input.
Take skin scrapings from the active untreated edge, plucked abnormal hairs for scalp disease and nail clippings plus subungual debris before systemic treatment.
For localised skin infection, terbinafine 1% cream once or twice daily for one to two weeks is usually effective; follow the exact product and site licence.
Confirm nail fungus before oral therapy and distinguish dermatophyte species where drug choice differs, especially scalp infection.
Avoid steroid–antifungal combination prescribing without a defined inflammatory indication and short plan; steroid alone produces tinea incognito.
Dry toe webs, change socks and footwear, avoid shared towels and treat infected household members or animals when confirmed rather than disinfecting indiscriminately.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Anthropophilic dermatophytes

Human-adapted Trichophyton species spread through skin contact, floors, footwear, combs and shared equipment and often cause relatively chronic inflammation.

Zoophilic and geophilic exposure

Animal- or soil-associated species can produce more inflamed lesions; pets and occupational exposure belong in the history and public-health plan.

Barrier and moisture

Maceration, sweating, occlusive footwear, minor trauma, diabetes and immune suppression favour invasion of keratinised stratum corneum, hair or nail.

Steroid modification

Topical corticosteroid suppresses the raised inflammatory edge while fungus expands, creating tinea incognito with less scale and more extensive atypical morphology.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Keratin digestion
Dermatophytes use keratin in superficial epidermis, hair and nail but generally do not invade living tissue in an immunocompetent host.
2
Centrifugal skin spread
Hyphae advance at the active scaly border while central inflammation settles, producing an annular plaque with apparent central clearing.
3
Hair-shaft invasion
Scalp organisms invade or surround hair shafts, causing breakage, black dots, alopecia and sometimes a destructive inflammatory kerion.
4
Nail reservoir
Subungual fungal growth thickens and separates nail and can repeatedly seed adjacent skin, although trauma and psoriasis mimic this appearance.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Advancing annular edge

Scale and papules are most active at an enlarging border while the centre becomes quieter or pigment-altered.

Interdigital and moccasin tinea

Toe-web maceration or diffuse powdery sole scale, often asymmetrical, supports tinea pedis and creates a cellulitis portal.

One hand two feet

Unilateral hyperkeratotic palmar scale with bilateral plantar disease is a classic distribution clue to dermatophyte infection.

Scalp hair invasion

Patchy scale, broken hairs, black dots and lymphadenopathy indicate tinea capitis even when inflammation is modest.

KerionRed flag

A tender boggy scalp plaque with pustules and loose hairs threatens follicular destruction and scarring alopecia.

Tinea incognito

Steroid exposure produces extensive poorly edged lesions with reduced scale, pustules or striae and an unexpectedly progressive course.

Red flags requiring action

Kerion with scarring risk, painful boggy scalp, bacterial superinfection, orbital proximity, extensive disease in immune compromise, diabetic foot ulceration or a rapidly spreading steroid-modified eruption requires urgent or specialist assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Skin scraping for microscopy and cultureFirst step
Why
Confirm dermatophyte at an active plaque edge before uncertain or systemic treatment.
Interpretation and limitations
Collect generous scale from untreated border; negative microscopy can coexist with later positive culture.
02
Hair pluck and scalp brushing
Why
Identify organism in suspected tinea capitis and guide oral drug plus contact action.
Interpretation and limitations
Sample broken abnormal hairs and scale, not smooth uninvolved scalp; treatment need not await culture in a convincing kerion.
03
Nail clipping and subungual debris
Why
Confirm onychomycosis before prolonged oral antifungal exposure.
Interpretation and limitations
Clip proximally into diseased nail and include debris; repeat a technically weak negative sample when suspicion remains.
04
Baseline liver and interaction assessment
Why
Prepare safely for systemic terbinafine, itraconazole or griseofulvin.
Interpretation and limitations
Testing and follow-up depend on drug, duration and comorbidity; reconcile warfarin, antidepressants, statins and contraception.
05
Bacterial swab of kerion or fissure
Why
Assess true secondary infection when pus, crust, cellulitis or fever is present.
Interpretation and limitations
Kerion inflammation itself can be sterile; do not replace systemic antifungal therapy with antibiotics alone.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Eczema and psoriasis

Symmetrical chronic plaques, poorly active margins, other classic sites and nail pitting support inflammatory disease, though fungal infection can coexist.

Candidal intertrigo

Moist confluent fold erythema with satellite pustules favours Candida, while dermatophyte groin infection often has a raised scaly edge and spares scrotal skin.

Erythrasma

Brown-red minimally scaly folds with characteristic coral-red Wood-lamp fluorescence suggest superficial Corynebacterium infection rather than fungus.

Alopecia areata or scarring alopecia

Smooth non-scaly patches favour alopecia areata; loss of follicular openings, pustules or scar requires urgent dermatology assessment.

Traumatic or psoriatic nail dystrophy

A thickened discoloured nail is not diagnostic of fungus, so confirm representative mycology before prolonged systemic treatment exposure.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Localised glabrous skinUse topical therapy correctlyFirst stepA limited corporis, cruris or pedis pattern is typical and hair, nail and severe host risk are absent.

1Scrape when uncertain or steroid-modified, then apply topical terbinafine across the lesion and one to two centimetres beyond its edge.
2Complete the product-specific one-to-two-week course, continue hygiene and treat fissures or eczema without potent steroid monotherapy.
3If no response, verify diagnosis, application, reinfection and mycology before extending or switching treatment.

02Scalp or beard hairTreat systemically and protect folliclesBroken hairs, black dots, alopecia, inflammatory kerion or beard-follicle involvement is present.

1Obtain hair and scale culture, assess contacts and animals, and arrange age-appropriate systemic antifungal treatment without topical monotherapy.
2Use species-informed oral terbinafine or griseofulvin through dermatology or local guidance; add antifungal shampoo to reduce shedding, not as cure.
3Urgently review kerion, scarring, eye proximity or systemic illness and document hair regrowth after inflammation settles.

03Nail or extensive diseaseConfirm before oral exposureMultiple body sites, hyperkeratotic disease or nail involvement makes topical penetration inadequate.

1Confirm fungus and species with adequate samples, assess liver disease, pregnancy, interactions and whether treatment benefit justifies systemic risk.
2Use the indicated oral regimen and baseline monitoring from current SmPC and specialist guidance rather than treating every dystrophic nail.
3Reassess clinical growth from the nail base or skin clearance, remembering that normal nail replacement takes months after fungal eradication.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Fungicidal first-line topical treatment for suitable localised dermatophyte skin infection.

Terbinafine 1% cream

Apply a thin layer once or twice daily to clean dry affected skin and a small surrounding margin for one to two weeks according to site and product directions.

Avoid eyes and mucosa, stop for significant irritation, and do not use topical treatment alone for scalp, beard-hair or established nail infection.

A broad topical azole option where dermatophyte or Candida is suspected in a suitable superficial site.

Clotrimazole 1% cream

Apply thinly two or three times daily for at least two weeks and continue according to product advice until symptoms resolve.

Local irritation can occur; avoid eyes and check excipients, and reassess diagnosis if a correctly applied course fails.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Kerion scarring alopecia

Intense scalp inflammation can destroy follicles permanently if systemic antifungal treatment and specialist review are delayed.

Secondary bacterial infection

Fissured toe webs and excoriated plaques permit bacterial cellulitis, particularly with diabetes, chronic oedema or poor peripheral circulation.

Id reaction

A distant itchy vesicular or papular eruption can reflect immune response to fungus and resolves when the primary infection is treated.

Treatment toxicity

Oral antifungals carry hepatic, haematological and important interaction risks, making diagnostic confirmation and medicine-specific safety monitoring essential.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review edge activity, scale, itch and new sites after the expected course rather than judging only residual hyperpigmentation.
Check scalp hair regrowth and follicular openings after kerion and refer persistent scarring or alopecia.
For systemic therapy, apply medicine-specific liver, blood and interaction monitoring and stop promptly for significant toxicity.
Re-sample recurrent or unresponsive disease before assuming resistance, documenting topical steroids and antifungals already used.
Inspect toe webs after lower-limb cellulitis and maintain dryness and antifungal control to reduce bacterial recurrence.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Sample the moving edge

The advancing border contains the highest viable fungal burden; a quiet centre commonly gives a false-negative result.

Hair requires bloodstream delivery

Cream cannot eradicate organisms inside a scalp hair shaft, making systemic treatment mandatory for tinea capitis.

Steroid hides the ring

Reduced redness and scale after corticosteroid can coexist with wider fungal growth and atypical pustulation.

Nail appearance is nonspecific

Trauma and psoriasis cause thick discoloured nails, so laboratory confirmation prevents months of needless systemic therapy.

11Common pitfallsFrequent interpretation and management errors.

01
Treating tinea capitis with shampoo alone and allowing scarring alopecia.
02
Taking scrapings from the treated quiet centre rather than the active border.
03
Prescribing potent topical steroid for an expanding annular plaque and creating tinea incognito.
04
Starting oral terbinafine for one dystrophic nail without mycological confirmation.
05
Ignoring infected pets, shared combs or occlusive footwear and interpreting reinfection as drug failure.