Intertrigo

Meet the patient

A 52-year-old woman with a body mass index of 38 and type 2 diabetes has a week of burning, weeping redness under both breasts and in the groins, worse with walking, sleepless with itch. Beneath the pannus the skin is sodden, bright red, and fissured at the deepest crease, with a few tiny pustules scattered just beyond the margin. She has tried "some steroid cream her sister had" with no improvement.^[1]

Hold the two questions that decide this whole topic: what is layered on the irritant base? (the coloniser — Candida, erythrasma, tinea, bacteria) and what is feeding the fold? (obesity, diabetes, incontinence, occlusion). Name the organism and dry the fold, and the disease resolves; miss either, and it recurs forever.^[1]

A descriptor, not a diagnosis — where intertrigo sits

Intertrigo (Latin intertrere, "to rub between") is the fold-occlusion member of the Moisture-Associated Skin Damage family. The MASD framework groups conditions in which prolonged moisture over-hydrates and erodes the stratum corneum: intertrigo (skin folds), incontinence-associated dermatitis, peristomal moisture damage, and peri-wound moisture damage. Recognising the moisture source is the key to prevention, because dryness — not drug selection — breaks the cycle.^[3]

The examiner's point is sharper than the definition: the bare word intertrigo denotes only the irritant, macero-inflammatory base. On top of that base a secondary coloniser establishes itself and colours the picture — most often Candida albicans, but also Staphylococcus aureus, beta-haemolytic streptococci, Corynebacterium minutissimum (erythrasma), or a dermatophyte. Naming the coloniser is what shifts the prescription from "barrier only" to "barrier plus targeted antimicrobial".^[1]

The classic trap: treating "intertrigo" with a steroid without naming the organism. Erythrasma is coral-red under Wood's lamp and needs clindamycin or clarithromycin, not an azole; tinea needs terbinafine, not a steroid; Candida needs an azole. A fold rash is a differential, not a diagnosis.^[1]

The three forces — moisture, friction, warmth

Friction between the two opposed surfaces chronically shears the stratum corneum. Moisture — sweat, urine, faecal enzymes, wound or stoma exudate — over-hydrates the stratum corneum, solubilises intercellular lipid, and strips corneocyte cohesion; the skin turns white, soggy, and easily torn (maceration). Warmth and occlusion then prevent evaporation and, by raising local pH towards the alkaline, create the incubator that selects for colonisation.^[1][3]

The cascade is self-reinforcing: occlusion traps a warm wet micro-environment, maceration denudes the barrier, fissures open at the deepest crease, colonisers move in, inflammation drives more exudate, and the itch-scratch-maceration loop makes the disease chronic. The molecular sequence — hydration leaching natural moisturising factor, alkaline pH activating serine proteases that cleave corneodesmosomes, and Candida switching from blastospore to invasive pseudohypha — is exactly why drying alone can interrupt the disease at any stage.^[1]

The molecular cascade — for the depth questionShowHide

A healthy stratum corneum is held together by intercellular lipids (ceramides, cholesterol, free fatty acids) and corneodesmosomes, kept mildly acidic at roughly pH 4.5 to 5.5 by the acid mantle. Occlusion does three things: it swells corneocytes and leaches water-soluble natural moisturising factor; trapped urea raises pH towards alkaline, activating serine proteases that cleave corneodesmosomes (the histology of maceration); and the now-permeable alkaline surface becomes a better substrate for microbial adhesion. Candida switches from blastospore to adherent pseudohypha. This is why removing moisture restores the acid mantle and halts the cascade — and why potent steroids, absorbed many-fold under occlusion, are uniquely hazardous here.

^[1]

Where it strikes — and what each fold tells you

Intertrigo is confined to folds and characteristically symmetrical, with involvement of the depth of the crease and sparing of surrounding flat skin — the geographical signature that separates it from a generalised eczema. The high-yield sites are inframammary and submammary, axillary, inguinal and crural, scrotal, abdominal pannus, intergluteal, neck (infants and the obese), retroauricular, interdigital toe- and finger-webs, and peristomal skin.^[1]

The fold involved often predicts the coloniser and the precipitant, so the site is itself a diagnostic clue. Submammary disease in a large-breasted or obese woman is the classic canvas for Candida and erythrasma — Wood's lamp is mandatory here. Axillary disease tracks with hyperhidrosis and occlusive deodorants. Inguinal and crural disease raises tinea and erythrasma, and carries the single highest-yield discriminator at viva: the scrotum is classically spared in tinea but involved in candidal and irritant disease.^[1]

Toe-web intertrigo — erythrasma, tinea, or streptococcal — is a recognised portal of entry for lower-limb cellulitis and must be treated, not dismissed. Peristomal disease is driven by effluent leakage: you refit the appliance, not just apply cream.^[1]

Name the coloniser — the differential that runs every fold rash

This is the heart of the topic at viva. Every fold rash must be run through the same competitors, because each carries a different treatment.^[1]

^[1]

The one-line discriminator beneath the table: satellite pustules beyond the margin → Candida; coral-red under Wood's lamp → erythrasma; annular scaly border that spares the scrotum → tinea; smooth salmon-pink with psoriasis elsewhere → inverse psoriasis; recurrent crusted erosions refractory to everything → Hailey-Hailey.^[1]

The highest-yield bedside test — coral-red means erythrasma

Wood's lamp examination is the single decision-changing test in fold disease, and it belongs in every non-straightforward intertrigo. Shine an ultraviolet lamp in a darkened room across the fold. Coral-red fluorescence is diagnostic of erythrasma — the porphyrin of Corynebacterium minutissimum — and instantly redirects treatment from an azole or steroid to topical clindamycin or oral clarithromycin. Candida, tinea, and inverse psoriasis are Wood's lamp negative.^[1]

The classic trap: a negative Wood's lamp does not exclude erythrasma if the lesion has been washed recently — the water-soluble porphyrin is easily removed, so examine before any cleansing. Potassium-hydroxide microscopy confirms the organism when the pattern is ambiguous: budding yeast and pseudohyphae = Candida; septate hyphae = dermatophyte. A bacterial swab is not a first-line test in uncomplicated intertrigo — reserve it for purulence, cellulitis, suspected MRSA, or empirical-therapy failure.^[1][4]

At the bedside — and when to investigate

Inspect every fold systematically — submammary, axillary, inguinal and crural, scrotal, abdominal pannus, intergluteal, neck, retroauricular, interdigital webs, peristomal — noting symmetry, confinement to the fold depth, maceration, fissuring, scale, and specifically the satellite lesions. Grade any cellulitis, lymphangitis, or abscess. Then run the two bedside tools liberally: Wood's lamp (coral-red = erythrasma) and KOH microscopy (pseudohyphae = Candida; septate hyphae = dermatophyte).^[1]

Intertrigo is a clinical diagnosis in the great majority of cases, and over-investigation is a recognised error. Reserve microbiology for purulent or resistant disease, fungal culture for ambiguous or recurrent disease, and biopsy for the chronic, recalcitrant, or ulcerated case where a mimic — inverse psoriasis, tinea incognito, Hailey-Hailey disease, or squamous cell carcinoma in a chronic fold ulcer — is plausible. When disease is recurrent or severe, screen the system: fasting glucose and HbA1c for diabetes, an HIV test, and urinalysis for glucosuria.^[1][4]

Management — the four pillars

No single agent works if the fold stays wet — which is why the general measures precede every drug. The definitive plan is built on four pillars that operate together.^[1]

^[1]

Pillar 2 — treat the organism, by name

Selecting the antimicrobial against the identified coloniser is the decisive therapeutic move. The doses below are the examinable ones:^[1]

^{[4] [9] [10] [11] [12]}

Never a potent steroid in a fold — the rule that protects the patient

When inflammation is severe, a mild topical corticosteroid — hydrocortisone 1 percent — for a short course of 5 to 7 days is acceptable and rapidly symptom-relieving. Potent steroids must never be used in folds. Occlusion multiplies percutaneous absorption many-fold, producing epidermal atrophy, striae, telangiectasia, and hypothalamic-pituitary-adrenal-axis suppression, sometimes within weeks — precisely at a site with an already-thinned, protease-damaged barrier.^[1]

For chronic, recurrent, or inverse-psoriasis-overlap disease, topical calcineurin inhibitors — tacrolimus 0.1 percent ointment or pimecrolimus 1 percent cream — are the steroid-sparing agents of choice, effective in flexural disease without the atrophy of corticosteroids.^[5]

A consultant confession: the commonest iatrogenic disaster in fold disease is a patient sent home with clobetasol or betamethasone "for the rash". The fold drinks it in; the skin thins and striae within weeks. If you must use a steroid, it is hydrocortisone 1 percent for a few days — and a calcineurin inhibitor for anything chronic.^[1]

Pillar 4 and prevention — fix the fold or it returns

No antimicrobial prevents recurrence if the fold environment persists. Weight loss (including bariatric surgery for morbid obesity) removes the deep folds that sustain disease; diabetes control lowers candidal colonisation; incontinence management dries the perineum; hyperhidrosis treatment (topical aluminium chloride, glycopyrrolate, or botulinum toxin for refractory axillary or groin sweating) reduces the moisture load; and stoma-appliance refitting addresses peristomal disease.^[1][2]

Prevention is indistinguishable from the first pillar of treatment, and it is the only reliable way to stop recurrence. Dry every fold completely after bathing (a cool hair-dryer reaches deep folds towels cannot), apply a daily barrier of zinc oxide, white soft paraffin, or a dimethicone-based film, wear loose breathable cotton, and use talc-free absorbent powders (cornstarch-based — talc is avoided for inhalation and ovarian-cancer concerns).^[1][7]

Two prevention pitfalls: first, cornstarch powder can feed Candida in an already-colonised fold — use a barrier cream rather than powder when candidal intertrigo is active, and reserve powder for prevention once healed. Second, over-washing with harsh soaps strips the lipid barrier and worsens maceration; use a gentle non-soap cleanser and pat, never rub, the folds dry.^[1][8]

When intertrigo is dangerous — the red flags

Intertrigo is rarely a dermatological emergency, but one red-flag question must be answered first: is this just a fold rash, or is there spreading infection or systemic toxicity? Spreading erythema with warmth, pain out of proportion, fever, or malaise escalates the diagnosis from intertrigo to cellulitis or, with rapid progression and systemic upset, to necrotising soft-tissue infection — intravenous antibiotics (flucloxacillin, with MRSA-guided agents where appropriate), blood cultures, surgical review, and admission, not topical therapy.^[1]

^[1]

Hailey-Hailey disease (benign familial chronic pemphigus) deserves its own line: a recurrent, relapsing flexural erosive dermatosis of the neck, axillae, and groin, autosomal dominant via ATP2C1, whose biopsy shows suprabasal acantholysis likened to a "dilapidated brick wall" — it masquerades as chronic intertrigo and is refractory to antifungals.^[6]

Special populations — the corners examiners test

Infants and neonates: candidal fold and napkin intertrigo involves the creases and shows satellite pustules — the discriminator from irritant nappy rash, which spares them. Treat with a topical azole plus a zinc-oxide barrier, avoiding potent steroids and talc.^[1]

Pregnancy: candidal intertrigo is common (oestrogen-driven); topical azoles are first-line and safe. Avoid oral azoles, particularly in the first trimester.^[1]

Diabetic: recurrent or severe candidal intertrigo is a screening trigger for HbA1c and fasting glucose; glycaemic control reduces recurrence, and toe-web intertrigo must be treated to protect against cellulitis.^[1]

Elderly, frail, bed-bound: immobility plus incontinence drive perineal and gluteal disease; the priority is prevention — repositioning, continence care, and skin barriers — and discriminating it from pressure injury and incontinence-associated dermatitis, all of which coexist.^[7][8]

Immunocompromised (HIV, transplant, chemotherapy): intertrigo may be persistent, atypical, or caused by unusual organisms and may require systemic antifungals.^[1]

Bariatric and stoma patients: deep folds resist drying and self-care — assist with hygiene, use barrier pastes, consider metabolic surgery to remove the fold environment, and refit leaking appliances.^[1][2]

Prognosis, and where to refer

Prognosis is excellent when treatment and correction of the cause are combined, and the disease usually resolves without scarring. Recurrence is the rule, not the exception, if the underlying fold environment persists. Review at two to four weeks: if resolved, pivot entirely to prevention education; if persistent, trigger the diagnostic escalation pathway — Wood's lamp, KOH, swab, and ultimately biopsy. Dermatology referral is for recurrent, resistant, diagnostically uncertain, or complicated disease.^[1]

The evidence, and where practice varies

The contemporary evidence base is anchored by the Romanelli and Voegeli 2023 review on diagnosis, management, and prevention in adults, the Voegeli 2020 narrative review, and the Wund-D.A.CH best-practice recommendation on MASD, which provides the unifying framework.^[1][2][3] The antifungal ladder rests on the Taudorf 2019 evidence-based review of cutaneous candidiasis.^[4] Regional guideline deltas are small because intertrigo is a clinical syndrome: European, American, and Australasian guidance converge on barrier and dryness first, topical azole for candidal disease, mild-only corticosteroids, and calcineurin inhibitors for chronic disease — differing mainly in formulary availability (clotrimazole versus miconazole versus econazole) and the stewardship status of fusidic acid.^[1]

The mnemonic, and the mantra

^[1]

The mantra: dry the fold, name the organism, barrier the skin, fix the cause — and never put a potent steroid where two surfaces meet.^[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the submammary rash in the woman with diabetes (answer)ShowHide

A 52-year-old obese diabetic woman has bright-red, weeping, glistening erythema under both breasts and in the groins, with satellite pustules beyond the margin. Name the coloniser, the bedside test, and the first-line treatment. Model: The satellite pustules and collarette scale make candidal intertrigo the lead. Confirm with potassium-hydroxide microscopy showing budding yeast and pseudohyphae (Wood's lamp is negative in candidal disease). Treat with a topical azole — clotrimazole 1 percent or miconazole 2 percent cream twice daily for 2 to 4 weeks — applied before the barrier, plus drying measures, weight and glycaemic counselling, and a check of the HbA1c because recurrent candidal intertrigo is a recognised clue to undiagnosed diabetes.^[1][4]

Stem 2 — the groin rash that is not responding to the azole (answer)ShowHide

A 40-year-old man has a chronic, reddish-brown, finely wrinkled rash in the groins and toe-webs that has not responded to two weeks of clotrimazole. What is the single most useful bedside test, and what does a coral-red result mean? Model: The picture and the azole failure point to erythrasma (Corynebacterium minutissimum). The highest-yield test is Wood's lamp examination in a darkened room: the characteristic coral-red fluorescence supports the diagnosis. Treatment moves from an azole to a targeted antibacterial — topical clindamycin or clotrimazole, or an oral agent (erythromycin or clarithromycin) when disease is extensive. This is the decision-changing test that belongs in every non-straightforward fold eruption.^[10][9]

Stem 3 — the chronic fold ulcer (answer)ShowHide

A 70-year-old man has a chronic, non-healing, indurated ulcer within a long-standing intergluteal intertrigo. The registrar plans another course of topical antifungal. What is the right move? Model: A chronic non-healing ulcer within a chronically inflamed fold is a red flag for squamous cell carcinoma — a Marjolin-type change in chronically inflamed or scarred skin. The right move is biopsy before any further empirical therapy, alongside reassessing the coloniser and the systemic drivers. Do not keep applying antifungal to a lesion that may be malignant.^[1]

References12ShowHide

1. [1]Romanelli M, Voegeli D, Colboc H, et al. The diagnosis, management and prevention of intertrigo in adults: a review J Wound Care, 2023.PMID 37405940
2. [2]Voegeli D. Intertrigo: causes, prevention and management Br J Nurs, 2020.PMID 32579453
3. [3]Dissemond J, Assenheimer B, Gerber V, et al. Moisture-associated skin damage (MASD): A best practice recommendation from Wund-D.A.CH J Dtsch Dermatol Ges, 2021.PMID 33942514
4. [4]Taudorf EH, Jemec GBE, Hay RJ, Saunte DM. Cutaneous candidiasis - an evidence-based review of topical and systemic treatments to inform clinical practice J Eur Acad Dermatol Venereol, 2019.PMID 31287594
5. [5]Reynolds KA, Pithadia DJ, Lee EB, Wu JJ. Treatments for inverse psoriasis: a systematic review J Dermatolog Treat, 2020.PMID 31100992
6. [6]Porro AM, Arai Seque C, Miyamoto D, et al. Hailey-Hailey disease: clinical, diagnostic and therapeutic update An Bras Dermatol, 2024.PMID 38789364
7. [7]Lichterfeld-Kottner A, El Genedy M, Lahmann N, et al. Maintaining skin integrity in the aged: A systematic review Int J Nurs Stud, 2020.PMID 31945604
8. [8]Fastner A, Hauss A, Kottner J Skin assessments and interventions for maintaining skin integrity in nursing practice: An umbrella review Int J Nurs Stud, 2023.PMID 37099847
9. [9]Radhakrishnan S, Logamoorthy R, Karthikeyan K, et al. Erythrasma: a systematic review of interventions Clin Exp Dermatol, 2025.PMID 40635638
10. [10]Holdiness MR. Management of cutaneous erythrasma Drugs, 2002.PMID 12010076
11. [11]Korting HC, Kiencke P, Nelles S, Rychlik R. Comparable efficacy and safety of various topical formulations of terbinafine in tinea pedis irrespective of the treatment regimen: results of a meta-analysis Am J Clin Dermatol, 2007.PMID 18039018
12. [12]Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo Cochrane Database Syst Rev, 2012.PMID 22258953