Erythrasma

Meet the patient

A 52-year-old man with type 2 diabetes and a body mass index of 34 has a slowly enlarging, mildly itchy brown-red patch in both groins; the border is sharp, the scale is fine, and there is no central clearing. He has used his wife's terbinafine cream for two weeks with no change.[1]

Two questions decide this rash: is it fungal or bacterial? and what glows under the lamp? Reach for the Wood's lamp before the potassium hydroxide — coral-red answers both questions in ten seconds and tells you why the antifungal failed.[1][6]

The bacterium that loves antifungal cream — definition in one breath

Erythrasma is a bacterial infection that walks, talks and often responds like a fungus. It is a chronic, superficial infection of the warm, moist, occluded intertriginous skin — groin, axillae, toe webs, submammary folds, gluteal cleft, umbilicus — caused by Corynebacterium minutissimum, a Gram-positive, aerobic, pleomorphic diphtheroid that lives as a harmless commensal on normal skin until the local microenvironment turns in its favour.[1][9]

Taxonomy is in flux and examiners know it. Modern molecular work has moved the organism, in some schemes, into the genus Kocuria (a Gram-positive coccus within the Micrococcaceae). Most clinical texts, microbiology reports and board questions still call it Corynebacterium minutissimum. Either name is accepted — recognise both and do not be thrown.[1]

Etymology for viva gold: erythrasma is from the Greek erythros, "red", for the colour of the patch; minutissimum is Latin for "smallest", a nod to the organism's tiny size when first established as the cause by Sarkany, Taplin and Blank in 1961.[9]

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Why the folds — the microenvironment that lets it flourish

The organism is on everyone's skin; the rash appears only where the skin stops breathing. Warmth, moisture, occlusion, friction and an alkaline pH let C. minutissimum overgrow in the stratum corneum — one sentence that explains every risk factor, every site of predilection and almost the entire prevention strategy.[1]

The disease is common and worldwide, but prevalence climbs steeply in hot, humid, tropical climates, where up to one in five people may carry or express it. Adults outnumber children because apocrine sweat, larger body mass, occlusive footwear and the rising tide of diabetes and obesity all favour the organism. A family history is irrelevant; shared footwear and living conditions are not, which is why toe-web disease clusters in households.[1]

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The risk factors split cleanly into the local and the systemic:[1]

• Local — hyperhidrosis, occlusive clothing and footwear, poor hygiene, deep skin folds from obesity, and tropical heat. All raise moisture, friction and surface pH.
• Systemic — diabetes mellitus (immune dysfunction, impaired neutrophil function, glucose-rich skin), immunosuppression (HIV, corticosteroids, chemotherapy, biologics) and obesity. These are the reasons to screen when disease is extensive, recurrent or resistant.[1]

The classic trap: treating the rash without treating the fold. A patient whose diabetes, obesity or hyperhidrosis stays unaddressed will relapse no matter how good the cream — the environment that grew the organism is still feeding it.[1]

Coral-red under Wood's lamp — the pathognomonic pigment

One pigment, made by one organism, glowing one colour, settles the diagnosis. C. minutissimum is non-spore-forming and non-motile, multiplies within the superficial stratum corneum without invading living tissue, and produces two classes of substance that explain every clinical feature.[1][9]

The first is coproporphyrin III, a water-soluble porphyrin that accumulates in the stratum corneum and emits the pathognomonic coral-red (salmon-pink) fluorescence under Wood's lamp (UV-A, 365 nm). Not every corynebacterium makes porphyrin, which is why this glow is specific to C. minutissimum and not a generic coryneform sign.[4][6]

The second is a set of proteolytic and keratolytic enzymes that digest the cornified layer into the fine, powdery scale seen clinically. Unlike dermatophytes, which invade keratin with hyphae, C. minutissimum stays on the surface — which is why potassium hydroxide microscopy is negative in pure erythrasma and why the inflammation is so muted.[1]

The consultant confession: the glow can outlive the rash. Coproporphyrin III lingers in the shedding stratum corneum for days after the patch has clinically cleared, so persistent fluorescence is not treatment failure — it is leftover pigment. Warn the patient, or you will both chase a phantom.[1]

The host response is deliberately quiet. Invasion below the stratum corneum is extraordinarily rare; when it does occur — bacteraemia, osteomyelitis, endocarditis — it is in profoundly immunocompromised hosts and is invasive corynebacterial infection, not "erythrasma" in the usual sense.[5]

Read the patch — distribution and morphology

Look for a sharp-bordered, reddish-brown, finely scaly patch in a fold that barely itches. The lesion is a macule or patch — well-demarcated, with a sharp geometric edge that contrasts with the diffuse, sloppy border of intertrigo or eczema. The colour is reddish-brown to coppery, not the bright red of candidal intertrigo or the salmon-pink of inverse psoriasis. The scale is fine and powdery, far less prominent than the active advancing border of tinea cruris.[1]

Most patients are asymptomatic or only mildly pruritic — and that lack of itch is itself a clue, because tinea cruris and candidal intertrigo are usually more symptomatic. The lesion does not blister, weep or crust unless a secondary infection or coexisting dermatitis has supervened.[1]

The classic sites are all intertriginous — memorise the list as a single principle, "where skin occludes skin":[1]

• Toe webs — the most common site overall; the 4th interdigital space is the single most frequent location. Look for maceration, fissuring, fine scale and sometimes malodour; tinea pedis and candidal intertrigo often coexist.
• Groin and crural folds — well-demarcated patches from the inguinal crease onto the inner thigh; mucosal surfaces are spared.
• Axillae — may coexist with trichomycosis axillaris, another corynebacterial infection.
• Submammary folds — commoner in women with obesity.
• Gluteal cleft and umbilicus — commoner in obese or diabetic individuals.
• Disseminated — rare; patches beyond the classic folds onto trunk and proximal limbs, strongly tied to diabetes, immunosuppression and tropical residence.[1]

The 4th-toe-web rule: if you see one well-demarcated, reddish-brown, finely scaling patch and you are not sure, examine every other fold — erythrasma is multifocal, and missing the toe webs is the commonest reason a "treatment-resistant groin rash" turns out to be untreated disease elsewhere.[1]

The differential fork — tinea, candida, psoriasis

Four mimics crowd the folds; the Wood's lamp and the potassium hydroxide separate them in a minute. Coral-red fluorescence is pathognomonic for erythrasma; a negative lamp plus hyphae on potassium hydroxide points to dermatophyte; satellite pustules on a bright-red moist base point to candida; smooth salmon-pink plaques with psoriasis elsewhere point to inverse psoriasis.[1]

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The one-line discriminator for each: coral-red glow — erythrasma; leading scaly advancing edge with hyphae — tinea; satellite pustules on a beefy base — candida; smooth salmon-pink plaque with psoriasis elsewhere — inverse psoriasis.[1]

If the Wood's lamp is genuinely negative, reconsider the diagnosis before reaching for another round of antifungal — perform potassium hydroxide microscopy to exclude dermatophyte or candidal infection, and remember that very early erythrasma may fluoresce faintly before porphyrin production is detectable.[1]

The Wood's lamp sign — how to do it and not be fooled

Wood's lamp is the diagnostic test of choice: rapid, cheap, non-invasive and highly specific. The coral-red fluorescence is produced by coproporphyrin III at a wavelength of UV-A 365 nm. Done well, it settles the diagnosis at the bedside without a swab.[4][6][7]

Do it properly, or you will get a false negative:[1]

• Darken the room and let the examiner's eyes adapt for at least a minute; even faint coral-pink is significant against a dark background.
• Hold the lamp close to the skin, at the correct wavelength (365 nm).
• Do not test wet or freshly washed skin — coproporphyrin III is water-soluble and washes off; some clinicians gently wipe with alcohol first to remove surface contaminants and moisture.
• Expect the glow to outlive the rash — residual porphyrin sheds over days, so persistent fluorescence after clinical clearance is leftover pigment, not failure.[1][6]

The Wood's lamp differential is core exam material — the colour tells you the organism before you send a single swab:[1]

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The classic trap: Malassezia (tinea versicolor) glows pale yellow-green, not coral-red — and Pseudomonas glows yellow-green too. If the colour you see is greenish rather than red-orange, you are looking at a different organism, and erythrasma is not the diagnosis.[1]

Microbiology and biopsy are rarely needed. Potassium hydroxide microscopy excludes fungus when the lamp is equivocal; Gram stain may show Gram-positive pleomorphic diphtheroid rods in the stratum corneum; culture on nutrient agar is slow and reserved for atypical or resistant disease; biopsy is not routine and shows only a mild superficial inflammatory infiltrate with organisms in the stratum corneum.[1]

Screen for underlying disease when it matters. In extensive, recurrent, disseminated or treatment-resistant erythrasma, send fasting plasma glucose and HbA1c for diabetes, weigh and measure for obesity, consider HIV testing and a medication review for immunosuppression, and take a focused history for hyperhidrosis. An isolated toe-web patch in a healthy adult needs none of these.[1]

Treatment — topicals first, macrolides for the deep end

The mantra, worth saying out loud on every ward round: coral-red under Wood's lamp — a bacterium that loves antifungal cream. Treatment is dictated by the extent of disease, the presence of co-infection, and the predisposing conditions underneath — and almost everyone starts with a topical.[1]

Step 1 — topical therapy for localised disease

For localised or limited erythrasma, a topical agent for 2 to 4 weeks is first-line, continued even after the rash looks better to cut recurrence. Cluster the six options as two imidazoles, two antistaphylococcal agents, two anti-corynebacterials:[1]

• Clotrimazole 1 per cent cream twice daily for 2 to 4 weeks — the imidazole workhorse; cheap, available everywhere, well tolerated.
• Miconazole 2 per cent cream twice daily for 2 to 4 weeks — the alternative imidazole with comparable efficacy.
• Fusidic acid 2 per cent cream twice daily for 2 weeks — a topical antibacterial reliable against Gram-positive organisms; a Scandinavian primary-care trial found it comparable to oral erythromycin for localised disease, which underwrites topical-first management.
• Mupirocin 2 per cent ointment twice daily for 1 to 2 weeks — useful in toe-web disease or when mixed bacterial infection is suspected.
• Erythromycin 2 per cent topical solution or gel twice daily for 2 weeks — targets C. minutissimum directly.
• Clindamycin 1 per cent topical solution or gel twice daily for 2 weeks — an alternative where macrolide resistance is a concern.[1][8]

The classic trap, and the favourite exam trick: imidazole antifungals clear erythrasma despite its being a bacterial infection. They work because they disrupt the membrane-synthesis pathways this diphtheroid shares with fungi — which is why the patient who "got better on his wife's clotrimazole" is a diagnostic clue, not a puzzle. Terbinafine, an allylamine, does not reliably cover erythrasma, which is why our patient's terbinafine failed.[1][3]

Step 2 — oral macrolides for extensive, recurrent or disseminated disease

When disease is widespread, multifocal, recurrent or unresponsive to topicals, go systemic. Macrolides — binding the 50S ribosomal subunit to block bacterial protein synthesis — are the traditional agents of choice:[1]

• Erythromycin 500 mg orally four times daily for 7 to 14 days — the most cited systemic regimen; nausea, cramping and diarrhoea are common, and CYP3A4 interactions matter.
• Clarithromycin 500 mg orally twice daily for 7 days — better tolerated, simpler schedule, a reasonable first-line systemic choice where available.
• Tetracycline 500 mg orally four times daily for 14 days — a historical alternative, generally less effective and constrained by photosensitivity and contraindications in pregnancy and children.
• Azithromycin has been used in reports but is less well supported than erythromycin or clarithromycin.[1][3]

Combine an oral macrolide with a topical and with the preventive measures below for extensive disease or mixed infection. The evidence base is thin — a 2025 systematic review found no single regimen clearly superior and emphasised that most cases are diagnosed clinically with Wood's lamp and managed without microscopy or culture.[1][2]

Step 3 — adjunctive and preventive measures

Relapse is the rule unless the fold is fixed. Every patient gets advice on the environment, not just the antimicrobial:[1]

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Escalation rules: escalate to oral therapy if lesions are extensive, multifocal, recurrent, or not improved after 4 weeks of appropriate topical therapy; reassess the diagnosis (repeat the Wood's lamp and potassium hydroxide, consider biopsy) if there is no response to two adequate courses; screen for diabetes and obesity in recurrent or extensive cases; refer to dermatology when the diagnosis is uncertain, treatment fails, or coexisting extensive dermatophyte infection needs oral antifungal therapy.[1]

When it gets dangerous — the rare escalation

Uncomplicated erythrasma is never an emergency, but two situations are. Almost every patient is managed electively in the outpatient setting — but watch for the two that change everything.[1]

First, secondary bacterial cellulitis or erysipelas: a fold that turns acutely tender, warm, swollen, with spreading erythema and fever is no longer erythrasma — it is deeper infection, usually Streptococcus pyogenes or Staphylococcus aureus. Manage as an urgent bacterial skin infection: blood cultures, intravenous flucloxacillin, cephalexin or clindamycin per local guidance, and assess for sepsis.[1]

Second, systemic infection with C. minutissimum: vanishingly rare, reported in profoundly immunocompromised hosts as bacteraemia, osteomyelitis, endocarditis or visceral abscess. Blood cultures, imaging and intravenous antibiotics guided by susceptibility, with infectious-disease input, are required.[5]

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The subtypes that bite — toe web, diabetes, pregnancy, immunocompromised

The presentation shifts with the host, and so do the thresholds. Toe-web erythrasma is the commonest form of all: the lateral 4th interdigital space is classic, but any web may be involved; look for white maceration, fissuring, fine scale and malodour that worsens after exercise or occlusive footwear. It routinely coexists with tinea pedis and candidal intertrigo, so treat every identified co-infection and insist on drying between the toes, cotton or wool socks, and rotated shoes.[1]

Erythrasma in diabetes tends to be extensive, recurrent and treatment-resistant — hyperglycaemia, immune dysfunction and obesity create a permissive environment. Combine an oral macrolide with rigorous glycaemic control, weight management and screening for fungal co-infection; recurrence is the rule until the diabetes is controlled.[1]

Erythrasma in pregnancy and breastfeeding: prefer topicals because systemic absorption is minimal — clotrimazole, miconazole, fusidic acid and topical erythromycin are generally considered safe. Oral erythromycin or clarithromycin is acceptable if topical therapy fails, but exhaust topicals first. Tetracycline is contraindicated in pregnancy and breastfeeding because of effects on fetal bone and teeth.[1]

In immunocompromised hosts — HIV, immunosuppressive therapy, corticosteroids, chemotherapy — expect more extensive, atypical or persistent disease, keep the rare systemic infection in mind, and lower the threshold for culture. In transplant recipients, beware drug interactions between macrolides and calcineurin or mammalian-target-of-rapamycin inhibitors; prefer topical therapy or a non-macrolide alternative with specialist input.[1]

Disseminated erythrasma — patches beyond the classic folds onto trunk and proximal limbs — is rare and strongly associated with diabetes, immunosuppression and tropical residence. Oral macrolides are required, and the predisposition must be addressed aggressively.[1]

In children, erythrasma is uncommon but does occur in groins and toe webs; topical therapy is preferred, and weight-based dosing applies if an oral macrolide is needed (erythromycin 30 to 50 mg per kg per day in divided doses, or clarithromycin 15 mg per kg per day in two divided doses, for 7 to 14 days). Tetracycline is contraindicated under 8 years because of permanent dental staining. In the elderly, deeper folds, reduced mobility, incontinence and higher rates of diabetes make extensive and recurrent disease commoner — manage practically, with attention to drying, footwear and incontinence, and watch for drug interactions and cardiac risk if macrolides are used.[1]

Why it comes back — recurrence, complications and prognosis

The prognosis of uncomplicated erythrasma is excellent — but the local environment, not the antibiotic choice, decides whether it returns. With appropriate therapy, improvement is visible within 1 to 2 weeks and clearance by 2 to 4 weeks, with no scarring because the infection never leaves the stratum corneum.[1]

The major determinant of recurrence is the fold: patients who stay warm, moist and occluded relapse. Addressing obesity, hyperhidrosis, occlusive clothing and diabetes is therefore as important as the antimicrobial — long-term drying, breathable clothing and weight management often matter more than the first prescription. Counsel patients about this at the outset.[1]

The complications are mostly diagnostic and recurrent rather than dangerous. Patients may not seek treatment for months, allowing spread to multiple folds; macerated skin can be superinfected with Staphylococcus aureus or Streptococcus pyogenes (cellulitis, erysipelas, lymphangitis); toe-web fissures can be painful and act as a portal for bacteria; and the psychological impact of a chronic, discoloured groin or axillary rash — embarrassment, social avoidance, reduced quality of life — is real and should not be dismissed.[1]

Disposition is almost always outpatient — primary care or dermatology clinic. Refer to dermatology when the diagnosis is uncertain, the disease is extensive or recurrent, coexisting fungal infection needs systemic therapy, or two adequate courses have failed; reserve infectious-disease referral for the rare systemic infection or the immunocompromised patient with atypical features.[1]

Exam pearls — what the viva rewards

Memorise these ten and the rest of the page slots around them. They are the points examiners on NEET-PG, INICET, USMLE and PLAB consistently test.[1]

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The mantra, one last time: coral-red under Wood's lamp — a bacterium that loves antifungal cream. Hold that line and the diagnosis, the treatment and the differential all fall into place.[1]

Ward-round test

Stem 1 — the terbinafine-resistant groin rash (answer)

A 52-year-old obese, diabetic man has a sharp-bordered, reddish-brown, finely scaly patch in both groins for three months that has not responded to two weeks of terbinafine cream. What is the likely diagnosis, the bedside test, and why did the terbinafine fail? Model: Erythrasma, a superficial bacterial infection by Corynebacterium minutissimum. The bedside test is Wood's lamp, which shows pathognomonic coral-red fluorescence from coproporphyrin III. Terbinafine failed because it is an allylamine antifungal and erythrasma is a bacterial infection — switch to an imidazole (clotrimazole or miconazole), which clear this diphtheroid despite being labelled antifungals, or a topical antibacterial such as fusidic acid; extensive disease gets an oral macrolide. Screen his diabetes and weight, because recurrence is the rule until both are addressed.[1]

Stem 2 — coral-red between the toes (answer)

A 34-year-old man has chronic, malodorous maceration of the 4th toe web with fine scale; the Wood's lamp glows coral-red. Name the organism, the pigment, and the two co-infections to look for. Model: The organism is Corynebacterium minutissimum and the pigment is coproporphyrin III (water-soluble, fluorescing coral-red at UV-A 365 nm). Toe-web erythrasma classically coexists with tinea pedis and candidal intertrigo, so look for and treat both — send potassium hydroxide microscopy if the lamp is equivocal. Treat the erythrasma with a topical imidazole or fusidic acid, dry the webs thoroughly, rotate shoes, and use cotton or wool socks.[1][6]

Stem 3 — the patient whose glow will not go away (answer)

A patient treated for erythrasma reports that the rash has cleared clinically but the patch still glows coral-red under Wood's lamp a week later. Is this treatment failure? Model: No. Coproporphyrin III is water-soluble and lingers in the shedding stratum corneum for days after clinical clearance, so persistent fluorescence is leftover pigment, not active infection. Reassure the patient, complete the planned course, and address the predisposing fold environment to prevent relapse. Reserve repeat treatment for true clinical recurrence, not persistent glow.[1][4]

Stem 4 — extensive erythrasma in an immunocompromised host (answer)

An HIV-positive patient develops widespread reddish-brown patches across the folds and trunk that glow coral-red. What is the management, and what rare complication must you exclude if he becomes febrile? Model: This is disseminated erythrasma in an immunocompromised host — extensive disease needs an oral macrolide (erythromycin 500 mg four times daily or clarithromycin 500 mg twice daily for 7 to 14 days) plus topical therapy, plus aggressive attention to the predisposing environment and HIV control. The rare complication to exclude if he becomes febrile is invasive C. minutissimum infection — bacteraemia, osteomyelitis or endocarditis — which demands blood cultures, imaging and intravenous antibiotics with infectious-disease input; culture is more useful in this population.[1][5]

References

1. [1]Forouzan P, Cohen PR. Erythrasma Revisited: Diagnosis, Differential Diagnoses, and Comprehensive Review of Treatment Cureus, 2020.PMID 33145138
2. [2]Radhakrishnan S, Logamoorthy R, Karthikeyan K, et al. Erythrasma: a systematic review of interventions Clin Exp Dermatol, 2025.PMID 40635638
3. [3]Holdiness MR. Management of cutaneous erythrasma Drugs, 2002.PMID 12010076
4. [4]Blasco-Morente G, Arias-Santiago S, Pérez-López I, et al. Coral-Red Fluorescence of Erythrasma Plaque Sultan Qaboos Univ Med J, 2016.PMID 27606125
5. [5]Sebaratnam DF, Lee S. <em>Corynebacterium minutissimum</em> infection: erythrasma Med J Aust, 2017.PMID 28987127
6. [6]Robles-Silva C, Hidalgo L, Vera-Kellet C, et al. Erythrasma and the role of Wood's light: A simple diagnosis pearl Med Clin (Barc), 2023.PMID 37517932
7. [7]Garcia-Souto F, et al. Visual Dermatology: Erythrasma Fluorescence Under Wood's Lamp J Cutan Med Surg, 2020.PMID 31994922
8. [8]Hamann K, Thorn P. Systemic or local treatment of erythrasma? A comparison between erythromycin tablets and Fucidin cream in general practice Scand J Prim Health Care, 1991.PMID 2041927
9. [9]Sarkany I, Taplin D, Blank H. The etiology and treatment of erythrasma J Invest Dermatol, 1961.PMID 14497222