Tinea corporis

Meet the patient

A 24-year-old wrestler arrives with an itchy, red, ring-shaped plaque on his shoulder that has been spreading outward for three weeks. The edge is raised, scaly and active; the centre has cleared. He has been applying a "ringworm cream" bought over the counter that contains a steroid, an antifungal and an antibiotic — and the lesion has only grown larger, flatter and stranger.[1][2]

Three questions now frame the whole topic: is the edge truly active and scaly with central clearing? (it is — so this is tinea), has a steroid masked it? (the cream says yes — so suspect tinea incognito), and where is the reservoir? (his feet and the wrestling mat). Scrape the active edge for KOH, stop the steroid, and the diagnosis is made before any culture grows.[1][9]

The ring — the active advancing edge with central clearing

The single most reproduced sign in a tinea stem is the annular plaque with a raised, scaly, active advancing edge and relative central clearing. That morphology is the disease's signature, and it exists because of how the fungus grows.[1]

Dermatophytes are keratinophilic fungi that digest keratin in the stratum corneum, hair and nails using secreted keratinases. They advance centrifugally from the inoculation point, radiating outward — so the leading edge is the zone of fresh invasion, intense inflammation and scale, while the centre clears because epidermal turnover (about 28 days) and the immune response have already shed the infected keratin.[1][5]

The first lesion is often the largest — the "mother" or "herald" patch — with smaller daughter lesions ringing it. Lesions are itchy, may carry pustules or vesicles at the active edge, and the inflammation runs hotter when the organism is zoophilic (from an animal) than anthropophilic (human-adapted).[1][6]

Etymology for viva gold: tinea is Latin for "a gnawing worm" — medieval physicians believed a worm burrowed under the skin to make the ring. Corporis simply means "of the body". The worm was wrong, but the ring it described was real, and the name stuck for six centuries.[1]

Confirm before you treat — KOH from the edge

The decisive bedside test is potassium hydroxide microscopy of skin scraped from the active scaly edge, and it takes five minutes. Branching septate hyphae under the microscope confirm a dermatophyte before you commit to weeks of therapy.[3]

Scrape the active edge, not the cleared centre — the centre has no fungus left. Sensitivity is about 70 to 80 percent and specificity above 90 percent, with a characteristic "chewed-spaghetti" or "rail-track" appearance. Fungal culture on Sabouraud dextrose agar with cycloheximide confirms the species and allows resistance testing, but takes 2 to 4 weeks.[3]

The classic trap: scraping the cleared centre, or scraping after the patient has applied a steroid, gives a false-negative KOH. Always scrape the active leading edge, and if the morphology has been steroid-altered, biopsy with PAS rather than trust a negative slide.[3][9]

Adjuncts round out the work-up. Wood's lamp fluoresces green-yellow only for some Microsporum species (M. canis, M. audouinii); T. rubrum and T. indotineae do not fluoresce, so a negative lamp means nothing for body tinea. PCR and ITS sequencing detect species and SQLE resistance mutations within 24 to 48 hours. Check LFTs and renal function before any systemic course.[3][11][12]

The three genera and three transmission routes

Three genera cause human dermatophytosis, and three transmission routes decide how inflamed the lesion looks. Cluster them and the history writes itself.[1][5]

The three genera:[1]

• Trichophyton — T. rubrum causes 60 to 80 percent of chronic tinea corporis, cruris, pedis and onychomycosis globally; T. tonsurans dominates tinea capitis and gladiatorum; and the emerging antifungal-resistant T. indotineae drives extensive, recurrent, terbinafine-refractory epidemics from South Asia.
• Microsporum — M. canis (zoophilic, from cats and dogs) is the commonest zoophilic cause; M. gypseum is geophilic, from soil.
• Epidermophyton floccosum — affects skin and nails but never hair, an important cause of tinea cruris.

[1] [5] [11]

The three transmission routes — and how inflamed each looks:[4]

• Anthropophilic (human-to-human, via towels, clothing, combs, gym mats) — chronic, indolent, minimally inflamed lesions; T. rubrum is the classic.
• Zoophilic (animal-to-human, from kittens, puppies, cattle) — acute, intensely inflamed, often pustular or kerion-like, because the host immune response is fierce against a poorly adapted organism.
• Geophilic (soil-to-human, M. gypseum from gardening) — intermediate inflammation, often a solitary lesion.

[4] [5] [6]

The number rule: the more foreign the organism is to its host, the angrier the inflammation — which is why a kitten-sourced M. canis plaque is a furious, boggy mess while a T. rubrum plaque from a shared towel is quiet and chronic.[4]

Why the ring forms — keratin, centrifugal spread, and the steroid trap

The organism cannot penetrate beyond the granular layer in an immunocompetent host, because deeper tissue is not keratinised. That is why tinea stays superficial — and why it clears centrally once the 28-day epidermal turnover sheds the infected keratin the fungus has already outrun.[1]

Every antifungal you will name works by attacking the fungal cell membrane's ergosterol. Allylamines (terbinafine) inhibit squalene epoxidase and are fungicidal; azoles inhibit lanosterol 14-alpha-demethylase and are fungistatic. That single distinction — cidal versus static — is why terbinafine is preferred where you can use it.[1][4]

Autoinoculation from coexisting tinea pedis, unguium or capitis maintains chronicity, which is why you must examine the feet, nails and scalp of every recurrent case: the reservoir on the foot re-seeds the groin every time the patient dresses.[1][2]

The annular differential — five mimics, one discriminator each

Five eruptions wear tinea's annular clothing, and each has a one-line giveaway. The decisive discriminator across all of them is KOH from the active edge — positive in tinea, negative in the rest.[1][6]

[1]

Add pityriasis versicolor (Malassezia; hypopigmented macules with fine scale and "spaghetti-and-meatballs" KOH, not branching septate hyphae), subacute cutaneous lupus (photosensitive annular plaques, ANA and anti-Ro positive), erythema annulare centrifugum (trailing scale on the inner edge), secondary syphilis (palmo-plantar lesions, moth-eaten alopecia, positive RPR), and fixed drug eruption (recurs at the same site). KOH is the arbiter.[1][6]

Tinea incognito — the steroid trap

Tinea incognito is tinea altered by a topical corticosteroid, and it is the commonest cause of "eczema that just won't go away". The steroid suppresses the local cell-mediated immune response: the active edge flattens, the scale disappears, and the lesion becomes an ill-defined erythematous patch that spreads silently.[7][9]

The recurring trainee error is to escalate the steroid — stronger potency, longer course — when the lesion "isn't responding". It is responding beautifully, by growing. The correct move is to stop the steroid cold, confirm with KOH or biopsy, and treat with a systemic antifungal, because incognito disease is usually extensive and has often invaded the follicle.[7][8]

The principal driver across South Asia is the AAA syndrome — the irrational over-the-counter sale of fixed-dose steroid-plus-antifungal-plus-antibiotic "triple action" creams, which mask tinea, select for resistance, and feed the epidemic of recalcitrant dermatophytosis. Warn every patient against them.[1][9]

Majocchi granuloma — the follicular trap

Follicular papules, nodules or pustules within or around a tinea lesion are Majocchi granuloma — dermatophyte invasion of the hair follicle — and topical therapy cannot reach them. This one always needs a systemic antifungal.[10]

It classically follows shaving (legs in women, beard in men), occlusion, topical steroid use, or immunosuppression. Histology shows fungal hyphae and arthrospores within the hair shaft surrounded by a mixed granulomatous infiltrate. Give 4 to 6 weeks of oral terbinafine or itraconazole, and address the trigger — stop the steroid, change the shaving habit, review the immunosuppression.[10]

The classic trap: treating Majocchi granuloma with a topical cream because "it's just folliculitis". It is not folliculitis, the fungus is in the follicle, and a topical will never reach it. If you see perifollicular papules in a tinea lesion, switch to oral.[10]

Trichophyton indotineae — the resistance threat

Trichophyton indotineae is the emerging terbinafine-resistant dermatophyte from the Indian subcontinent, now spreading globally, and it is the answer when tinea fails standard oral terbinafine. It produces extensive, pruritic, polycyclic tinea corporis, cruris and faciei that does not respond to the usual 2 to 4 weeks of terbinafine.[11][12]

The mechanism is point mutations in the squalene-epoxidase gene — SQLE F397L, L393F, A448T and S443P — that change the terbinafine binding pocket and shift the MIC up to 100-fold. Send fungal cultures for ITS sequencing and SQLE PCR. Treatment is itraconazole pulse 200 mg BD for 1 week per month over 3 to 4 pulses, with oral voriconazole 200 mg BD or posaconazole in refractory disease.[11][12]

Consider T. indotineae in any patient with extensive, recurrent, terbinafine-refractory tinea and a travel or family link to India, Pakistan or Bangladesh — and screen household contacts, because it spreads within families.[11][12]

The antifungal ladder — topical first, systemic when it counts

[1]

The ladder runs topical to systemic, and the rung you choose depends on extent, depth and resistance. Localised disease gets a topical; extensive, follicular, incognito or immunocompromised disease gets a systemic; refractory disease gets culture and resistance testing.[1][4]

Topical antifungals — first-line for localised tinea corporis and cruris:[4]

• Terbinafine 1 percent cream, BD for 1 to 2 weeks — the preferred topical, because the allylamine is fungicidal and beats the fungistatic azoles in head-to-head trials.
• Azoles — clotrimazole 1 percent, miconazole 2 percent, econazole 1 percent, ketoconazole 2 percent, sertaconazole 2 percent, luliconazole 1 percent; apply BD for 2 to 4 weeks where terbinafine is unavailable or cost-restricted.
• Other topicals — ciclopirox 0.77 percent (also antibacterial and anti-inflammatory), tolnaftate (less effective), selenium sulfide shampoo as an adjunct.
• Apply to the lesion and 2 cm beyond, continue for 1 to 2 weeks after clinical resolution, and treat coexisting tinea pedis and unguium. Avoid steroid-antifungal combinations — they cause tinea incognito.

[1] [4]

Systemic antifungals — for extensive, refractory, Majocchi, incognito or immunocompromised disease:[1]

• Terbinafine 250 mg daily for 2 to 4 weeks (corporis and cruris) — first-line systemic; fungicidal allylamine; accumulates in keratin; check LFTs at baseline and at 4 to 6 weeks if prolonged; watch for rare hepatotoxicity and taste or smell disturbance.
• Itraconazole 200 mg BD for 1 week (one pulse), or 100 to 200 mg daily for 1 to 2 weeks — triazole, broad-spectrum; a potent CYP3A4 inhibitor, so avoid with simvastatin, ergots, colchicine and quinidine; contraindicated in heart failure; check LFTs.
• Fluconazole 150 to 300 mg weekly for 2 to 4 weeks — well-tolerated alternative when terbinafine and itraconazole are contraindicated.
• Griseofulvin — superseded for body tinea but still used for capitis; a CYP450 inducer, teratogenic, contraindicated in pregnancy and porphyria.
• Voriconazole and posaconazole — for refractory T. indotineae in specialist hands.

[1] [11] [1] [4]

Site-specific dosing — the region decides the regimen

Two-thirds of recurring "treatment failure" is simply the wrong drug or the wrong duration for that body region. The thick stratum corneum of the palm, the keratin of the nail, and the hair shaft of the scalp each demand a longer or deeper regimen than trunk skin.[1][2]

The site-specific rules that examiners quote:[1]

• Tinea cruris — spares the scrotum and penis (unlike candida intertrigo, which involves it); coexists with tinea pedis, so examine the toes. Topical terbinafine 1 percent BD for 2 weeks for localised disease; oral terbinafine 250 mg OD for 2 weeks for extensive disease. Recurrence approaches 20 percent if the foot reservoir is not cleared.
• Tinea manuum — usually unilateral, with bilateral tinea pedis ("two feet one hand syndrome", pathognomonic of T. rubrum). Topical agents fail on the thick palm, so give oral terbinafine 250 mg OD for 4 weeks.
• Tinea pedis — interdigital (maceration, usually the 4th web space), hyperkeratotic "moccasin", or vesiculobullous. Interdigital gets topical terbinafine 1 percent BD for 1 to 2 weeks; hyperkeratotic or extensive gets oral terbinafine 250 mg OD for 2 to 4 weeks; vesiculobullous adds an oral antibiotic if secondarily infected.
• Tinea unguium (onychomycosis) — confirm with KOH and culture first, because only about half of dystrophic nails are fungal. Oral terbinafine 250 mg OD for 6 weeks (fingernails) or 12 weeks (toenails) is most effective (70 to 80 percent mycological cure); itraconazole pulse 200 mg BD for 1 week per month over 2 pulses (fingernails) or 3 to 4 pulses (toenails) is the alternative.
• Tinea capitis — always systemic, never topical, because the fungus is within the hair shaft. Griseofulvin 20 to 25 mg/kg/day (maximum 1000 mg) for 6 to 12 weeks remains the gold standard; oral terbinafine is weight-based (62.5 mg/day below 20 kg, 125 mg/day for 20 to 40 kg, 250 mg/day above 40 kg). Kerion adds prednisolone 0.5 to 1 mg/kg/day for 1 to 2 weeks to reduce scarring alopecia.

[1] [2] [1] [2] [1]

Traps, confessions and preventable harm

Everyone reaches for the steroid-antifungal combo cream. That is how you manufacture tinea incognito. The combination masks the disease, flattens the active edge, and lets the fungus spread silently — and across South Asia it is the principal driver of recalcitrant dermatophytosis. The rule is simple: a tinea plaque never gets a topical steroid.[1][9]

Everyone forgets the reservoir. Tinea corporis that "keeps coming back" is almost always being re-seeded from an untreated foot, nail or scalp. Examine the feet and nails of every recurrent case, treat the reservoir, and the relapse rate collapses.[1][2]

Consultant confession: the single highest-yield question in a tinea clinic is not "what does it look like?" but "what have you been putting on it?". The over-the-counter triple-action cream is the diagnosis hiding in plain sight — and the answer to why the lesion grew stranger instead of better.[1][7]

The preventable-harm list:[1]

• Applying a steroid-antifungal combination to a tinea plaque — manufactures tinea incognito.
• Treating Majocchi granuloma with a topical — the fungus is in the follicle and the cream cannot reach it.
• Giving 2 weeks of terbinafine to a toenail — it needs 12 weeks; under-treatment is the commonest cause of "failure".
• Missing tinea capitis in a child treated topically — it is always systemic because the fungus is in the hair shaft.
• Missing T. indotineae in extensive, terbinafine-refractory tinea — culture and switch to itraconazole pulse.

[1] [11]

The mantra: scrape the active edge, never steroid a tinea, treat the reservoir, and go systemic when the follicle or the nail is involved.[1]

Prevention and household control

Tinea recurs because the reservoir survives. Clear it by treating coexisting pedis, unguium and capitis; laundering towels and bedding above 60 degrees Celsius; screening and treating household contacts (and the kitten with patchy alopecia for M. canis); keeping skin cool and dry; and for contact-sport athletes, excluding from play until lesions resolve and disinfecting the mats.[1][6]

The IADVL and ICRF consensus targets the AAA (abuse, application, addiction) syndrome — the irrational over-the-counter fixed-dose steroid-plus-antifungal-plus-antibiotic creams that drive tinea incognito and resistance across South Asia. Patient education against these products is itself a public-health intervention.[1][9]

The ward-round test

Click to reveal the stems — answer before you open each one

Stem 1. A wrestler has an itchy annular plaque on his shoulder with a raised scaly edge and central clearing. Name the bedside test, the result, and the first-line treatment with dose and duration.[1]

Answer: KOH microscopy of the active edge shows branching septate hyphae. First-line is topical terbinafine 1 percent BD for 1 to 2 weeks (or oral terbinafine 250 mg OD for 2 to 4 weeks if extensive), plus exclusion from contact sport until clear.[1]

Stem 2. A woman has a facial annular plaque that lost its scale and spread after six weeks of a steroid-antifungal cream. What is the diagnosis and the first action?[7][9]

Answer: Tinea incognito. Stop the steroid cold, confirm with KOH or biopsy, and treat with systemic antifungal (oral terbinafine 250 mg OD for 2 to 4 weeks) — warn the patient about unmasking as it flares before it improves.[7][9]

Stem 3. A man has perifollicular nodules and pustules within a tinea plaque on his shin after shaving. What is the diagnosis and why must treatment be systemic?[10]

Answer: Majocchi granuloma — dermatophyte invasion of the hair follicle. Treatment must be systemic (oral terbinafine or itraconazole for 4 to 6 weeks) because a topical cannot penetrate the follicle.[10]

Stem 4. Extensive, polycyclic, intensely itchy tinea corporis in a patient recently arrived from India fails 4 weeks of oral terbinafine. Name the organism, the resistance mechanism, and the treatment.[11][12]

Answer: Trichophyton indotineae, with SQLE F397L (or L393F, A448T) mutations conferring terbinafine resistance. Treat with itraconazole pulse 200 mg BD for 1 week per month over 3 to 4 pulses, screen household contacts, and avoid the AAA creams.[11][12]

[1]

References

1. [1]Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review Drugs Context, 2020.PMID 32742295
2. [2]Sahoo AK, Mahajan R. Management of tinea corporis, tinea cruris, and tinea pedis: A comprehensive review Indian Dermatol Online J, 2016.PMID 27057486
3. [3]Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and management of tinea infections Am Fam Physician, 2014.PMID 25403034
4. [4]Barac A, Stjepanovic M, Krajisnik S, et al. Dermatophytes: Update on Clinical Epidemiology and Treatment Mycopathologia, 2024.PMID 39567411
5. [5]Moskaluk AE, VandeWoude S. Current Topics in Dermatophyte Classification and Clinical Diagnosis Pathogens, 2022.PMID 36145389
6. [6]Kovitwanichkanont T, Chong AH. Superficial fungal infections Aust J Gen Pract, 2019.PMID 31569324
7. [7]Arenas R, Moreno-Coutiño G, Vera L, et al. Tinea incognito Clin Dermatol, 2010.PMID 20347654
8. [8]Kokandi AA. Tinea Incognito Clin Cosmet Investig Dermatol, 2024.PMID 38737948
9. [9]Shony S, Lobo C, Kaimal S. Tinea incognito Cleve Clin J Med, 2025.PMID 40312118
10. [10]Boral H, Durdu M, Ilkit M. Majocchi's granuloma: current perspectives Infect Drug Resist, 2018.PMID 29861637
11. [11]Lockhart SR, Chowdhary A, Gold JAW. The rapid emergence of antifungal-resistant human-pathogenic fungi Nat Rev Microbiol, 2023.PMID 37648790
12. [12]Gupta AK, Susmita, Nguyen HC, et al. Trichophyton indotineae: Epidemiology, antifungal resistance and antifungal stewardship strategies J Eur Acad Dermatol Venereol, 2026.PMID 40613321