Key Takeaways
- Tinea is caused by dermatophyte fungi — Trichophyton, Microsporum, and Epidermophyton — not by worms. The clinical name (tinea corporis, tinea pedis, etc.) tells you the body site, not the organism.
- Most skin infections respond to topical antifungals like terbinafine 1% cream or clotrimazole 1% applied for the full prescribed duration. Stopping early is the leading reason for treatment failure.
- Tinea capitis (scalp ringworm) and onychomycosis (nail fungus) require oral antifungal therapy — topical creams cannot penetrate deeply enough to clear these infections.
- Tinea incognito is a clinically altered fungal infection caused by applying topical steroids to an unrecognized tinea lesion. It spreads widely, loses its classic ring appearance, and is frequently misdiagnosed as eczema or psoriasis.
- In children with tinea capitis, oral treatment is mandatory. Terbinafine (dosed by weight) for 4–6 weeks is first-line for Trichophyton species, which account for over 89% of U.S. cases.[1]
- Nail fungus treatment is long — 12 weeks of oral terbinafine for toenails — and the nail may not look visually normal for another 6–12 months after the infection has cleared.
Fungal skin infections are among the most common dermatologic conditions in clinical practice. In my experience, the biggest problem isn't diagnosis — it's the pattern of partial treatment, premature stopping, and the cascade of complications that follow. A patient who uses an antifungal cream for three days instead of two weeks, or who is given a steroid cream for what is actually a fungal rash, often ends up with a significantly worse infection than when they started.
The word "tinea" simply means fungal infection of the skin, hair, or nails caused by dermatophytes. The full name identifies where on the body the infection is: tinea pedis on the feet, tinea capitis on the scalp, tinea unguium on the nails. The organism doesn't change — what changes is the anatomy involved, and that anatomy determines how you treat it.
This guide covers all the major types, how they're diagnosed, what the current evidence says about treatment, and the clinical traps — especially tinea incognito and scalp infections in children — that lead to prolonged, worsening infections when handled incorrectly.
The Fungi Behind Tinea: Dermatophytes Explained
Three genera of fungi cause virtually all dermatophyte infections: Trichophyton, Microsporum, and Epidermophyton. All three are keratinophilic — they digest keratin, the structural protein in skin, hair, and nails. This keratin dependence explains both where these infections occur (surface skin, hair shaft, nail plate) and why they don't invade deeper tissues in immunocompetent patients.
Trichophyton rubrum is the dominant species worldwide and accounts for the majority of tinea pedis, tinea unguium, tinea corporis, and tinea cruris cases.[1] In the United States, Trichophyton tonsurans causes more than 89% of tinea capitis cases — a clinically important fact because terbinafine outperforms griseofulvin against Trichophyton species, while griseofulvin retains superiority for Microsporum infections, which are more common in certain regions of South America, Europe, Africa, and the Middle East.[1]
Dermatophytes are transmitted three ways: person-to-person contact (anthropophilic species), animal-to-person contact (zoophilic species — cats and dogs are common vectors), and from soil (geophilic species). Microsporum canis, a zoophilic species acquired from cats and dogs, is a frequent cause of tinea capitis outside the United States and should be considered in patients with recent animal contact.
The AAD has flagged Trichophyton indotineae — a strain spreading globally, originally from South Asia — as a serious emerging concern. This organism causes extensive, treatment-resistant dermatophytosis that does not respond to standard terbinafine therapy. Prolonged oral antifungal therapy and specialized diagnostic testing are needed for these cases. If a patient presents with widespread, refractory tinea that fails standard topical and oral treatment, especially with recent international travel history, referral to dermatology and fungal culture are warranted.[3]
Types of Tinea by Body Location
Tinea Corporis (Body Ringworm)
Tinea corporis is the classic "ringworm" — a circular or oval scaly plaque with a raised, advancing border and relative clearing at the center. It appears on smooth (glabrous) skin of the trunk, arms, or legs. The lesion expands centrifugally as the fungus progresses outward, which is why the border is the most active zone and the best place to scrape for KOH preparation. Itching is common but variable.
Topical terbinafine 1% once daily for 1–2 weeks is highly effective for limited tinea corporis and clears most cases.[2] Clotrimazole 1% or miconazole 2% twice daily for 2–4 weeks are reasonable alternatives. Oral therapy is reserved for extensive or refractory disease.
Tinea Pedis (Athlete's Foot)
Tinea pedis is the most common dermatophytosis globally, affecting an estimated 15–25% of the population at any given time. Three clinical patterns exist: interdigital (scaling, maceration, and fissuring in the web spaces — most common), moccasin-type (dry, diffuse scaling over the plantar surface and heel), and vesiculobullous (blisters, usually on the instep, often with intense itch).
Topical terbinafine is the first choice. For the dry moccasin type, twice-daily application for at least 2 weeks is needed because the thickened stratum corneum limits penetration. The interdigital type responds faster — often within 1 week of terbinafine. Recurrence is high without attention to footwear hygiene, moisture management, and treating any associated tinea unguium (which re-seeds the skin).
Tinea Cruris (Jock Itch)
Tinea cruris involves the inguinal folds, inner thighs, and perianal area. It characteristically spares the scrotum in men — a useful clinical feature that helps distinguish it from candidal intertrigo, which more often involves the scrotum. The advancing edge is sharply demarcated and may have a papular or vesicular component.
Topical antifungals applied twice daily for 10–14 days clear most cases.[3] Keeping the area dry, wearing breathable fabric, and avoiding tight clothing are essential supportive measures. Tinea pedis frequently coexists and should be treated simultaneously to prevent re-infection from the feet.
Tinea Capitis (Scalp Ringworm)
Tinea capitis infects the scalp and hair shafts, presenting most often in prepubertal children. The classic pattern is patchy hair loss with scaling and broken hairs at the scalp surface ("black dot" pattern with T. tonsurans). "Gray patch" tinea, caused by Microsporum species, produces larger patches of scaling with fluorescence under Wood's lamp. A kerion — a boggy, tender, inflamed mass on the scalp — represents the host's inflammatory response to the fungus and can cause scarring alopecia if not treated promptly.
Oral treatment is mandatory for tinea capitis. Topical agents do not penetrate the hair follicle.[4] This is a point I cannot overstate when speaking with parents who ask about just using a shampoo. An antifungal shampoo reduces spore shedding and transmission risk, but it will not cure the infection — a course of oral medication is non-negotiable. This is covered in detail in the section below on pediatric treatment.
Tinea Unguium / Onychomycosis (Nail Fungus)
Onychomycosis is the most treatment-resistant and longest-duration tinea infection. It affects an estimated 10% of the general population, rising to 20–30% in those over age 60.[2] The classic presentation is distal subungual onychomycosis: yellow-brown discoloration, nail thickening, subungual debris, and onycholysis (nail plate separation) starting at the free edge and advancing proximally. Toenails are affected far more often than fingernails.
What I tell patients is this: treating nail fungus is a long commitment. Even after the infection is mycologically cured, the nail takes months to grow out looking normal. Set that expectation early, because patients who see a still-thickened nail at their six-week follow-up frequently stop taking their medication — exactly the wrong decision.
Diagnosing Tinea: KOH Prep and Fungal Culture
Most tinea infections can be diagnosed clinically, but laboratory confirmation matters when the presentation is atypical, when first-line treatment has failed, or when you're about to start oral antifungal therapy — especially in children or patients with liver disease.
KOH Preparation (Potassium Hydroxide Prep)
The KOH prep is a rapid, inexpensive office test. Skin scrapings (from the advancing edge of the lesion), nail clippings, or hair stubs are placed on a slide, treated with 10–40% potassium hydroxide solution, and examined under microscopy. KOH dissolves keratin and host cell material, leaving fungal hyphae clearly visible as branching, septate filaments. A positive KOH prep confirms dermatophyte infection within minutes.[1]
Sensitivity varies with technique and specimen quality. For nail infections, 40% KOH with dimethyl sulfoxide (DMSO) improves clearing. Scraping from the periphery — not the center — of a tinea corporis lesion yields more fungal elements.
Fungal Culture
Culture on Sabouraud dextrose agar or dermatophyte test medium (DTM) identifies the specific organism and provides susceptibility data — important when choosing between terbinafine and griseofulvin for tinea capitis, or when managing suspected resistant infection. The major drawback is time: cultures take 2–6 weeks to yield results. In most straightforward cases, empiric treatment is started while culture results are pending.
I perform a KOH prep when: (1) the diagnosis is uncertain, (2) the lesion is not responding to empiric topical treatment after 2 weeks, (3) I'm about to prescribe oral antifungals and want confirmation, or (4) the presentation looks like it could be tinea incognito. A 2-week trial of topical antifungal (without a steroid) is a reasonable first step when testing isn't immediately available — if the lesion doesn't improve or clearly worsens, that redirects the workup.[1]
Tinea Incognito: The Steroid-Masked Infection
Tinea incognito is one of the more consequential diagnostic pitfalls in dermatology. The sequence is predictable: a patient presents with a scaly, itchy rash; the clinician (or the patient themselves, using an OTC steroid) identifies it as eczema or contact dermatitis and applies a topical corticosteroid. The steroid suppresses the inflammatory response, which makes the rash less red and less itchy — temporarily. The patient is initially satisfied. Then the rash returns, spreads, and looks nothing like a typical tinea lesion.
The potassium hydroxide prep is the exit from this diagnostic loop. Because steroids mask the classic ring-shaped border and reduce the erythema, tinea incognito can mimic eczema, seborrheic dermatitis, discoid lupus, psoriasis, or rosacea — depending on where it appears on the body.[5] A positive KOH at that point reveals the fungal etiology that was present all along.
Treatment requires two steps: stop the steroid, then treat the fungal infection. The skin may briefly look worse after steroid withdrawal before it improves — a phenomenon that needs to be explained to the patient in advance. Oral antifungals are frequently needed for tinea incognito because the infection has usually spread beyond what topical therapy can reach.
Combination antifungal-corticosteroid creams (such as clotrimazole-betamethasone) are widely available and frequently misused. They suppress symptoms while allowing the fungal infection to spread. Clinical guidelines specifically discourage their use for tinea management outside of very limited circumstances.[1] If you're unsure whether a rash is fungal or inflammatory, a plain antifungal cream (no steroid) is the safer empiric choice. A lesion that is truly eczema will not worsen from a brief antifungal trial.
Tinea Capitis in Children: Why Oral Treatment Is Non-Negotiable
Parents frequently ask whether a medicated shampoo will clear their child's scalp ringworm. The short answer is no — and this distinction is worth explaining clearly.
The dermatophyte in tinea capitis infects the hair shaft itself, residing inside the follicle. Topical agents, regardless of concentration or duration of use, cannot penetrate deeply enough to reach the fungus at that level. Systemic antifungal therapy is the only way to deliver therapeutic drug concentrations to the site of infection.[4] Antifungal shampoos (selenium sulfide 1–2.5%, ketoconazole 2%) are useful adjuncts to reduce transmission and spore shedding for the first 2 weeks of oral treatment — but they are not substitutes.
Choosing the Right Oral Agent
In the United States, where T. tonsurans dominates, oral terbinafine is the preferred first-line agent for tinea capitis. It has shorter treatment duration than griseofulvin and equivalent or superior efficacy against Trichophyton species.[1] Dosing is weight-based:
| Child's Weight | Terbinafine Dose | Duration |
|---|---|---|
| 10–20 kg | 62.5 mg/day | 4–6 weeks (Trichophyton); 8–12 weeks (Microsporum) |
| 20–40 kg | 125 mg/day | 4–6 weeks (Trichophyton); 8–12 weeks (Microsporum) |
| >40 kg | 250 mg/day | 4–6 weeks (Trichophyton); 8–12 weeks (Microsporum) |
Griseofulvin (micronized, 20–25 mg/kg/day for 6–12 weeks) remains preferred for Microsporum species infections and is FDA-approved for pediatric use. It is taken with a fatty meal to improve absorption. The long course and potential for GI side effects (nausea, headache) reduce compliance — worth anticipating in practice.[4]
If a child develops kerion — the tender, boggy, abscess-like variant of tinea capitis — a short course of oral corticosteroids may be added alongside antifungal therapy to reduce the inflammatory response and lower the risk of scarring alopecia. The underlying infection still requires full antifungal treatment.
School attendance: children being treated for tinea capitis do not need to be excluded from school once oral therapy has been started, per current guidance. The transmission risk decreases substantially within the first week of effective treatment.
Antifungal Treatment: Topical vs. Oral
Topical Antifungals
For tinea on the body, groin, or feet without nail or hair follicle involvement, topical therapy is the appropriate first approach. The allylamine class (terbinafine, butenafine) is generally more effective than the azole class (clotrimazole, miconazole, ketoconazole) because allylamines are fungicidal rather than merely fungistatic — they kill the organism rather than just inhibiting its growth.[2]
| Agent | Class | Typical Regimen | Best Used For |
|---|---|---|---|
| Terbinafine 1% (Lamisil AT) | Allylamine | Once daily, 1–2 weeks | Tinea corporis, tinea cruris, tinea pedis — first choice |
| Butenafine 1% (Lotrimin Ultra) | Benzylamine | Once daily, 1–4 weeks | Tinea pedis, tinea corporis, tinea cruris |
| Clotrimazole 1% | Azole | Twice daily, 2–4 weeks | All smooth-skin tinea types; OTC availability |
| Miconazole 2% | Azole | Twice daily, 2–4 weeks | All smooth-skin tinea types; combination antifungal |
| Ketoconazole 2% | Azole | Once daily, 2–4 weeks | Broad spectrum; tinea versicolor, seborrheic dermatitis |
| Ciclopirox 8% lacquer | Hydroxypyridone | Once daily, up to 48 weeks | Mild-moderate onychomycosis without matrix involvement |
The most common reason topical treatment fails is stopping too early. Even if the rash looks cleared, stopping before the recommended duration leaves residual fungal elements that cause rapid relapse. Complete the full course.
Oral Antifungals: When They're Required
Oral therapy is necessary when topical treatment is insufficient: tinea capitis, onychomycosis, extensive or refractory tinea corporis/pedis, or immunocompromised patients.
| Agent | Indication | Dose & Duration | Key Notes |
|---|---|---|---|
| Terbinafine 250 mg | Onychomycosis (toenail), tinea capitis, extensive tinea | 250 mg/day × 6 weeks (fingernail) or 12 weeks (toenail); 4–6 weeks for tinea capitis | First-line for Trichophyton. Fungicidal. Check LFTs in patients with hepatic disease. Taste disturbance in ~3%. |
| Itraconazole 200 mg | Onychomycosis, tinea capitis (alternative), extensive tinea | Continuous: 200 mg/day × 12 weeks (toenail); Pulse: 400 mg/day × 1 week/month × 3 months (toenail) | Equally effective to terbinafine for onychomycosis. Drug interactions (CYP3A4). Take with food for best absorption. |
| Griseofulvin | Tinea capitis, extensive tinea | Ultramicrosize: 10–15 mg/kg/day × 6–8 weeks (tinea capitis); up to 12 weeks if needed | Preferred for Microsporum species; FDA-approved for children. Take with fatty meal. GI side effects limit compliance. |
Onychomycosis: The Long Game
Nail fungus is the condition where patient education matters most, because the timeline is counterintuitive. The antifungal drug stops the infection within the treatment window, but nails grow slowly — toenails at roughly 1.5 mm per month. After completing 12 weeks of terbinafine, the proximal nail matrix is clear, but the visibly abnormal portion of the nail that existed at treatment start has to physically grow out before the nail looks healthy. That can take another 9–12 months.
What I tell patients is: "Think of the drug as pulling up the weed by the root. But the old dead plant is still there — it just has to grow out. Keep your follow-up appointments and don't judge success by how the nail looks at the end of your pill course."
Pulse Dosing with Itraconazole
Itraconazole's unique pharmacokinetics make pulse dosing possible and clinically rational. The drug accumulates in the nail plate and keratin-containing tissues at concentrations that persist for months after therapy ends. Studies demonstrate itraconazole remains detectable in the distal nail for several months after the final pulse.[6]
The standard pulse regimen is 400 mg/day (200 mg twice daily) for 1 week per month, repeated for 2 cycles for fingernails or 3 cycles for toenails. Cure rates of approximately 77–82% mycological cure have been reported with three-pulse toenail regimens.[6] Pulse dosing reduces total drug exposure compared to continuous therapy, with similar efficacy — a meaningful advantage for patients with drug interaction concerns or cost sensitivity.
Confirming the Diagnosis Before Starting Oral Therapy
Not all thick, discolored nails are fungal. Trauma, psoriasis, lichen planus, and other conditions produce onychomycosis-like nail changes. Before committing to 12 weeks of oral terbinafine or itraconazole, confirm the diagnosis. Nail clipping for KOH and fungal culture is the standard approach. Sending the clipping with subungual debris increases sensitivity.
Tinea vs. Eczema vs. Psoriasis
These three conditions share enough visual overlap to generate frequent misdiagnosis. The consequences matter: treating eczema or psoriasis with a topical steroid is correct; treating tinea with a steroid makes it dramatically worse. Here's a practical clinical comparison:
| Feature | Tinea | Eczema (Atopic Dermatitis) | Psoriasis |
|---|---|---|---|
| Border | Sharply raised, advancing, scaly edge with central clearing | Indistinct, merges with surrounding skin | Well-defined, sharp plaque border |
| Scale | Fine scale at periphery; less at center | Fine scale, may weep or crust | Thick, silvery-white ("micaceous") scale |
| Distribution | Asymmetric; spreads outward from point of inoculation | Symmetric; inner elbows, behind knees, face, neck | Elbows, knees, scalp, sacrum, nails |
| Itching | Moderate; variable | Intense; worse at night | Burning or stinging; less intense itch than eczema |
| KOH prep | Positive (hyphae visible) | Negative | Negative |
| Response to steroids | Temporary improvement, then worsening and spread (tinea incognito) | Improves with steroids | Improves with steroids; rebound possible on stopping |
| Triggers/history | Animal contact, shared items, locker rooms, warm/moist skin | Allergens, soaps, stress, known atopic history | Stress, infection, skin trauma, family history |
The single most useful differentiating test is a KOH preparation. When the clinical picture is unclear and you're considering starting a corticosteroid, do the KOH prep first. It's rapid, inexpensive, and the result changes management in a clinically significant way.
Prevention: Moisture, Hygiene, and Pets
Dermatophytes thrive in warm, moist environments. Preventing tinea is largely about managing those conditions and limiting contact with known sources.
Moisture Management
Athlete's foot and tinea cruris are both strongly associated with persistent moisture on the skin. Dry thoroughly between the toes after bathing. Change out of wet workout clothes promptly. Wear moisture-wicking socks and change them if they become wet. Antifungal powders (miconazole or tolnaftate formulations) in shoes and on the feet can reduce recurrence risk in people with a history of tinea pedis.
Personal Items and Shared Spaces
Don't share towels, washcloths, clothing, hats, combs, or nail clippers. Tinea capitis spreads through shared combs and hats among children — this is the primary transmission route in school-age outbreaks. In shared locker rooms and pool areas, wear flip-flops or shower shoes. These measures are low-effort and genuinely reduce transmission.
Pet Transmission
Zoophilic dermatophytes — particularly Microsporum canis from cats and dogs — are a meaningful source of tinea in households with pets. A cat or dog with patchy hair loss, scaly skin, or bald spots on the muzzle should be evaluated by a veterinarian. Family members with unexplained tinea corporis, especially on the face or arms, should consider their pet as a potential source. Treating the animal is necessary to prevent ongoing reinfection of household contacts.
Household and Clothing Decontamination
For tinea capitis in children, washing pillowcases, hats, and combs with hot water and regular detergent is sufficient to reduce environmental spore burden. Dermatophytes do not survive long on inanimate objects, so elaborate disinfection protocols are not necessary — basic hygiene is.
Dermatology and Tinea via Telehealth
Many tinea infections — particularly tinea corporis, tinea cruris, and uncomplicated tinea pedis — are well-suited to telehealth evaluation. A physician can review photos of the rash, assess the clinical pattern, evaluate the history (duration, prior treatment, associated symptoms), and prescribe topical or oral antifungals without an in-office visit.
Telehealth has specific practical value for tinea because the most common treatment error is incorrect diagnosis followed by a steroid application. Getting an accurate diagnosis early — even by video — prevents the tinea incognito cascade. A patient who calls in with a ring-shaped scaly rash can have that diagnosis confirmed and receive an appropriate antifungal prescription the same day.
Conditions requiring in-person evaluation include: tinea capitis where a culture is needed to guide therapy (especially if Microsporum is suspected), kerion requiring physical examination, onychomycosis where nail clipping and KOH are needed for confirmation before committing to 12 weeks of oral antifungals, and cases with suspected secondary bacterial infection. The TeleDirectMD team can assess which of these apply to your situation and coordinate referral when needed.
For questions about tinea or fungal skin infections, contact us at 678-956-1855 or contact@teledirectmd.com.
Red Flags: When to Seek Prompt Evaluation
- A rash that spreads despite 2 weeks of topical antifungal — suggests either tinea incognito (if steroids were applied), an incorrect diagnosis, or a resistant organism
- A child with scalp hair loss and scaling — do not attempt topical treatment; tinea capitis requires oral therapy and culture guidance
- A tender, boggy scalp mass (kerion) — risk of permanent scarring; needs prompt oral antifungal ± steroid treatment
- Nail changes in a diabetic patient — nail fissures can serve as entry points for bacterial infection; confirm the diagnosis and treat
- Widespread tinea in an immunocompromised patient — HIV, organ transplant, or high-dose steroid patients are at risk for invasive or extensive dermatophytosis requiring specialist management
- Prior treatment with a combination antifungal-steroid cream — the infection may now have atypical features; KOH and culture are needed before restarting treatment
Frequently Asked Questions
No — the name is misleading. Ringworm is a fungal infection caused by dermatophytes, not worms of any kind. The name comes from the characteristic ring-shaped rash that tinea corporis can produce on smooth skin. The fungi responsible — Trichophyton, Microsporum, and Epidermophyton — feed on keratin, the protein in your skin, hair, and nails. No parasitic worms are involved.
For tinea on the body, groin, or feet, yes — OTC antifungal creams containing terbinafine 1%, clotrimazole 1%, or miconazole 2% are effective for most cases. Apply for the full recommended duration (1–4 weeks depending on the product and location). Stopping early because the rash looks better is the most common reason for recurrence. Tinea on the scalp and nail infections cannot be cleared with topical creams and require prescription oral antifungals.[1]
For skin infections treated topically, meaningful improvement typically appears within 1–2 weeks, but the full course must be completed. Tinea capitis with oral terbinafine usually clears in 4–6 weeks. Nail fungus is the slowest — 12 weeks of oral terbinafine for toenails clears the infection, but visual nail improvement requires months of nail regrowth. The nail itself can take 6–12 months to look normal even after the fungus is gone. This does not mean treatment failed; it means nails grow slowly.
Yes. Dermatophyte infections spread through direct skin-to-skin contact, contact with contaminated items (towels, combs, locker room floors), and from infected animals. Tinea capitis spreads easily among children sharing hats or combs. Cats and dogs with patchy hair loss or scaly skin can transmit Microsporum canis to family members. Avoid sharing personal items, wear footwear in shared wet areas, and have any household pet with suspicious skin changes evaluated by a veterinarian.
Several possibilities: a steroid cream may have been applied (which worsens tinea by suppressing the immune response while the fungus continues to spread — this is tinea incognito), treatment may have been stopped too early, or reinfection is occurring from contaminated clothing, bedding, or a household contact. Toenail fungus can continuously re-seed a treated skin infection if it isn't addressed simultaneously. A KOH preparation confirms whether you're still dealing with a fungal infection or whether the diagnosis needs to be reconsidered.[5]
Almost always. Topical nail lacquers (ciclopirox, efinaconazole, tavaborole) are an option for very mild cases — specifically, infections limited to the distal nail tip without matrix involvement. Most onychomycosis, especially cases where the nail root or more than a third of the nail is involved, requires oral terbinafine or itraconazole. Oral terbinafine 250 mg daily for 6 weeks (fingernails) or 12 weeks (toenails) is first-line. Confirm the diagnosis with KOH and culture before committing to oral therapy.[1]
Tinea capitis infects the hair shaft inside the follicle. Topical creams — even prescription-strength — cannot penetrate deeply enough to reach the fungus at that level. Oral antifungal therapy is the only effective approach. Antifungal shampoos reduce surface spore counts and lower transmission risk, and are used alongside oral therapy for the first 2 weeks — but as an adjunct, not a replacement. Oral terbinafine dosed by weight is standard first-line for the Trichophyton species that dominate in the U.S.[4]
Tinea typically has a raised, scaly border with some central clearing, spreads outward asymmetrically, and often has a traceable exposure (gym, pet, contact). Eczema tends to be symmetric, affects skin folds (inner elbows, behind knees), and is associated with allergens or soaps. Psoriasis produces well-defined, thick, silvery-scaled plaques on the elbows, knees, and scalp. The definitive differentiator is a KOH prep — it shows fungal hyphae in tinea and is negative in eczema and psoriasis. If applying a topical antifungal for 2 weeks doesn't help or makes things worse, reconsider the diagnosis.
References
- Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and Management of Tinea Infections. American Family Physician. 2014;90(10):702–711. https://pmc.ncbi.nlm.nih.gov/articles/PMC12707599
- Nenoff P, Krüger C, Ginter-Hanselmayer G, Tietz HJ. Mycology — An Update. Part 1: Dermatomycoses: Causative Agents, Epidemiology and Pathogenesis. Journal of Fungi. 2018;4(3):99. https://pmc.ncbi.nlm.nih.gov/articles/PMC6162762/
- American Academy of Dermatology. Ringworm: Diagnosis and Treatment. Accessed March 2026. https://www.aad.org/public/diseases/a-z/ringworm-treatment
- Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the Management of Tinea Capitis in Children. Pediatric Dermatology. 2010;27(3):226–228. Also: Management of Tinea Capitis in Childhood. Clinical, Cosmetic and Investigational Dermatology. 2010;3:89–98. https://pmc.ncbi.nlm.nih.gov/articles/PMC3047946/
- Sahoo AK, Mahajan R. Tinea Incognito: Challenges in Diagnosis and Management. Journal of Clinical Medicine. 2024;13(11):3237. https://pmc.ncbi.nlm.nih.gov/articles/PMC11172699/
- Gupta AK, et al. Antifungal Pulse Therapy for Onychomycosis: A Pharmacokinetic and Pharmacodynamic Basis for Intermittent Dosing. Archives of Dermatology. 1996;134(1). https://pubmed.ncbi.nlm.nih.gov/8546481/
- Hay RJ. Itraconazole Pulse Therapy for Onychomycosis and Dermatomycoses: An Overview. Journal of the American Academy of Dermatology. 1997;37(3 Pt 2):S28–S32. https://pubmed.ncbi.nlm.nih.gov/9418766/
- American Academy of Family Physicians. Common Tinea Infections in Children. American Family Physician. 2008;77(10):1415–1420. https://www.aafp.org/pubs/afp/issues/2008/0515/p1415.html