Ringworm (Tinea Corporis and Tinea Capitis)

"Ringworm" is a lay term for dermatophyte (tinea) infection, named for the classic annular, ring-shaped lesion of tinea corporis — a smooth-skin infection of the trunk, limbs, or neck, most often caused by Trichophyton rubrum or other Trichophyton species, that expands outward while clearing centrally and responds reliably to topical antifungal therapy alone in the great majority of cases.^[1] Tinea capitis, the scalp equivalent, is overwhelmingly a disease of young children and looks superficially related, but differs from tinea corporis in a way that is genuinely decisive for treatment: the dermatophyte invades the hair shaft and follicle itself, not just the surface stratum corneum, so a topical cream — however appropriate it would be for a skin lesion — simply cannot reach the infection.^[1] Systemic antifungals should be used to treat tinea capitis because topical agents do not penetrate hair follicles, and this single distinction is the organizing principle of this entire chapter: tinea corporis is genuinely a self-care condition with an appropriately chosen topical agent, while any patient with suspected tinea capitis needs to be recognized and referred for oral prescription therapy, not managed with an OTC cream or shampoo alone.^[1] Both conditions also carry a transmission dimension worth building into routine counselling: direct contact with an infected person, contact with an infected household pet (cats and dogs, particularly kittens), and contact with a contaminated shared object — a comb, hairbrush, hat, or pillowcase — can all seed a new infection, and spores can remain viable on such objects for months.^[2][3]

Tinea corporis: the classic ring

Tinea corporis presents as a red, annular (ring-shaped), scaly, pruritic plaque with an active, raised, scaly border and a zone of central clearing — the lesion expands centrifugally as the fungus advances outward through the stratum corneum, leaving relatively normal-appearing skin behind it in the middle.^[1] Lesions are typically 1-5 cm but can be larger, and several lesions can appear at once or merge into a single irregular plaque with multiple advancing edges.^[1] A history of pruritus, recent contact with an infected person, pet, or contaminated object, and a well-demarcated advancing border on examination are the key clinical clues.

Two tinea corporis ("ringworm") lesions on the forearm, showing the classic raised, scaly active border and central clearing that give the condition its lay name. (Grook Da Oger, CC BY-SA 3.0, Wikimedia Commons)

Tinea capitis: 2 organism-driven presentations in children

Tinea capitis is the most common dermatophyte infection of childhood and presents differently depending on the causative organism and how it invades the hair shaft.^[2]

Tinea capitis in a young child — a single, rounded, hairless patch caused by a zoophilic Microsporum infection acquired through contact with a cat, illustrating the zoonotic transmission pathway discussed below. (Wikimedia Commons contributor, CC BY-SA 4.0)

Beyond hair loss and scale, look specifically for posterior cervical, suboccipital, or postauricular lymphadenopathy — a genuinely useful bedside finding, since tinea capitis (unlike its common mimics, seborrheic dermatitis and psoriasis) frequently produces regional lymph node enlargement.^[3]

Kerion: the inflammatory complication

A kerion is a severe, delayed hypersensitivity reaction to the fungal infection presenting as a boggy, tender, fluctuant, often pustular inflammatory mass on the scalp with associated hair loss — it can look alarmingly like a bacterial abscess, but is a fungal-driven immune reaction, not a primary bacterial infection.^[3][2] Left untreated, or if incision/drainage and antibiotics are pursued instead of antifungal therapy, a kerion carries a real risk of permanent, scarring alopecia. The Canadian Paediatric Society is explicit that a kerion responds to oral terbinafine and usually does not require antibiotics or surgical drainage — the correct next step is prompt, adequately dosed oral antifungal therapy, not incision and drainage.^[2]

A kerion — a boggy, tender, pustular inflammatory mass with hair loss, the delayed-hypersensitivity complication of tinea capitis that responds to oral antifungal therapy rather than antibiotics or drainage. (Grook Da Oger, CC BY-SA 4.0, Wikimedia Commons)

• Household pet ownership, particularly kittens and cats, and stray-cat contact — the classic source of zoophilic Microsporum canis infection.^[3]
• Sharing combs, hairbrushes, hats, helmets, headphones, pillowcases, towels, or headrests — fungal spores on these fomites can remain viable for months.^[2][3]
• Close-contact activities: wrestling and other skin-to-skin contact sports for tinea corporis; classroom, daycare, and household contact for tinea capitis, which spreads readily among young children.^[2]
• Age: tinea capitis is overwhelmingly a disease of preschool and school-age children; it is uncommon, though not absent, in adults — consider it in postmenopausal women and immunosuppressed adults with new scalp scaling or hair loss.
• African heritage and shared hair-care practices/tools (braiding, pomades, communal grooming implements) — a genuine epidemiologic driver of the North American predominance of Trichophyton tonsurans tinea capitis.^[2][3]
• Warm, humid climates and occlusive clothing or heavy sweating, which favour tinea corporis on the trunk and limbs.
• A disrupted skin barrier — concurrent atopic dermatitis or minor skin trauma — makes inoculation of tinea corporis easier.
• Immunosuppression, which can produce more extensive or atypical disease at either site.
• An untreated household member, sibling, or classmate with active tinea corporis or tinea capitis.

History

• Onset, distribution, and whether the lesion is expanding; pruritus; and, for scalp involvement, hair loss, scaling, or a tender/boggy area.
• Exposure history: household pets (especially kittens/cats), stray animal contact, close-contact sports, daycare/school contacts with similar symptoms, and sharing of combs, hats, or pillowcases.^[2][3]
• Prior treatment, including any topical corticosteroid applied to the lesion before the correct diagnosis was considered (risk of tinea incognito).
• Immunosuppression or diabetes.

Examination

For tinea corporis, confirm the annular shape with an active, scaly, slightly raised border and central clearing. For suspected tinea capitis, examine for scaling, patchy alopecia, black-dot stubble versus larger grey-patch scaling, a boggy/fluctuant kerion, and regional (posterior cervical, suboccipital, postauricular) lymphadenopathy, which favours tinea capitis over its non-infectious mimics.^[3]

Wood's lamp examination

A Wood's lamp (UV-A light) can support the diagnosis of tinea capitis, but its result must be interpreted by organism: hairs infected with Microsporum species fluoresce bright green under Wood's lamp, while Trichophyton tonsurans — the endothrix organism that predominates in North America — does not fluoresce.^[3] This is a genuinely important pitfall: a negative Wood's lamp examination does not rule out tinea capitis, since the most common North American organism will not fluoresce regardless of how active the infection is. A positive fluorescence is a useful positive finding; a negative one is not reassuring on its own.

KOH microscopy and culture

Potassium hydroxide (KOH) wet-mount microscopy of a skin scraping taken from the active border (tinea corporis) or of plucked hairs and scale from the affected area (tinea capitis) rapidly confirms hyphae or spores under light microscopy and can be performed at the point of care.^[1][3] Fungal culture takes 1-3 weeks to result but is the reference standard for species identification, and the Canadian Paediatric Society specifically recommends it for persistent or recurrent tinea capitis, since the causative species (Trichophyton versus Microsporum) directly changes the expected treatment duration.^[2] Because culture is slow, empiric oral therapy for clinically clear tinea capitis should not wait for culture results, but a specimen is worth sending at the outset so species-directed adjustments can be made if the initial response is inadequate.

Differential diagnosis

• Achieve mycological cure, not just symptomatic improvement.
• Match the treatment route to the site: topical therapy for tinea corporis; oral therapy is mandatory for any tinea capitis, since topical agents cannot penetrate the infected hair follicle.
• For tinea capitis, prevent scarring alopecia, particularly with a kerion, through prompt, adequately dosed oral therapy rather than delay or inappropriate antibacterial/surgical management.
• Reduce household, classroom, and daycare transmission through appropriate antifungal therapy and fomite/pet decontamination.
• Prevent recurrence by identifying and addressing an ongoing reservoir — an infected pet, an untreated household contact, or shared grooming items.

• Have household pets — particularly kittens and cats — checked and, if infected, treated by a veterinarian when a zoonotic source is suspected or when a household's tinea capitis keeps recurring despite adequate therapy.^[3]
• Do not share combs, hairbrushes, hats, helmets, headphones, towels, or pillowcases; disinfect or launder these items in hot water, since fungal spores can remain viable on fomites for months.^[2][3]
• For tinea capitis specifically, wash pillowcases, hats, and hair accessories in hot water and consider soaking combs and hairbrushes in a diluted bleach solution during the early treatment period.
• Keep tinea corporis lesions covered during contact sports (wrestling, judo, and similar), and shower promptly after practice or competition to reduce transmission to teammates.
• Screen household members, siblings, and close contacts for similar lesions or scalp scaling, since an unaddressed contact is a common source of reinfection.
• Once appropriate oral antifungal therapy for tinea capitis has begun, most experts do not consider school or daycare exclusion necessary — reinforce ordinary hygiene precautions (no head-to-head contact, no sharing of hats or combs) rather than routine exclusion, unless local public health guidance specifies otherwise.
• Set the expectation explicitly: continue treatment for the full prescribed duration, and for tinea corporis specifically, at least 14 days past the point the skin looks clear — stopping as soon as symptoms improve is a common, avoidable cause of relapse.^[2]

Pregnancy

Breastfeeding

Topical antifungals are compatible with breastfeeding given minimal systemic absorption. Data on the oral agents in lactation are more limited; the prescribing clinician should weigh the same benefit/risk considerations as in pregnancy.

Pediatrics

Tinea capitis is overwhelmingly a pediatric disease, most common in preschool and school-age children, and disproportionately affects children of African heritage in North America given the predominance of Trichophyton tonsurans and shared hair-care practices.^[2] Use weight-based oral terbinafine dosing as above, and remember that most experts do not consider school exclusion necessary once appropriate oral therapy has begun.

Adults

Tinea capitis is uncommon in adults but does occur, particularly in postmenopausal women and immunosuppressed patients, and is frequently misdiagnosed initially as seborrheic dermatitis given the overlapping scalp scaling — a genuine reason to keep tinea capitis on the differential for adult scalp scaling with hair thinning, not just in children.

Immunosuppression

Presentation of either condition can be more extensive or atypical, and warrants a lower threshold for prescriber involvement, culture confirmation, and oral therapy even for what would otherwise be straightforward tinea corporis.

For tinea corporis, reassess at the end of the planned topical course (14-21 days plus 14 days beyond visible clearing); persistent or worsening lesions warrant reconsidering the diagnosis (mimic, tinea incognito, Majocchi granuloma) rather than simply repeating the same topical agent.^[2]

1. Confirm the diagnosis is genuinely tinea and not a mimic — obtain KOH microscopy or fungal culture rather than assuming the same drug simply needs more time; granuloma annulare, psoriasis, seborrheic dermatitis, alopecia areata, and (for a single expanding non-scaly ring) erythema migrans are common misdiagnoses that will not respond to an antifungal.
2. For tinea corporis, confirm a topical corticosteroid was not applied at any point (tinea incognito), and confirm adherence to the full prescribed duration, including the 14 days beyond visible clearing.
3. For tinea corporis that is deep, follicular, or has arisen after shaving over a lesion or after topical steroid use, consider Majocchi granuloma and refer for oral therapy rather than continuing a topical agent.
4. For tinea capitis, confirm oral (not topical) therapy was actually used, confirm correct weight-based dosing, and if response is inadequate at the expected duration, reconsider the causative organism — obtain or repeat fungal culture, since Microsporum species need a substantially longer course than Trichophyton and may need griseofulvin if accessible.{C(cps)}
5. Screen and address household contacts and pets that were not previously addressed — an untreated reservoir will keep reseeding the infection regardless of which antifungal is used.
6. Persistent infection despite an adequate, adherent oral course, or any lesion behaving atypically, warrants referral to dermatology or infectious diseases rather than an empiric change to a further oral agent.

• Dispensing or recommending a topical antifungal cream or shampoo as the sole treatment for suspected tinea capitis — topical agents cannot penetrate the hair follicle, and this is the single most consequential error to avoid in this chapter.^[1]
• Treating a kerion as a bacterial abscess with antibiotics and/or incision and drainage instead of recognizing it as a fungal-driven inflammatory complication that needs oral antifungal therapy.^[2]
• Trusting a negative Wood's lamp examination to rule out tinea capitis — Trichophyton tonsurans, the predominant North American organism, does not fluoresce.^[3]
• Applying a topical corticosteroid to an undiagnosed annular lesion, risking tinea incognito and a delayed, more atypical-looking diagnosis.
• Missing erythema migrans by treating a single, non-itchy, non-scaly expanding ring as tinea corporis without asking about tick exposure.
• Assuming griseofulvin is routinely available to prescribe for tinea capitis in Canada without confirming access, given it is no longer commercially available outside compounding pharmacies.^[2]
• Recommending an antifungal shampoo alone for tinea capitis, or presenting it as equivalent to oral therapy rather than as an adjunct that reduces spore shedding.^[2]
• Not asking about household pets, shared grooming items, or symptomatic contacts, leaving an ongoing transmission or reinfection source unaddressed.
• Unnecessarily excluding a child from school or daycare once appropriate oral therapy has begun, rather than reinforcing simple hygiene precautions.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Allylamines (topical and oral)

First-line class at both sites: fungicidal, generally shorter courses, and — for oral use — fewer clinically significant drug interactions than the oral azoles.

Azoles (topical)

CPS reports little difference in efficacy among the topical azoles and topical terbinafine for tinea corporis; choice can reasonably be guided by cost, availability, or patient preference.

Azoles (oral)

Reserved for tinea capitis when first-line terbinafine fails, is not tolerated, or (for itraconazole) on specialist direction — not first-choice agents.

Griseofulvin (oral)

Historically the gold-standard oral agent for tinea capitis, with the longest-established pediatric track record and particular strength against Microsporum species — but note the Canadian availability issue below before assuming it can be prescribed.

Adjunctive antifungal shampoos

Reduce fungal spore shedding and household/school transmission during tinea capitis treatment. These are adjuncts only and are never a substitute for oral antifungal therapy.

Hydroxypyridones (topical)

Broader-spectrum topical option for tinea corporis when secondary bacterial or candidal colonization is also suspected.