What are the transmission routes, prevention strategies, and treatment options for dermatophytosis (ringworm) in humans?

Ringworm Transmission Routes and Prevention

Ringworm transmits through direct skin-to-skin contact with infected individuals, contact with infected animals (particularly cats and dogs), contaminated fomites (towels, clothing, athletic equipment), and environmental surfaces harboring fungal spores that can persist for years. 1, 2, 3

Transmission Routes

Direct Human-to-Human Contact

• Anthropophilic dermatophytes (primarily Trichophyton tonsurans, accounting for 50-90% of UK scalp infections) spread through direct skin contact between infected and susceptible individuals, particularly common in prepubertal children in inner-city communities. 4, 1
• Athletes in contact sports (wrestlers, rugby players, judo practitioners) face elevated transmission risk due to repeated skin-to-skin contact during competition and training. 1

Zoonotic (Animal-to-Human) Transmission

• Zoophilic dermatophytes, especially Microsporum canis (the most common organism across Europe), transmit from infected cats, dogs, and other animals to humans through direct contact or handling. 4, 1
• Multiple animal species can harbor ringworm and remain contagious, including livestock (lambs with Trichophyton species) and zoo animals (documented M. canis infection from a hand-reared tiger cub affecting 23 persons). 1

Environmental and Fomite Transmission

• Geophilic dermatophytes exist as soil-associated organisms that can infect humans through contact with contaminated soil containing keratinous materials. 2, 3
• Fungal spores persist for years in the environment on hair, skin scales, and contaminated surfaces, making fomites (shared towels, clothing, combs, brushes, athletic equipment, wrestling mats) significant transmission vectors. 2, 3

Prevention Strategies

Personal Hygiene and Behavior Modifications

• Never share personal items including towels, clothing, combs, brushes, or athletic equipment to prevent fomite transmission. 1
• Wear protective footwear in communal areas such as locker rooms, showers, and pool decks where contaminated surfaces pose transmission risk. 1
• Limit exposure to swimming pools recently associated with known outbreaks. 1

Environmental Decontamination

• Clean wrestling mats with freshly prepared household bleach solution (1 quarter cup bleach in 1 gallon water) applied for minimum 15 seconds contact time, at least daily and preferably between matches. 1
• Regularly disinfect shared surfaces and equipment in athletic facilities to eliminate persistent fungal spores. 1

Screening and Exclusion Protocols for High-Risk Settings

• Pre-competition examination of wrestlers and rugby players for vesicular or ulcerative lesions on exposed body areas and around mouth or eyes by personnel familiar with mucocutaneous infections. 1
• Exclude athletes with suspicious lesions from competition until all lesions are fully crusted or a physician provides written statement that the condition is noninfectious. 1
• Systematic screening is critical because athletes often do not recognize or may deny possible infection. 1

Reducing Transmission from Infected Individuals

• Topical antifungal shampoos (povidone-iodine, ketoconazole 2%, or selenium sulfide 1%) reduce transmission of spores from infected scalp lesions, though topical therapy alone is insufficient for cure. 4
• Start treatment promptly in high-risk populations when diagnosis is strongly suspected clinically (presence of kerion, scaling, lymphadenopathy, or alopecia) to prevent further spread, even before culture confirmation. 4

Treatment Options

Oral Antifungal Therapy (Primary Treatment)

• Oral therapy is required to achieve eradication of the organism, clinical and mycological cure, symptom alleviation, prevention of scarring, and reduction of transmission to others. 4
• Treatment regimens vary by causative organism: protocols should reflect local epidemiology and the most likely culprit organism based on clinical presentation. 4

Griseofulvin

• Griseofulvin remains the only licensed product for tinea capitis treatment in children in the UK, with over 50 years of clinical experience. 4
• Dosing: 20-25 mg/kg daily for 6-8 weeks (may require prolonged treatment for resistant cases); taking with fatty food increases absorption. 4
• Species-specific efficacy: 88.5% response rate for Microsporum species versus 67.9% for Trichophyton species; 8 weeks of griseofulvin is significantly more effective than 4 weeks of terbinafine for confirmed Microsporum infections. 4

Terbinafine

• Terbinafine shows superior efficacy compared to placebo with significantly higher clinical cure rates (RR 4.51,95% CI 3.10-6.56, NNT 3). 5
• Unlicensed in UK children but widely used; a granule formulation (125-mg or 1875-mg packets sprinkled on food) is licensed for children >4 years in the USA. 4

Topical Antifungal Therapy

Monotherapy (Limited Role)

• Topical therapy alone is not recommended for tinea capitis management, though a small percentage of patients with tinea corporis/cruris may clear with topical agents. 4, 5
• Terbinafine topical and naftifine 1% demonstrate effectiveness for body/groin ringworm (naftifine: RR 2.38 for mycological cure, RR 2.42 for clinical cure versus placebo, NNT 3). 5
• Clotrimazole 1% shows mycological cure superiority over placebo (RR 2.87, NNT 2). 5
• Azoles (various formulations) are effective with minimal difference between azoles and benzylamines (RR 1.01 for mycological cure). 5

Adjunctive Use

• Antifungal shampoos (ketoconazole 2%, selenium sulfide 1%, povidone-iodine) reduce spore transmission when used alongside oral therapy for scalp infections. 4

Combination Therapy Considerations

• Azole-corticosteroid combinations show higher clinical cure rates at end of treatment compared to azoles alone (RR 0.67), but similar mycological cure rates (RR 0.99). 5
• Use requires caution: corticosteroids may suppress local immune response, potentially allowing persistent infection or deeper tissue invasion; contraindicated in children <12 years, facial lesions, occluded areas, and immunosuppressed patients. 6
• If used: limit to low-potency nonfluorinated corticosteroids for symptomatic inflamed lesions in healthy adults, never exceeding 2 weeks for groin/body infections, and substitute with pure antifungal once symptoms resolve. 6

Diagnostic Confirmation

Laboratory Testing

• Microscopy and culture should be performed on all scalp scrapings and plucked hairs to confirm fungal presence and identify the causative organism, directing species-specific therapy. 4
• Specimen collection: scalp lesions sampled by scalpel scraping, hair pluck, brush, or swab; body ringworm scales collected from active edges of lesions. 4, 2
• Culture requires 2-4 weeks for results; susceptibility testing is not indicated as resistance development shows little evidence. 4

Clinical Pitfalls

• Misdiagnosis is common, particularly with inflammatory variants (kerions) mistaken for bacterial abscesses, leading to inappropriate management delays. 4
• Clinical signs can be subtle and highly variable depending on causative organism, hair invasion type, and host inflammatory response. 4