Dermatophytoses (Tinea Infections)

Organisms/Shared Trait

3 genera: Trichophyton, Microsporum, Epidermophyton. KERATINOPHILIA — keratinases digest keratin as nutrient. NEVER extends past dead keratinized layer into living tissue = superficial, non-invasive by nature (contrast systemic/subcutaneous mycoses).

Site Tropism (KEY testable fact)

Trichophyton = ONLY genus infecting all 3. Microsporum NEVER nail. Epidermophyton NEVER hair.

Clinical Patterns (by site, not organism)

Tinea capitis (scalp/hair): mainly children. Trichophyton/Microsporum. Patchy hair loss+scaling, “black dot” pattern (broken stubs), or KERION (inflammatory, boggy, pus-discharging — intense HOST IMMUNE reaction, not bacterial superinfection per se, though can complicate).

Tinea corporis (“ringworm”): classic annular, scaly, centrally-clearing, advancing edge plaque.

Tinea cruris (“jock itch”): groin, warm/moist/occluded skin, more males, sharp advancing edge onto inner thigh.

Tinea pedis (“athlete’s foot”): COMMONEST dermatophytosis overall. Interdigital/moccasin/vesiculobullous patterns. Reservoir for autoinoculation to groin/hands.

Tinea unguium (onychomycosis): ONLY Trichophyton or Epidermophyton (NEVER Microsporum). Thickened, discolored, crumbly nail. HARDEST to cure (poor drug penetration into nail).

Tinea manuum (hand), tinea barbae (beard) — less common, same biology.

Laboratory Diagnosis

KOH mount: standard 1st line. 10% KOH (higher/overnight for nail) digests keratin, hyphae visible (see General Mycology for technique/pitfalls).

Wood’s lamp (UV): useful adjunct for tinea capitis. Microsporum = BRIGHT GREEN fluorescence (fungal metabolite). MOST Trichophyton = NO fluorescence. → fast genus-narrowing before culture. Also school screening use.

Culture (SDA): definitive species ID (colony morphology, pigmentation, macro/microconidia shape). 1-4 weeks, not needed routine, mainly refractory cases/epidemiology.

Treatment

Localized (corporis/cruris/pedis): TOPICAL antifungals (terbinafine, clotrimazole/azoles), several weeks.

Systemic/oral REQUIRED for:

• Tinea capitis (topicals can’t penetrate follicle)
• Tinea unguium (topicals can’t penetrate nail keratin) Oral terbinafine or itraconazole, weeks-months (reflects slow keratin structure turnover, esp. nail).

Griseofulvin: largely superseded for most indications, but STILL specifically used for tinea capitis in CHILDREN (long safety track record).

The Organisms and Their Shared Trait: Keratinophilia

Dermatophytoses are superficial fungal infections confined to keratinized tissue — skin, hair, and nail — caused by three related genera collectively called dermatophytes: Trichophyton, Microsporum, and Epidermophyton. Their single defining biological property is keratinophilia: these fungi produce keratinases that digest keratin as a nutrient source, which is exactly why infection never extends past the dead, keratinized outer skin layer into living tissue — dermatophytes simply cannot survive or invade below the keratin layer, which is what makes these infections superficial and non-invasive by nature, in genuine contrast to the systemic and subcutaneous mycoses covered elsewhere.

Site Tropism — the Single Most Testable Fact in This Topic

Which of the three genera can infect which keratinized tissue is fixed and worth memorizing precisely, since it’s exactly the kind of distinction exams (and real differential diagnosis) hinge on:

Trichophyton alone can infect all three tissue types; Microsporum never infects nail; Epidermophyton never infects hair. This division of labour is the reason different clinical patterns of tinea (below) are caused by different genus combinations depending on which tissue is involved.

Clinical Patterns of Tinea

Nomenclature follows anatomical site rather than organism, with the causative genus/species varying by site and region:

• Tinea capitis (scalp/hair) — mainly children, caused by Trichophyton or Microsporum species; presents as patchy hair loss with scaling, sometimes broken-off hair stubs at the follicle (“black dot” pattern) or a more inflammatory, boggy, pus-discharging mass (kerion) representing an intense host immune reaction to the fungus rather than bacterial superinfection per se, though secondary bacterial infection can complicate it.
• Tinea corporis (“ringworm” of the body) — the classic annular (ring-shaped), scaly, centrally-clearing, advancing-edge plaque that gives dermatophytosis its lay name.
• Tinea cruris (groin, “jock itch”) — favours warm, moist, occluded skin; more common in males, often with a sharply demarcated advancing edge extending onto the inner thigh.
• Tinea pedis (“athlete’s foot”) — the commonest dermatophytosis overall, with interdigital, moccasin, or vesiculobullous patterns; a genuinely important reservoir for autoinoculation to other sites (groin, hands) via the patient’s own scratching.
• Tinea unguium (onychomycosis, nail) — caused only by Trichophyton or Epidermophyton (never Microsporum, per the tropism table above); thickened, discoloured, crumbly nail, notoriously the hardest tinea pattern to cure given poor drug penetration into nail keratin.
• Tinea manuum (hand) and tinea barbae (beard area) — less common site-specific patterns following the same underlying biology.

Laboratory Diagnosis

KOH mount of skin scraping, hair, or nail clippings is the standard first-line test — 10% KOH (higher concentrations, or overnight incubation, for thicker nail material) digests host keratin, leaving fungal hyphae visible under the microscope (see General Mycology for the full KOH technique and its pitfalls). Wood’s lamp examination (UV light) is a genuinely useful, rapid adjunct specifically for tinea capitis: Microsporum species characteristically fluoresce a bright green under Wood’s lamp (from a fungal metabolite), while most Trichophyton species do not fluoresce at all — making Wood’s lamp a fast way to narrow the likely genus before culture confirmation, and also useful for screening/scalp-check purposes in outbreak settings (school screening for tinea capitis).

Culture on Sabouraud’s dextrose agar (see General Mycology) provides definitive species identification, based on colony morphology, pigmentation, and microscopic conidial morphology (macroconidia and microconidia shape/arrangement differ characteristically between genera and species) — though culture takes 1–4 weeks and is not needed for routine clinical management, mainly reserved for treatment-refractory cases or epidemiological purposes.

Treatment

Localized tinea corporis/cruris/pedis typically responds to topical antifungals (terbinafine, clotrimazole, or other azoles) applied for several weeks. Systemic (oral) therapy is required for tinea capitis (topical agents cannot penetrate the hair follicle adequately) and for tinea unguium/onychomycosis (topical drugs cannot adequately penetrate nail keratin) — oral terbinafine or itraconazole, given for weeks to months depending on site, reflecting how slowly infected keratin structures (especially nail) are replaced by healthy growth. Griseofulvin, though largely superseded by newer agents for most indications, remains specifically useful and still commonly used for tinea capitis in children, given its long track record of safety in that population.

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