Dermatophytosis & Superficial Fungal Infections

Superficial fungal infections are among the highest-yield, most image-heavy topics in NEET PG Dermatology. They span keratin-loving dermatophytes (the "tineas") and the yeast Malassezia (pityriasis versicolor). Master the KOH patterns, Wood's lamp colours, and the terbinafine-vs-griseofulvin-vs-azole decision tree and you bank easy marks.

Definition & classification

Superficial mycoses involve only the keratinised tissues — stratum corneum, hair, and nails — and the immediate epidermis. They are broadly divided into:

1. Dermatophytoses (tinea/ringworm) — caused by keratinophilic moulds of three genera: Trichophyton, Microsporum, Epidermophyton. They digest keratin using the enzyme keratinase.
2. Yeast infections — Malassezia (pityriasis versicolor, Malassezia folliculitis) and Candida (intertrigo, paronychia, oral thrush).
3. Non-dermatophyte/superficial saprophytes — Hortaea werneckii (tinea nigra), Trichosporon/Piedraia (piedra).

Dermatophytes are also classified ecologically — a favourite single-best-answer angle:

Type	Reservoir	Examples	Inflammation
Anthropophilic	Humans	T. rubrum, T. tonsurans, E. floccosum	Mild, chronic
Zoophilic	Animals	M. canis (cats/dogs), T. verrucosum (cattle)	Intense, kerion
Geophilic	Soil	M. gypseum	Moderate

High-yield: Zoophilic and geophilic species evoke the most intense inflammatory reaction (e.g., kerion), while anthropophilic T. rubrum causes chronic, low-grade, recalcitrant disease. T. rubrum is the commonest cause of dermatophytosis worldwide (and of tinea pedis, cruris, corporis, and onychomycosis).

Clinical patterns of tinea (named by site)

Lesions are named by anatomical region, not by organism. Classic morphology: an annular, scaly plaque with an active, raised, vesicular advancing edge and central clearing ("ringworm").

Site	Tinea	Key clinical points
Scalp/hair	capitis	Children; alopecia + scaling; kerion; favus
Trunk/limbs	corporis	Annular plaque, central clearing
Groin	cruris	"Jock itch"; spares scrotum (vs candida)
Feet/web spaces	pedis	"Athlete's foot"; interdigital maceration
Nails	unguium (onychomycosis)	Subungual hyperkeratosis, onycholysis
Face	faciei	Often misdiagnosed; loses annular look
Beard	barbae	Zoophilic; pustular
Hands	manuum	"Two feet–one hand" syndrome
Body-wide	incognito	Modified by topical steroids — loses scaling/border

High-yield: Tinea cruris classically spares the scrotum, whereas candidal intertrigo involves the scrotum and shows satellite pustules. This single distinction is repeatedly tested.

Tinea capitis subtypes (very high-yield)

Patterns of hair invasion determine Wood's lamp fluorescence and clinical look:

• Ectothrix — arthrospores coat the outside of the hair shaft. Microsporum species. Fluoresces green under Wood's lamp.
• Endothrix — spores within the shaft (cuticle intact). T. tonsurans, T. violaceum. Does NOT fluoresce. Causes "black dot" tinea capitis (hairs break at scalp surface).
• Favus — chronic, T. schoenleinii; scutula (cup-shaped yellow crusts) + scarring alopecia; dull green-blue Wood's fluorescence; "mousy/cheesy" odour.
• Kerion — boggy, tender, pus-discharging inflammatory mass from a zoophilic species; risk of scarring alopecia.

Mnemonic for ectothrix (fluorescent) species — "Cats And Dogs Sometimes Fight & Growl": Microsporum canis, M. audouinii, M. distortum, M. ferrugineum, M. gypseum — though for NEET PG it is enough to remember most Microsporum = ectothrix = fluoresce, and T. tonsurans/T. violaceum = endothrix = no fluorescence.

Pityriasis (tinea) versicolor — the Malassezia disease

Caused by the lipophilic yeast Malassezia furfur (formerly Pityrosporum ovale/orbiculare) converting from yeast to hyphal (mycelial) form. It is a normal skin commensal that becomes pathogenic with heat, humidity, sweating, oily skin, Cushing's, and immunosuppression.

• Lesions: well-demarcated, finely scaly macules on the upper trunk, neck, shoulders. Hypo- OR hyper-pigmented (hence "versicolor"). Hypopigmentation is due to azelaic acid produced by the yeast inhibiting tyrosinase/melanocytes.
• Signs: "coup d'ongle" / Besnier's scratch sign — scraping produces fine scale.
• KOH: "spaghetti and meatballs" appearance — short hyphae + round spores.
• Wood's lamp: yellow-gold / coppery-orange fluorescence.

High-yield: Pityriasis versicolor is NOT a dermatophyte — it is a yeast (Malassezia). KOH = spaghetti and meatballs; Wood's lamp = golden-yellow; pigment change is due to azelaic acid.

Etiology & pathophysiology

Dermatophytes invade keratin via keratinases, elastases and proteases. Spread is favoured by moisture, occlusion, sharing fomites (combs, towels), communal baths, diabetes, immunosuppression, and tight clothing. Host defence relies on cell-mediated immunity (Th1); a strong delayed-type hypersensitivity reaction limits infection but produces inflammation. A weak/Th2-skewed response (atopy, T. rubrum) permits chronic, widespread disease.

An important immunological phenomenon: the id reaction (dermatophytid) — a sterile, distant vesicular eruption (often on hands) triggered by a brisk immune response to a remote focus (e.g., kerion or tinea pedis). KOH of the id lesion is negative; it resolves when the primary infection is treated.

Diagnosis & investigation of choice

Stepwise approach: Clinical morphology → KOH mount of scrapings (investigation of choice / first-line) → Wood's lamp (screening for capitis/versicolor) → fungal culture (Sabouraud Dextrose Agar — gold standard for speciation) → histopathology with PAS stain if needed.

KOH microscopy (most-tested investigation)

• Collect scales from the active advancing edge; for nails take subungual debris; for hair pluck affected hairs.
• Use 10% KOH for skin/hair, 20–40% KOH for thick nail/keratin; DMSO speeds clearing.
• Dermatophytes show branching, septate hyphae with arthrospores.
• Versicolor shows spaghetti and meatballs; Candida shows pseudohyphae + budding yeast.

High-yield: KOH mount is the first and quickest investigation (highest yield in exams as "investigation of choice/first step"). Sabouraud Dextrose Agar culture is the gold standard for identifying the species. Cycloheximide is added to SDA to suppress contaminant saprophytes.

Wood's lamp (365 nm UV) — colour table

Condition	Organism	Fluorescence
Tinea capitis (ectothrix)	Microsporum spp.	Bright green
Tinea capitis (endothrix)	T. tonsurans/violaceum	None
Favus	T. schoenleinii	Dull green-blue
Pityriasis versicolor	Malassezia	Golden-yellow / coppery
Erythrasma (not fungal)	Corynebacterium minutissimum	Coral-red
Pseudomonas	P. aeruginosa	Green
Porphyria (urine)	—	Pink-red

High-yield: Erythrasma → coral-red (porphyrin/coproporphyrin III) is a perennial trap — it is bacterial, not fungal, and treated with erythromycin/topical clindamycin, mimicking tinea cruris.

Management & drug of choice

Topical agents suffice for limited corporis/cruris/pedis and versicolor. Oral therapy is mandatory for tinea capitis, onychomycosis (unguium), extensive/recalcitrant disease, and tinea barbae, because topical drugs cannot penetrate hair follicles or the nail plate adequately.

Topical options

• Azoles: clotrimazole, ketoconazole, luliconazole, sertaconazole.
• Allylamines: terbinafine (fungicidal), naftifine.
• Others: ciclopirox olamine (broad), amorolfine (nail lacquer for limited onychomycosis), tolnaftate, selenium sulphide / ketoconazole shampoo / zinc pyrithione for versicolor.

Systemic drug of choice by condition

Condition	Drug of choice	Notes
Tinea capitis (Microsporum)	Griseofulvin	Traditional DOC for Microsporum
Tinea capitis (Trichophyton)	Terbinafine	More effective for T. tonsurans
Onychomycosis (nail)	Terbinafine	Toenail 12 wks, fingernail 6 wks
Pityriasis versicolor	Topical (ketoconazole/selenium sulphide); oral fluconazole/itraconazole if extensive	Avoid oral terbinafine — ineffective for Malassezia
Extensive corporis/cruris	Terbinafine or itraconazole	—
Candidiasis	Fluconazole / topical nystatin	—

High-yield: Oral terbinafine is the drug of choice for onychomycosis, but it is ineffective against pityriasis versicolor (Malassezia) because the yeast is relatively resistant — use an azole or selenium sulphide instead. This is a classic NEET PG trap.

High-yield: Griseofulvin must be taken with a fatty meal (improves absorption), is fungistatic, acts by disrupting microtubules/mitotic spindle, and is the traditional DOC for tinea capitis (Microsporum). It is contraindicated in pregnancy and porphyria, can cause a disulfiram-like reaction with alcohol, and induces hepatic CYP enzymes (reduces warfarin/OCP efficacy).

Mechanisms (one-line memory hooks)

• Allylamines (terbinafine): inhibit squalene epoxidase → squalene accumulation, ergosterol deficiency → fungicidal.
• Azoles: inhibit lanosterol 14-α-demethylase (CYP450) → block ergosterol synthesis → fungistatic.
• Griseofulvin: binds tubulin, deposits in keratin → fungistatic.
• Polyenes (nystatin/amphotericin): bind ergosterol, form membrane pores.

High-yield: Pulse itraconazole (e.g., 1 week/month) is a recognised regimen for onychomycosis. Terbinafine is the most hepatotoxic of the common antifungals — baseline LFTs are advised for prolonged courses; it can also cause taste disturbance (dysgeusia).

Current Indian problem — recalcitrant dermatophytosis

India faces an epidemic of chronic, recurrent, steroid-modified tinea (tinea incognito) driven by rampant OTC topical steroid–antifungal–antibacterial combination creams. Emerging terbinafine resistance is linked to Trichophyton mentagrophytes / T. indotineae with squalene epoxidase gene mutations. Management emphasises stopping steroid creams, treating all affected sites and contacts, longer oral courses, hygiene, and switching to itraconazole where terbinafine fails.

Complications

• Scarring (cicatricial) alopecia from kerion or favus.
• Secondary bacterial infection (impetiginisation, Staph aureus).
• Id reaction (dermatophytid) — sterile distant eruption.
• Chronic widespread tinea / tinea incognito with steroid misuse.
• Onychodystrophy and recurrent cellulitis (tinea pedis as an entry portal for bacterial cellulitis/erysipelas — a high-yield link).
• Psychological/cosmetic morbidity in versicolor (persistent dyspigmentation even after cure, until repigmentation occurs over weeks).

Key differentials

Mimic	Distinguishing feature
Nummular eczema	Coin-shaped but no central clearing, no active scaly border, KOH negative
Psoriasis	Silvery scale, Auspitz sign, symmetrical, KOH negative
Pityriasis rosea	Herald patch, "Christmas-tree" pattern, collarette scale
Erythrasma	Coral-red Wood's lamp, Corynebacterium, treat with erythromycin
Candidal intertrigo	Scrotum/satellite lesions involved, beefy-red, pseudohyphae on KOH
Granuloma annulare	No scale, dermal papules, KOH negative
Seborrhoeic dermatitis	Greasy scale on scalp/face; overlaps with Malassezia
Vitiligo	Versicolor mimic but complete depigmentation, no scale, no fluorescence

High-yield: A "ringworm" lesion that is KOH-negative and lacks a scaly active edge should prompt thoughts of nummular eczema, granuloma annulare, or psoriasis rather than tinea.

Recently asked / exam angle

• Photograph identification: annular plaque with central clearing → tinea corporis; "spaghetti and meatballs" KOH → pityriasis versicolor; scutula on scalp → favus; boggy scalp swelling → kerion.
• Wood's lamp colour matching (coral-red erythrasma, golden versicolor, green Microsporum) — repeatedly tested in single-best-answer and matching formats.
• DOC questions: terbinafine for onychomycosis; griseofulvin for Microsporum capitis; why terbinafine fails in versicolor.
• Mechanism MCQs: squalene epoxidase (terbinafine) vs 14-α-demethylase (azoles) vs microtubule (griseofulvin).
• Ecological classification: which organism causes kerion (zoophilic, e.g., T. verrucosum/M. canis).
• Tinea incognito / steroid-modified tinea and terbinafine-resistant T. indotineae — a hot, contemporary Indian topic.
• Investigation of choice: KOH (first-line) vs SDA culture (gold standard) vs PAS (histology).
• Trap: erythrasma is bacterial, not fungal.

Rapid revision

1. T. rubrum = commonest dermatophyte overall (pedis, cruris, corporis, unguium).
2. KOH mount = quickest/first-line investigation; SDA culture = gold standard for speciation; cycloheximide suppresses contaminants.
3. Endothrix (T. tonsurans/violaceum) → "black dot" tinea capitis, no Wood's fluorescence; ectothrix (Microsporum) → green fluorescence.
4. Favus = T. schoenleinii, scutula, scarring alopecia, dull green Wood's light.
5. Kerion = boggy inflammatory mass from a zoophilic species → scarring; treat with oral antifungal ± short steroid.
6. Tinea cruris spares scrotum; candidal intertrigo involves scrotum with satellite lesions.
7. Pityriasis versicolor = Malassezia yeast; spaghetti and meatballs on KOH; golden-yellow Wood's lamp; hypopigment from azelaic acid.
8. Erythrasma = Corynebacterium minutissimum, coral-red Wood's lamp, treat erythromycin — a bacterial mimic, NOT fungal.
9. Terbinafine (squalene epoxidase inhibitor, fungicidal) = DOC for onychomycosis, but ineffective in versicolor.
10. Griseofulvin = microtubule inhibitor, fungistatic, take with fatty meal, DOC for Microsporum capitis, contraindicated in pregnancy & porphyria, disulfiram-like + enzyme inducer.
11. Tinea incognito = steroid-modified tinea (loss of scale/border); India sees terbinafine-resistant T. indotineae → use itraconazole.
12. Id reaction (dermatophytid) = sterile, KOH-negative distant eruption that clears when the primary focus is treated.