Mycology

Pathogenic features – refer diagram

a. Normal continual shedding of stratum corneum – protects from dermatophytes

b. Inflammatory reactions following dermatophytoses
1. Penetration of stratum corneum – CMI response
2. Vesiculation occurs in severe cases
3. Stratum corneum contains nucleated cells!
- Inflammatory reaction increases epidermal cell division rates – pass more rapidly
through epidermis
- Full differentiation of cells of different strate does not take place
4. Loss of normal translucency causing
- stratum corneum to appear white
- And dermal vessels to dilate
5. Mononuclear inflammatory cells infiltrate the dermis

NOTE: A crude extract called TRICHOPHYTON from certain dermatophyres produces a tuberculin-like
response in most adults

This contains 2 moieties of galactomannan

- Carbohydrate  immediate response

- Peptide  Delayed Type Hypersensitivity and probably immunity, too.

CLINICAL FINDINGS

 Superficial mycoses named according to site of infection.

 These usually correspond to site of local inoculation.
 Degree of inflammation often dictated by the nature of the environment from which fungus
originates.
 Anthrophilic dermatophytes – milder IR in humans
 e.g: microsporum dermii

TINEA CAPITIS (SCALP RINGWORM)

 Mainly affects prepubertal children ages 4-14

 Often seen in
- Crowded living conditions
 - Areas of poverty
 Infection of hair shaft:
 Ectothrix – fungi that produces arthrospores ON hair shaft. Present with gray or
scaling patches of alopecia with or without inflammation.
 Black dot appeatance seen.
 Kerions and prominent inflammatory lesion +.
 Kerions = nodular, circumscribed exudative tumefaction (swelling) covered with
pustules (usually M. canis, rarelt y T. verruocosum or T. mentagrophytes)
 Endothrix – Fungus that grows INSIDE the hair shaft.
 Cuticle not destroyed
 Clinically appears as simple scaling of scalp
 May resemble
– seborrheic dermatitis
– dandruff
 There may be gray patches of alopecia with or without inflammation or ‘black dot
alopecia in which hair breaks off at roots’
 Favus – infection leads to crusting and matter hair on the scalp with such severe
invasion that permanent alopecia often results.
 Usually seen in Eastern Europe and Africa.

TINEA BARBAE

 Like tinea capitis, but affects the hair follicles and shafts of the facial area. May
develop into tumourlike abscess
 Usual aetiologies: T. mentagrophytes, T. verrucosum

TINEA CORPORIS
  Affects non-hairy, glabrous (smooth & bare) skin.
 Can be the extensions of scalp or groin infections.
 Range from mild to highly inflamed lesions with pustules.
 Central areas may become brown / hypoigmented and less scaly.

TINEA CRURIS (JOCK ITCH)

 Commonly in men. May involve perineum, perianal and thighs.

 Rarely affects srotum (cf Candida – typically involves scrotum)
 Typically presents with bilateral erythematous plaques with central healing. Erythematous
border – active.
 May have vesicles and papules.
 Pruritus and burning sensations most common complaints.
 Infection usually transmitted from foot to groin.
 Predisposing factors – sweating, wet/many layered clothing

TINEA PEDIS (ATHLETE’S FOOT)

 Most common dermatophytosis

  Usual cause – T. rubrum
 Occlusive footwear – warmth and wet – for fungal growth
 Presents in 4 general fashions:
1. Interdigital infection with erythema, maceration and scalin.
2. Moccasin foot – erythema and thick hyperkeratotic scales
3. Inflammatory infections with vesicles, usually on the medial foot
4. Less common ulcerative infection affecting the web spaces of the toes
 If tinea unguium (of the nails) + tinea pedis may persist due to reinfections.

TINEA UNGUIUM (ONYCHOMYCOSIS)

 Infection causes nails to become opaque, chalky or yellowish.

 May become thickened and brittle.
 Toenails more frequently unvolved.
 Incidence increases with age.

DERMATOPHYTID or ‘ID’ REACTION

 Allergic response to tinea processes that cause sterile dermatitis at distant sites.
 Most common – Tinea pedis – itching and burning near the creases.
 Vesicles and bullae may form.
 Lesions may persist until primary process resolves.

TINEA VERSICOLOR

Aetiology:

 Genus: Malassezia
 Species: Malassezia furfur (formerly Pityrosporum orbiculare/ovale)
 Organisms: Lipophilic and makes use of medium-chain length fatty acids
 Excess heat, humidity, pregnancy, oral contraceptives, malnutrition, burns and
corticosteroids promote their proliferation.

Clinically:

 Begins as small circular macules of various colours (versicolor) – white, pink or brown
depending on host’s response – reddish; hyperaemic inflammation
 Hypopigmented/hyperpigmented – depends on melanosome formation in individual
  Upper trunk most commonly affected. Highes numbers in areas of increases sebaceous
activity. Usuall asuymptomatic. Itch when inflamed.

DERMATOPHYTOSIS – DIAGNOSIS

 Clinical manifestations
 UV (Wood’s) light examination in darkened room
 M. audouinii, M. canis & T. schoenleinii all give off a blue-green colour.
 Tinea versicolor: whitish-yellow fluorescence.
 Skin/nail scrapings (keratinized/flaking material)/cutting:
- +10-20% KOH – direct microspopy – hyphae
- Cellophane tape – Tinea versicolor.
- ‘spaghetti and meatballs’ appearance.
 Culture – Sabouraud’s agar 1-3 weeks.
- Identified by colony colour, texture
 Light microscopy – morphologic patterns

TREATMENT

 Most tinea infections: Topical agent – imidaole b.d x 2-3/52

 Severe cases: oral
- Itraconazole
- Fluconazole
- Terbinafine
 Tinea versicolor:
- 2.5% selenium sulphide suspension (Selsun shampoo) entire body 10 minutes x 7.7
- Single dose oral keto/itra/flunazole

PREVENTION & CONTROL

- Keep clean
- Dry body surfaces all the time