58. Mucosal and Cutaneous Fungi

Question 1

dermatophytes?

Answer 1

• Microsporum spp (more common worldwide, can’t cause onychomycosis/tinea unguium)
• epidermophyton floccosum (tinea cruris only)
• Trichophyton spp (most common in USA)

Question 2

pathogenesis of dermatophytosis?

Answer 2

use keratin as a nutrient source, involvement of underlying and surrounding tissues results from allergic or inflammatory host responses to fungi, cellular immunity is a key host defense (HIV ), and subtleties in iron metabolism

Question 3

dermatophytes by environmental reservoir?

Answer 3

• Anthropophilic species are adapted to live in humans and thus elicit a more mild response (T.tonsurans)

Zoophilic species are adapted to live in animals and thus elicit a more severe response (M. canis  take pet to vet for treatment)

Geophilic species are adapted to the soil and commonly infect avid gardeners (M.gypseum)

Question 4

onchomycosis is caused by what?

Answer 4

T.rubrum or T.mentagrophytes

Question 5

onchomytosis causes what?

Answer 5

Source of pain, ambulatory dysfuntion, and paronychia (skin infection near the nails, commonly S.aureus)

Question 6

increased risk for onchomytosis?

Answer 6

• Increased risk: diabetes, HIV/AIDS, other compromised hosts, elderly

Question 7

3 clinical types of onchomycosis?

Answer 7

Proximal subungual (PSO)

• T.rubrum
• Immunocompromised hosts and is an early indicator of HIV infection
• Mechanism of invasion: infection enters at the cuticle and involves the proximal nail bed; spreads distally to eventually invole the entire nail plate if untreated

Distal subungual (DSO) (90% of cases)

• T.rubrum (also T.tonsurans, T.mentagrophytes, and E.floccosum)
• Mechanism of invasion: hyphae enter distally under the nail plate and spread proximally, digesting the stratum corneum of the nail bed as well as the nail plate
• Subungual hyperkeratosis, paronychia, and onycholysis can occur as the infection spreads

White superficial (WSO) (only 10% of cases)

• T.mentagrophytes
• Dorsal surface of the nail plate is attacked, resulting in minimal inflammation as viable tissue is not involved

Question 8

lab testing for onchomycosis?

Answer 8

o KOH w/calcofluor direct exam and culture of the nail is definitive diagnostic tool

Question 9

treatment/prevention for onchomycosis?

Answer 9

o Oral therapy: terbinafine, itraconazole

Question 10

superficial mycoses?

Answer 10

Superficial Mycoses: fungal infections of the superficial stratum corneum that do not elicit a host response

Tinea Versicolor: superficial mycotic infection of young and middle-aged adults caused by lipophilic yeast Malessezia furfur usu involving upper trunk, neck, and arms (dx w/pale yellow flourescense on Wood’s light exam or spaghetti and meatballs on KOH microscopy)

Also recently, M.furfur has been implicated in other conditions like pityriasis folliculitis, seborrheic dermatitis, atropic dermatitis, and dandruff

Tx: scraping, topical selenium sulfide shampoo or short course PO itraconazole/fluconazole

Question 11

tinea capitis patients infected?

Answer 11

• infants, children, and young adolescents

- urban infection usu African American or Hispanic preschoolers (w/poor access to healthcare and crowded living)

Question 12

tinea capitis pathophysiology?

Answer 12

• ectothrix: arthroconidia form on the outside of the hair shaft and the cuticle is destroyed (M. canis, M.gypsium, T.equinum)
• Endothrix: arthroconidia form within the hair shaft, leaving the cuticle intact (T.tonsurans)

Question 13

tinea capitis pathology?

Answer 13

• primary lesions may be papules, pustules, plaques or nodules on the scalp. Inflammation results in scaling, alopecia, erythema, exudate and edema
• kerion forms as a result of increased cell-mediated immune response, demonstrated by severe inflammation, hair loss and cervical lymphadenopathy
• breakage of hairs = black dot alopecia

Question 14

tinea capitis disease?

Answer 14

Ectothrix: more inflammatory but better prognosis

Endothrix: irreversible alopecia (less inflammatory but more destructive)

Question 15

tinea captitis dx?

Answer 15

• KOH exam of extracted hair if caused by Trichophyton species, as spores can attach or reside on the hair shaft. Culture the extracted hair (not painful because follicle already destroyed)
• if caused by M.audouinii or M.canis can also test re: fluoresces blue-green under Wood’s light examination

Question 16

tinea captitis treatment?

Answer 16

Oral antifungal: terbinafine, ketoconazole, itraconazole, or fluconazole plus reduce fungal shedding with ketoconazole shampoo and prevent spread to family members by cleaning contaminated combs and brushes, selenium sulfide lotion for family members

Question 17

tinea capitis bugs?

Answer 17

• Trichophyton (tonsurans) (80%)

- Microsporum (more common worldwide)

Question 18

tinea corporis pathology?

Answer 18

• ringworm (erythematous, round, scaly plaque or patch w/a red, raised, advancing border – edge can contain papules or pustules)

Question 19

tinea dx (besides capitis)?

Answer 19

KOH or calcofluor preparation of scale scraped from leading edge of the lesion (KOH dissolves squamous epith to leave just hyphae)
- cx to confirm

Any dermatophyte growth found is a pathology/is significant!

Question 20

tinea tx (besides capitis)?

Answer 20

• treat the pet/animal
• topical therapy:
  Miconazole, Clotrimazole, Ciclopirox, econazole, ketoconazole, terbinafine
  If exensive/severe: PO fluconazole or terbinafine

Nafitine also for tinea pedis

Question 21

tinea pedis patients infected?

Answer 21

• most common dermatophytosis (70% adults)
• troops
• athletes

Question 22

tinea pedis disease?

Answer 22

• interdigital
• moccasin (painful, overt)
• vesiculobullous
  (may present with onchomycosis)