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Microbiology Exam 6 > Stratum Corneum/Keratin Layers > Flashcards

Stratum Corneum/Keratin Layers Flashcards

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Biology 101 flashcards
1
Q

lipophilic organism (saprophyte)

A

Malassezia furfur

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2
Q

spaghetti and meatball appearance w/ KOH prep

A

Malassezia furfur

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3
Q

Pathogenic phase of Malassezia furfur

A

Hyphal phase

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4
Q

Hypopigmentation associated with Pityriasis versicolor is due to

A

a substance produced by the organism that inhibits melanosome production

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5
Q

Hyperpigmentation associated with Pityriasis versicolor is due to

A

production of larger, unpacked, and heavily melanized melanosomes

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6
Q

Pityrosporum folliculitis results from

A

hyperkeratosis that plugs the follicle

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7
Q

Atopic dermatitis caused by Malassezia furfur results from

A

induction of beta-defensins in the skin

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8
Q

tinea versicolor is associated with what climate/season

A

tropics, warmer months

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9
Q

risk factors for tinea versicolor

A

Warm temperature, high humidity, use of oily creams, greasy skin, hyperhidrosis
Steroid use, antibiotic use
Malnutrition, diabetes, immunosuppression, slow rate of epithelial cell turnover

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10
Q

Describe the lesions of tinea versicolor

A

Reddish/pale-brown, non-pruritic, non-inflammatory hypopigmented/hyperpigmented

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11
Q

Location of lesions of tinea versicolor

A

trunk, upper arms, scalp, face and flexural areas

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12
Q

Septicemia of Malassezia furfur is

A

Rare, increasing in stem cell transplant pts

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13
Q

Malassezia furfur appearance w/ Wood’s Lamp

A

pale fluorescence

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14
Q

Malassezia furfur appearance w/ KOH stain

A

yeast and hyphae “spaghetti and meatballs”

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15
Q

Treatment for tinea versicolor

A

1-2.5% Selenium sulfide ointment or Zinc Pyrithione, Ketoconazole, Ciclopirox

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16
Q

Acute occurrence of tinea versicolor can be treated w/

A

Calcineurin Inhibitor – Primecrolimus, Tacrolimus

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17
Q

Treatment for tinea versicolor hyperpigmentation

A

Cycloserine

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18
Q

Treatment for Seborrheic dermatitis caused by Malassezia furfur

A

2% Ketoconazole gel

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19
Q

Treatment to decrease relapse rate of Seborrheic dermatitis caused by Malassezia furfur

A

Toll-like receptor 2 modifiers (decrease the topical IL-8 expression)

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20
Q

Tinea Nigrans is caused by what agent

A

Hortaea (Exophiala) werneckii

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21
Q

Typical pt with Tinea Nigrans

A

< 18 y/o, female, living/travel to Central or South America

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22
Q

Tinea Nigrans is transmitted by

A

contact w/ decaying vegetation, wood, or soil

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23
Q

Describe the lesion of Tinea Nigrans

A

Discrete, 1-8cm dark, brown-to-black, mottled, macule on the palmar surface of the fingers (occasionally the soles)

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24
Q

Treatment for Tinea Nigrans

A

Topical keratinolytic agents

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25
Q

Defenses against Tineas

A

Alpha-2-macroglobulin keratinase inhibitor
Unsaturated transferrin (fungus can’t use Fe)
Epidermal desquamation
Lymphocytes, macrophages, epidermal Langerhans cells, dermal dendritic cells, neutrophils, and mast cells

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26
Q

Tineas infect which layer

A

keratinized layers

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27
Q

Immune required for fighting Tineas

A

CMI predominantly, humoral also

28
Q

Risk Factors for Tinea infections

A

Warmer months, males, post-pubescents, family member with infection, contact w/ contaminated instruments/textiles/animals
Obesity, hydration, and humidity
Steroid use, antibiotic use

29
Q

Microsporum and superficial pityriasis both

A

fluoresce apple to blue green

30
Q

Brilliant coral red fluorescence

A

Erythrasma, bacterial infection of Corynebacterium minutissimum

31
Q

Culture Tineas on

A

Dermatophyte Test Medium or Sabouraud-glucose agar containing chloramphenicol and cycloheximide + Cellufluor white

32
Q

dermatophytid or “id” reaction

A

sterile vesicle which appears at a site distant from the focus indicating a CMI response or Type IV HSN - DTH

33
Q

Tinea Incognito

A

altered clinical appearance due to inappropriate treatment – usually topical steroids

34
Q

Lesions of Tinea Incognito

A

Appears less raised, less scaly, more pustular, more extensive

35
Q

Long-term use of topical steroids on Tinea infections results in

A

atrophy (thin skin + striae in skin folds), purpura, telangiectasia

36
Q

Classic Ringworm lesion

A

annular lesion w/ an active border and central clearing

37
Q

Does ringworm involve mucosal membranes?

A

No

38
Q

single/multiple fissures at corner of mouth + red, scaly adjacent skin rash

A

Candida – Perleche

39
Q

Treatment for Tinea infections

A

o Potassium permanganate 1:5000
o Salicylic acid
o 20% Sodium hyposulfite
o Gentian violet
o Whitfield’s, Sulfur, Tolnaftate, Desenex, Haloprogin, Clotrimazole, Naftin, Imidazole, Griseofulvin
o Oral Antifungals: Lamisil, Itraconazole, Griseofulvin, Ketoconazole

40
Q

Tinea pedis etiologic agents

A
  1. Trichophyton mentagrophytes
  2. Trichophyton rubrum
  3. Epidermophyton floccosum
41
Q

Symptoms of Tinea pedis are due to

A

interaction of fungi and bacteria

42
Q

Lesion of typical Tinea pedis

A

Pruritic, inflamed, Pruritic, inflamed, scaling -> vesicular -> ulcers -> crusted lesions on soles and b/w toes

43
Q

Intertriginous form of Tinea pedis

A

peeling, maceration of skin b/w toes, foul odor

44
Q

Chronic, papulosquamous, hyperkeratotic form (moccasin type) form of Tinea pedis

A

pink skin covered by fine silvery-white scales, very persistent and difficult to treat

45
Q

Moccasin type of Tinea pedis is caused by which agent

A

T. rubrum

46
Q

Vesiculobulbous form of Tinea pedis

A

vesicles, vesiculopustules, or bullae on the plantar surface

47
Q

“id” reaction is most common with what form of Tinea pedis

A

Vesiculobulbous form

48
Q

Tinea manuum etiologic agents

A
  1. Trichophyton rubrum (predominately)
  2. Trichophyton mentagrophytes
  3. Epidermophyton floccosum
49
Q

Risk Factors for Tinea manuum

A

occupation that compresses interdigital spaces, concomitant tines pedis

50
Q

Tinea cruris etiologic agents

A
  1. Epidermophyton floccosum (predominately)
  2. Trichophyton rubrum
  3. Trichophyton mentagrophytes
51
Q

Describe lesion of Tinea cruris

A

Reddish-brown lesions, sharply demarcated, raised, erythematous margins, pruritic

52
Q

Tinea unguium etiologic agents

A

T. rubrum and T. metagrophytes

53
Q

Distal Subungual Onychomycosis

A

nail thickens and often discolors

distal-> proximal

54
Q

Proximal Subungual Onychomycosis

A

begins in nail fold (proximal) -> spreads distally

55
Q

White Superficial Onychomycosis (Leukonychia mycotica)

A

nails lose luster, become opaque, brittle, and have a crumbling consistency

56
Q

What is the most common tinea unguium form?

A

Distal Subungual Onychomycosis

57
Q

What is the most common tines unguium form in AIDS patients?

A

Proximal Subungual Onychomycosis

58
Q

If you find Proximal Subungual Onychomycosis, what test should be ordered?

A

CD4 count, P24 antigen

59
Q

Treatment for tinea unguium?

A

3-4 months/fingernail infection; 4-6 months/toenail infection of antifungals

60
Q

What test is done to confirm tinea unguium?

A

Periodic Acid-Schiff stain

61
Q

Tinea corporis etiologic agents

A
  1. Trichophyton

2. Microsporum

62
Q

Tinea corporis lesions

A

Single or multiple, dry, scaly, annular lesions , red borders w/ central clearing (classic ringworm)

63
Q

Iris form or vesicular form of Tinea corporis lesions

A

highly inflammatory lesion composed of pustules, vesicles, and marked erythema

64
Q

Tinea faciei lesions

A

Non-bearded areas - Annular red patches or, more commonly, indistinct red areas w/ little or no scaling

65
Q

Tinea faciei worsens with

A

sunlight exposure

Microbiology Exam 6 (5 decks)

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