Infectious skin diseases Flashcards Preview

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Flashcards in Infectious skin diseases Deck (81):
1

How does the skin offer a first line of defense against microbial infection?

physical barrier; low pH, sebaceous fluid, fatty acids; normal flora deters further colonization

2

What is the most common means bacteria infect the skin?

penetration of the skin barrier

3

What are the 3 steps of bacterial pathogenesis?

bacterial adherence to host; invasion of tissue w/ evasion of host; elaboration of toxins

4

Which organisms are produce superantigens?

virulent S. aureus and S pyogenes

5

How do superantigens work?

bind conserved portions of T cell receptors and activate large numbers of T cells leading to cytokine storm and inflam response

6

What is impetigo

a superficial cursting of epidermal skin infections presenting in bullous and nonbullous forms

7

Who/What/By whom/characteristic feature of impetigo

young children; face; S. aureus and S. pyogenes; honey colored crust

8

Define Erysipelas

streptococcal infection of superficial dermal lymphatics w/ sharply demarcated, raised borders

9

Define cellulitis and causative agent

infection of deeper dermis and subcutaneous tissue w/ poorly demarcated borders; majority streptococcal

10

cutaneous abscess

collections of pus in the dermis and subcutaneous tissue

11

Define folliculitis

superficial infection of hair follicles w/ pus accumulation in epidermis

12

Define furuncles

deeper involvement of hair follicles in which infection extends into the subcutaneous tissue

13

Define carbuncle

adjacent furuncles coalesce to form single inflamed area

14

Who/What/By whom of Staphyloccal scalded skin syndrome

infants/kids, adults w/ renal failure, immsprsd;
granular layer split of epidermis;
exotoxin producing S. aureus

15

What are the clinical features of Staph scalded skin syndrome?

diffuse generalized erythema, superficial desquamation w/ flural accentuation; **uninvolved mucous membranes**; perioral, periocular crusting, radial fissures

16

What is staph scalded skin syndrome Tx?

Antibiotics and supportive care

17

What is the pathogenesis of staph scalded skin syndrome?

exotoxin bind to desmoglein 1 and cleave leading to loss of cell-cell adhesion

18

define necrotizing fasciitis

insidious and deadly soft tissue infections associated w/ widespread tissue necrosis

19

Who is subject to necrotizing fasciitis?

patients after minor trauma and surgical wounds; most are immunocompromised, diabetic, alcoholic, or obese

20

What is an early warning sign of necrotizing fasciitis? What happens if it is ignored?

**pain out of proportion to clinical findings**; ignoring leads to rapid progression and delay may be fatal (red to purple skin w/in 36 hours)

21

What type of emergency is necrotizing fasciitis?

surgical emergency associated with debridement

22

What is toxic shock syndrome?

S. aureus caused disease that produces TSST-1 toxin classically from tampons, surgery or deep abscesses

23

How does toxic shock syndrome present?

sunburn-like erythema and sandpaper papules progressing to desquamation of hands and feet

24

Toxic shock syndrome Treatment

antibiotics and remove agent

25

What are general features of bacterial skin diseases?

pus forming infections: staphylococcal except in periorifical abscesses that are anaerobic

26

What accounts for the majority of serous bacterial SSTIs?

cellulitis

27

How is a diagnosis made in bacterial skin diseases?

clinical presentation and Hx; culture to confirm and base Tx from

28

In fungal diseases, where are superficial infections?

confined to dead keratinous tissue, epidermis and hair follicles

29

What causes superficial fungal diseases?

dermatophytes; nondermatophyte molds; yeasts (candida)

30

in fungal diseases, where are deep infections?

all skin layers and some extend into the subcutaneous tissue

31

How do deep infections typically occur?

direct inoculation of skin such as sporotrichosis, mycetoma, chromomycosis

32

Where are systemic fungal infections typically found?

since inhaled, least common cutaneous and have pulmonary focus even though a skin lesion may tip the infection

33

What does the most common cause of superficial fungal infections feed on?

dermatophytes digest keratin as nutrient source

34

Where will dermatophytes likely colonize?

stratum corneum; nail plate; hair follicles

35

What are the dermatophytes virulence factors?

enzymes: adherence to keratin; invasion of keratin by secretized enzymes

36

What are the dermatophyte genera that cause superficial fungal infections?

Trichophyton (most common); microsporum; epidermophyton

37

How is a tinea infection characterized?

intensely pruritic, annular lesions with peripheral scale, central clearing and variable inflammation

38

What is the most common cause of tinea pedis?

95% dermatophytes due to occlusive footwear

39

What is the result of tinea unguium/onchomycosis?

infection of nail plate/bed leading to deformity with thickening and discoloration (onchodystrophy and hyperkeratosis)

40

Where is tinea corporis located?

trunk and limbs

41

Where is tinea cruris? clinical presentation?

jock itch of groin: erythematous patch of inner thigh and inguinal folds **spares scrotum and penis**

42

What is the common cause of tinea capitis?

infection of scalp and hair from superficial infection w/ T. tonsurans

43

What are 3 distinctive features of superficial fungal diseases regarding histopathology?

neutrophils present in stratum corneum;
hyphae in corneum visible on PAS stain (pink-red);
culture material scraped from area for ID

44

Where does candidiasis typically present?

skin, mucus membranes, nails or GI tract

45

Who is candidiasis more common in?

women (vulvovaginal candidiasis); immunosuppressed

46

What is a typical presentation of tinea versicolor?

recent tropical visit; Malassezia overgrowth causing harmless hypo/hyper pigmented patches with fine scaling

47

What disease presents as off-white/pink macules and papules with a spaghetti and meatball appearance?

Tinea versicolor

48

What is significant about most viruses affecting the skin?

produce chronic/life long infection

49

Describe the infection and reactivation of HSV 1,2 infections

initial via mucosa or abraded skin; travel retrograde along sensory neuronal axons to nuclei during latency; reactivate at previous primary infection site

50

HSV reactivations lead to what?

shedding of viral particles w/o symptomatic disease contributing to disease spread

51

What causes herpes labialis? how is it spread?

HSV-1 and spread through contact with oral secretions

52

What causes herpes genitalis?

HSV-2 (increasing overlap from HSV-1)

53

What is the typical presentation of HSV infection?

variable depending on immune status of host with prodrome tingling or pain in diseases region

54

How could HSV-1 and HSV-2 infections be differentiated other than location?

HSV-1: asympptomatic
HSV-2: severe, painful vesicle form, ulceration, fever, lethargy

55

How does HSV-1 reactivations typically present?

grouped vesicles on erythematous base for 2-3 days; lesions develop ulceration w/ crusting then heal in 4-5 days

56

How are HSV infections diagnosed?

**most clinical eval alone**; Tsanck smear, viral culture, direct fluorescnt Ab study; serologic testing

57

What are the dermatologic disease manifestations of HSV infections?

eczema herpeticum (atopic dermatitis); herpetic whitlow (digital infection); herpes gladiatorum (corporeal)

58

How should a HSV infection be treated?

Acyclovir; valacyclovir; famciclovir; foscarnet; cidofovir

59

What is the MOA of acyclovir?

inhibits viral DNA polymerase after phosphorylation by herpes specific thymidine kinase

60

How does resistance arise to acyclovir?

viral thymidine kinase deficiency

61

How is VZV transmitted and incubation period?

very contagious airborne or direct contact with incubation 11-20 days

62

What describes the primary infection of VZV?

pruritic eruption spreading from face/scalp to trunk/ to extremities resembling drops on a rose petal

63

VZV under histology has what characteristic finding?

multinucleated acanthoytic keratinocyte

64

What are the vaccines for VZV?

varivax (live attenuated prevents/decreases risk)
Zostavax (persons at least 60y/o)

65

What causes molluscum contagiosum? What does it look like?

DNA poxvirus of the molluscipox genus;
smooth, dome-shaped, umbilicated papules

66

What does molluscum contagiosum look like on histologic exam?

Henderson-Patterson bodies => intracytoplasmic inclusions within keratinocytes

67

How does molluscum contagiosum progress?

self limited disease in healthy patients

68

What is the genome of HPV?

icosahedral, naked, circular ds DNA

69

HPV are very genetically simple. How does this help the virus?

implies strong host dependence and few targets for anti-virals

70

What are the 3 domains of the HPV genome?

upstream regulatory region; early and late regions;

71

What proteins of HPV may lead to cancer? How?

E6 protein leads to degradation of p53; E7 inactivates Rb protein

72

How does HPV infect a person?

through basal keratinocytes through minor abrasions in skin/mucosa => direct contact; cell entry L1/L2 proteins and cell surface receptors

73

How does the virus replicate and divide?

replicates in nucleus; divides and spreads laterally and migrates upward to suprabasal cell layers

74

What does HPV-1 cause?

palmoplantar warts on volar aspect of palms/soles and fingers/toes

75

What does HPV-2, 4 cause?

common warts => verrucous papules on glaberous skin

76

What does HPV-3, 10 cause?

flat warts=> slightly elevated flesh colored papules that are smooth or hyperkeratotic

77

What does HPV-6, 11 cause?

genital warts=> scaly and papular to smooth and flesh colored

78

How will the histology of the HPV-6, 11 be viewed?

hyperkeratosis; papillomatosis; hypergranulosis

koilocytes: vacuolated superficial keratinocytes w/ pyknotic raisin like nuclei

79

How should warts from HPV be treated?

most are self limited in healthy patients but Tx tailored to site involved

80

What causes an increase risk in cervical cancer?

condylomata associated with HPV will increase cervical cancer risk

81

What are the 2 types of vaccines associated with HPV?

Quadrivalent composed of L1 VLP from 6, 11, 16, 18;
bivalent HPV 16, 18 that is a VLP vaccine