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Infectious skin diseases Flashcards

pathogenesis of skin infections; bacterial, fungal, viral skin diseases; (81 cards)

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1
Q

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

A

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

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2
Q

What is the most common means bacteria infect the skin?

A

penetration of the skin barrier

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3
Q

What are the 3 steps of bacterial pathogenesis?

A

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

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4
Q

Which organisms are produce superantigens?

A

virulent S. aureus and S pyogenes

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5
Q

How do superantigens work?

A

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

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6
Q

What is impetigo

A

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

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7
Q

Who/What/By whom/characteristic feature of impetigo

A

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

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8
Q

Define Erysipelas

A

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

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9
Q

Define cellulitis and causative agent

A

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

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10
Q

cutaneous abscess

A

collections of pus in the dermis and subcutaneous tissue

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11
Q

Define folliculitis

A

superficial infection of hair follicles w/ pus accumulation in epidermis

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12
Q

Define furuncles

A

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

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13
Q

Define carbuncle

A

adjacent furuncles coalesce to form single inflamed area

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14
Q

Who/What/By whom of Staphyloccal scalded skin syndrome

A

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

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15
Q

What are the clinical features of Staph scalded skin syndrome?

A

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

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16
Q

What is staph scalded skin syndrome Tx?

A

Antibiotics and supportive care

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17
Q

What is the pathogenesis of staph scalded skin syndrome?

A

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

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18
Q

define necrotizing fasciitis

A

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

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19
Q

Who is subject to necrotizing fasciitis?

A

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

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20
Q

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

A

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)

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21
Q

What type of emergency is necrotizing fasciitis?

A

surgical emergency associated with debridement

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22
Q

What is toxic shock syndrome?

A

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

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23
Q

How does toxic shock syndrome present?

A

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

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24
Q

Toxic shock syndrome Treatment

A

antibiotics and remove agent

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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

Dermatology path (11 decks)

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