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Microbiology Part 2 > Lec48 Infectious disease of skin > Flashcards

Lec48 Infectious disease of skin Flashcards

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Biology 101 flashcards
1
Q

What causes warts?

A

HPV

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2
Q

What types of dermo findings for HPV1 and 2?

A
  • palmoplantar [palms and soles] and common warts
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3
Q

What type of dermo findings for HPV6 and 11?

A
  • genital warts
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4
Q

What are effects of HPV16/18?

A

cervical/genital cancer

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5
Q

What is pathogenesis of HPV infection?

A
  • spread by direct contact with broken skin –> virus enters basal –> induces cellular proliferation
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6
Q

What is appearance of HPV warts?

A
  • verrucuous papule/plaque with thrombosed capillaries
  • thrombosed capillaries show as black dots
  • elevated, rough skin
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7
Q

How do you distinguish corn/callous from wart?

A

wart ablates skin lines

corn/callous does not

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8
Q

What is typical therapy for warts?

A
  • mechanical destruction –> cryotherapy [freezing] or salicylic acid plasters
  • induce immune response: inject candida to cause local immune response
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9
Q

What is sign of HSV derm?

A

crop of vesicles on erythematous base

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10
Q

Which type of herpes primarily responsible for labial herpes? genital herpes?

A 
HSV1 = labial [lips]
HSV2 = genital
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11
Q

What is pathogenesis of HSV? transmission?

A
  • virus contacts skin –> replicates in dermis/erpidermis –> infects and latent in trigeminal or sacral sensory ganglion –> recurs focally where nerve innervates

transmission by direct contact –> contagious until crusted

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12
Q

What triggers HSV reinfection?

A

stress, UV light, fever

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13
Q

What is manifestation of HSV prodrome?

A

tenderness/burning –> then skin pressentation/blister

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14
Q

What happens if HSV near eye?

A

can lead to eye infection –> keratitis/blindness

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15
Q

When do you get eczema herpeticum?

A
  • spreads along contiguous skin due to compromised barrier [eczema, burn, etc]
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16
Q

What is disseminated HSV? who gets it?

A
  • spreads more widely than one area, can have more scattered individual lesions
  • occurs in immunocompromised
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17
Q

Where does ZVZ stay latent?

A

sensory nerve root

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18
Q

What is life cycle involved in shingles? clinical signs?

A
  • dermatomal rash, does not cross midline [vs HSV crosses midline]
  • can have post-herpetic nerualgia in affected sensory nerve
  • lytic life cycle
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19
Q

Who gets disseminated VZV? sign?

A
  • in immunocompromised

- have dermatomal rash + individual lesions via hematogenous spread

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20
Q

How is VZV transmitted?

A
  • contagious –> by contact
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21
Q

How do you diagnose HSV/VZV?

A
  • tzanck spear [only tells you part of herpes family]
  • DFA –> anti HSV/VZV antibodies
  • viral culture
  • PCR
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22
Q

What is treatment for HSV/VZV?

A
  • acyclovir, valganciclovir, famciclovir

- foscarnet [for resistant]

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23
Q

What can cause mononucleosis?

A
  • usually EBV [human herpesvirus 4]

- also could be CMV, toxoplasmosis rarely

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24
Q

What are clinical features of infectious mono?

A
  • triad: pharyngitis, fever, lymphadenopathy [esp cervical]
  • periorbital edema
  • hepatosplenomegaly
  • can have rash beginning on trunk with later extension to face
  • 90% have hypersensitivity skin rxn to ampicillin/amoxicillin
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25
Q

How do you diagnose mono?

A
  • > 50% lymphocytes, > 10% LFTs

- monospot test: detects IgM antibodies in wk 2]

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26
Q

How do you treat mono?

A
  • coritcosteroid in case of complications

- otherwise supportive

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27
Q

What causes erythema infectiosum? Other names?

A

other names: fifth disease, slapped cheek disease

- due to human parvovirus B19

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28
Q

What type of properties human parvovirus B19 [strandedness, DNA or RNA]?

A
  • single strand

- DNA

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29
Q

What are clinical features of erythema infectiosum?

A
  • prodrome: fever, headache, myalgia
  • exanthem: bright red macular erythema [= bright red patches esp on face]
  • may have arthralgia or arthritis
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30
Q

What is pathogenesis of erythema infectiosum?

A
  • initially infect respiratory –> B19 viremia with decrease in reticulocytes –> viremia ends with IgM Ab –> IgG appears with rash and arthralgia after a few days
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31
Q

What clinical disorders associated with parvovirus B19?

A
  • erythema infectiosum
  • adults: arthropathy: may be without exanthem
  • aplastic anemia [in sickle cell pts] –> ab pain, resp symptoms
  • paupular purpuric gloves and socks syndrome [purpura on hands and feet and oral mucosa]
32
Q

What are outcomes of congenital parvovirus B19 infection? when is infection the greatest risk?

A

greatest risk = first 20 wks gestation

effects: fetal hydrops, intreuterine demise, still birth

33
Q

How do you diagnose parvovirus B19?

A
  • serology [anti B19 IgM Ab]

- PCR

34
Q

What is treatment for parvovirus B19?

A
  • no specific antiviral treat

- symptomatic support

35
Q

How is measles transmitted?

A

respiratory droplets

36
Q

What are clinical features of measles:

A

prodrome: fever, cough, koplik spots, nasal congestion
exanthem: erythematous macules and papules begin on face and move down = irregulary shaped bright red spots with blueish white central dot

37
Q

What are possible complications of measles?

A
  • pneumonia, encephalitis, subacute sclerosing panencephalitis
38
Q

What causes molluscum contagiosum?

A

poxvirus

39
Q

What is mech of molluscum contagiosum transmission?

A
  • by direct contact
  • in adults –> sexually transmitted
  • in children see it with atopic diathesis
40
Q

What is the appearance of molluscum contagiosum?

A

umbilicated papule

41
Q

What is treatment for mollscum contagiosum?

A
  • self limited, can scrape off but may leave scar
42
Q

What are the 3 superficial fungal infections of the skin?

A
  • dermatophytes
  • candida
  • pityriasis [tinea] versicolor
43
Q

What organisms cause dermatophytes?

A

most common: trichophyton rubrum

also: microsporum canis and T. tonsurans

44
Q

What types of lesions are dermatophyte lesions?

A

pruritic

45
Q

How do you diagnose dermatophytes?

A

KOH [potassium hydroxide] and/or culture

46
Q

What is another name of tinea corporis?

A

ring worm

47
Q

What is tinea capitis?

A
  • dermatophyte of head

- fungus invades hair follicle and shaft

48
Q

Is tinea capitis contagious? How is it spread?

A
  • it is contagious
  • spread by sharing hats, bedding
  • pets can be a source
49
Q

What are three types of tinea capitis?

A

black dot tinea capitis = hair break near scalp looks like black dots

kerion = boggy inflammatory plaque, inflammatory red

favus = extensive hairloss with scarring and hyperkeratotic yellow crusts called scutula, most severe type

50
Q

What is manifestation of tinea corporis?

A

round red rash

51
Q

What is favus?

A

type of tinea capitis = extensive hairloss with scarring and hyperkeratotic yellow crusts called scutula

52
Q

What is kerion?

A

type of tinea capitis = boggy inflammatory plaque

53
Q

What is tinea unguium?

A

dermatophyte infection of nail

54
Q

What is appearance of tinea unguium?

A

yellow discoloration of nail

dystrophy

55
Q

What is treatment for dermatophytes?

A

topical: terbinafine best, others [ketoconazole, clotrimazole, econazole]
oral: terminafine or itraconazole

56
Q

What is appearance of tinea cruris?

A
  • aka jock itch
  • red paches, may have pustule at border
  • spares the scrotum [vs candidal intergrigo affects scrotum
  • no satellite lesions
57
Q

What is different tinea cruris and candidal intertrigo

A
  • tinea spares the scrotum [vs candidal intergrigo affects scrotum]
  • tinea has no satellite lesions [vs candida does]
58
Q

How do you treat tinea capitis?

A
  • oral a
59
Q

What is side effect of terbinafine?

A

possible hepatotoxicity

60
Q

Which dermatophytes can you treat topically?

A

with limited area [groin, small area body]

tinea capitis –> use shampoo

61
Q

Which dermatophytes do you treat orally?

A
  • tinea unguium

- tinea capitis

62
Q

What is sign of oral candidiasis?

A
  • creamy white cottage cheese like plaques that are easily scraped off [pseudomembrane]
  • burning, pain, pruritis [itching]
63
Q

Where do you get oral candidiasis lesions?

A
  • dorsal tongue
  • buccal mucosae
  • palate
  • pharynx
64
Q

How do you get oral candidiasis?

A
  • inhaled steroids for asthma

- immunocompromised [HIV]

65
Q

What is treatment for oral candidiasis?

A
  • fluconazole, clotrimazole or nystatin
66
Q

Where do you get candidal intertrigo?

A

any skin folds, also get satellite lesions

67
Q

How do you prevent candidal diaper dermatitis?

A
  • barrier cream after diaper change –> irritant feces and urine contact cream not skin
68
Q

How do you treat candidal diaper dermatitis?

A
  • oral antifungals –> candida can colonize gut
69
Q

What are risk factors for candidal angular chelitis?

A
  • chronic lip licking, drooling
70
Q

How do you get candidal paronychia / what is it?

A

cuticle gets inflamed from chronic water exposure

71
Q

What are signs of systemic candidiasis [candidemia]?

A
  • generalized papules and pustules

- neutropenia

72
Q

What causes tinea [pityriasis] versicolor?

A

pityrosporum orbiluare

73
Q

What are signs of tinea versicolor?

A
  • hyper and hypopigmented pathces with fine scale on chest and back
  • can be asymptomatic
74
Q

How do you diagnose tinea versicolor?

A
  • clinical inspection

- KOH scraping –> shows spaghetti and meatballs [hyphae and spores]

75
Q

What is treatment for tinea versicolor?

A
  • ketoconazole, keratolytics
76
Q

Who gets deep [invasive] fungal skin infections? How do they usually appear?

A
  • seen in immunocompromised

- usually ulcerated plaques or disseminated papules

Microbiology Part 2 (30 decks)

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