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Unit 3 D&D > DD 03-10-14 09-10am Skin Infections and Infestations slides notes > Flashcards

DD 03-10-14 09-10am Skin Infections and Infestations slides notes Flashcards

1
Q

Human Papilloma Virus - Prevalences

A

Prevalence – up to 10% of children

Genital HPV infection in 20+ million in US

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2
Q

Human Papilloma Virus – Ways to Acquire

A

Breaks in skin/mucosa
Person-to-person contact
Fomites

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3
Q

Skin Defense mechanisms

A

Physical barrier
Desquamation (40,000 min)
Localized immune response (cellular & immunoglobulins)
Anti-microbial peptides (alpha-definsins)
Skin pH

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4
Q

HPV Virology – Family, Types, Structure

A
  • Family Papoviridae (papovavirus)
  • Many many types (over 200 at least; likely to be reinfected w/another type)
  • Non-enveloped double-stranded DNA virus
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5
Q

Warts – how they develop & types

A

= overgrowth of normal skin cell (virus tells cell to proliferate)

  • Verruca vulgaris
  • Verruca plantaris (on plantar surface of foot)
  • Verruca plana (flat warts) – often on mens’ face & women’s legs (spread by shaving)
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6
Q

Diagnosis of HPV infection

A

Clinical + Biopsy + In-situ hybridization

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7
Q

Treatment of warts

A

Can’t target virus, so blow up its house

  • Cryotherapy (freeze), Curettage (scrape), Laser (CO2, PDL)
  • Salicylic acid, Podophyllin, Cantharidin
  • Occlusion (duct tape)
  • Imiquimod (Aldaral ), 5% 5-flurouracil, Intralesion candida –> to wake up immune system in the area
  • Time (spontaneous involution in many, but continued appearance of new warts)
  • Do not need to treat, unless immunosuppressed
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8
Q

Herpes Simplex virus infection – Epidemiology

A

HSV-1 in >90% by age 2

HSV-2 seroprevalence increased with increasing sexual partners

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9
Q

Herpes Simplex virus infection – How to Acquire

A

Through breaks in skin/mucosa

Saliva, vaginal secretion, vesicular fluid, direct skin contact

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10
Q

Herpes Simplex Virology – Family, Location of different types, structure

A

Herpesvirus group

HSV-1 = lips
HSV-2 genitalia

Enveloped double-stranded DNA virus

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11
Q

Persistances of HSV

A

HSV persists in autonomic or sensory ganglia – no cure once infected

Primary & Recurrent Herpes Labialis (cold sore)

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12
Q

Herpes – manifestations

A

Group of blisters on red base, especially recurrent = Herpes until proven otherwise

  • Herpetic whitlow –on fingertips
  • Herpes progenitalis – on genitals
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13
Q

Herpes simplex infection & HIV

A

Serious infection quickly, may present atypically

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14
Q

Diagnosis of HSV infection

A

Clinical presentation – grouped blisters on red base + story (recurrences, triggers)

Tzanck preparation – scraping & staining on slides (confirms HSV or VZV, but not between them)

Biopsy (cytopathic changes, immunoperoxidase)

Viral culture

HSV type-specific DNA probes/Abs

Serologic evaluation

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15
Q

Treatment of HSV infection

A

Acyclovir – for all types of herpes (five times a day)

Famciclovir, Valacyclovir – longer half-life (once or twice a day; also for suppressive therapy)

Foscarnet (acyclovir-resistance HSV)

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16
Q

Varicella-Zoster Infection – Epidemiology

A

> 90% of adults has VZV antibodies

> 90% in susceptible household contacts

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17
Q

Varicella-Zoster– How to acquire

A

Primarily spread by respiratory route

Very communicable

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18
Q

Chickenpox

A

= primary VZV infection

Incubation: ~14 days

Initially: Fever, don’t feel good

Lesion: single thin-walled vesicles on erythematous base (dewdrop on rose petal) (not grouped – one dewdrop on one rose petal)

New crops for 3-5 days (lesions in multiple stages of development)

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19
Q

Herpes Zosters

A

= reactivation of dorsal root ganglion varicella zoster virus

*Called Herpes zoster, but NOT herpes infection

Long-lasting post-herpatic neuralgia (often reason for presentation)

Not scarring (unless excoriated)

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20
Q

Diagnosis of VZV infection

A

Clinical presentation
Tzank preparation
Biopsy, Viral culture, Serology
Direct immunofluorescence, PCR

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21
Q

Impetigo – epidemiology & how to acquire

A

Most common superficial bacterial infection of kids

Person-to-person contact

Less commonly through fomite

Predisposing factors: high humidity, cutaneous carriage, poor hygiene

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22
Q

Bacteria involved in Impetigo

A

Strep pyogenes

Staph aureus

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23
Q

Streptococcal Non-Bullous Impetigo (Impetigo Contagiosa)

A

Most commonly affects face & in children

Typically begins as single lesions & becomes multiple

Primary lesions: honey-colored yellow crust

Occasionally mild lymphadenopathy & mild fever, but usually feel fine

Up to 5% are associated w/acute post-strep glomerulonephritis

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24
Q

Staphylococcal Non-Bullous Impetigo

A

Most commonly affects face

Any age group but more commonly in adults

Often a secondary lesion of superficial injury or dermatitis

Primary lesion: Yellow to amber-colored crust w/variable erythema

Often inoculate from your own nose (where staph is carried)

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25
Q

Diagnosis of Impetigo

A

Clinical presentation

Gram stain, Biopsy of blister, Culture w/Antibiotic sensitivity test

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26
Q

Cellultis – epidemiology

A

Increase sensitivity in:

  • very young or old
  • immunocompromised (though occur in healthy ppl)
  • IV drug users
  • pts w/ chronic ulcers

Poste-surgical complication

Increased incidence in summer

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27
Q

Cellulitis – how to acquire

A

Infections occur through skin breaks

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28
Q

Bacteriology of Cellulitis - Eryiseplas

A

= facial variant of cellulitis

<– Group A Beta-hemolytic streptococci

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29
Q

Bacteriology of Cellulitis – Cellulitis

A 
Non-face variant of cellulitis
Group A Beta-hemolytic streptococci
Staph aureus
Haemophilus influenza (children)
Less commonly: other streptococci, Pneumococcus, Klebsiella, Yersinia, mixed flora
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30
Q

Erysipelas – location, incubation, appearance

A

Confined to face

Incubates 2-5 days

Bilateral facial involvement

Painful, bright red, indurated, sharp border (“cliff drop border”)

+/- Lymphadenopathy

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31
Q

Staphylococcal cellulitis

A

Primary lesion – tender, ill-defined area of painful erythema w/variable induration

Lymphatic streaking is common

Lymphadenopathy is variable

32
Q

Cellulitis Diagnosis

A

Clinical presentation

CBC (leukocytosis variably)

Biopsy consistant w/ organisms is HARD to find

Culture + gram stain more sensitive & specific (occasionally used)

Blood culture = + in 10%

33
Q

Sexually transmitted disease – Risk from single sexual contact & incidence

A

~30%

Incidence peaked in 90s, but now going up again since 2006

34
Q

Syphilis – cause

A

Terponema pallidum
= Spirochete w/6-14 spirals
= 7-15 microns long, 0.25 micron width
= can’t cultured; must ID in other ways

35
Q

Syphilis – Clinical Classifications

A

Primary
Secondary (early latent – 1-2 years; late latent)
Tertiary
Congenital

36
Q

Primary syphilis - time & lesion type

A

Incubation 10-90 days (inversely proportional to inoculum’s size)

In regional lymph nodes in 30 min

Painless chancres full of spirochetes, highly communicable

37
Q

Chancre in primary syphilis

A

Non-tender, Indurated

Genital or extragenital

May be unnoticeable if in hidden location

Heals in 3-6 weeks

Lymphadenopathy

38
Q

Secondary syphilis – time

A

Begins 4-10 weeks after onset of chancre

Original chancre may be present

Lymphadenopathy in 90%

Several types of secondary skin lesions

Typically lasts 2-12 weeks

*typically pts present w//secondary syphilis

39
Q

Secondary syphilis – types of skin lesions

A
  • Non-pruritic papulosquamous lesions
  • Condylomata lata
  • Nonscarring “moth eaten” alopecia
  • Split papules at oral commissures
  • Annular lesions on face
  • Oral lesions
  • Lesions on palms & soles (rarely involved except in syphilis)

*If you look at a rash & don’t know what it is, always safe to put syphilis, sarcoid, & drug rxn in

40
Q

Diagnosis of syphilis

A

Clinical presentation – rash + lymphadenopathy, palms & soles, etc.

Darkfield microscopy

Biopsy

Serology

  • Nontreponemal (VDRL, RPR) tests
  • Treponemal (FTA-ABS, MHA-TP) tests
41
Q

Dermatophytes

A

Fungi that eat keratin (skin, hair, nails)–> can’t get deep infection, rarely get septic

Ex: epidermophyton (sock & jocks, no hair), trichophyton, microsporum

42
Q

Fungal skin infections – how to acquire

A

Human or Animal (farm, cats) contact
Water, soil
Fomites, Clothing

43
Q

Tinea capitis

A

Hair infection (esp. w/short dark curly hair)

Gray patch tinea = perfectly round, associated hair loss, occipital lymphadenopathy

Black dot tinea capitis

Kerion tinea capitis – so much fungi that there is a pus pocket; scaling on scalp is rarely bacterial – don’t use antibiotics, use antifungals

44
Q

Tinea faciei

A

affects face

annular placques w/some central clearing

45
Q

Tinea barbae

A
  • on face

- from men, barbershops, animals

46
Q

Tinea corporis

A

on body

47
Q

Tinea cruris

A

groin (often spares scrotum, penis)

48
Q

Tinea pedis

A
  • on feet
  • annular placques moving outward from central ring;
  • can be hyperkeratotic
49
Q

Tinea manum

A
  • on hands

- usually only affects 1 hand (–> 2-feet-1-hand syndrome)

50
Q

Majocchi’s granuloma

A
  • Tinea corporus w/ involvement of hair follciles

- Deeper granulomatous infection (must use systemic antifungals now)

51
Q

Onychomycosis w/Tinea pedis/manus

A

Subungual (under nail) infection, lifting of nail

52
Q

Diagnosis of tinea fungal infections

A

KOH test on leading edge
Dermatophyte test medium
Biopsy of leading edge

53
Q

Treatment of tinea pedis

A

Topical naftifine

OTC topical antifungals: Tinactin>Lotrimin

54
Q

Candidiasis – epidemiology & location

A

Increased prevalence in

  • diabetes mellitus
  • occlusion
  • corticosteroid use
  • broad-spectrum antibiotics

Affects mucous membranes & skin

Normal flora

55
Q

Mycology – food source, most common species

A

Preferred food source = glucose or serum

Most common pathogenic species

  • Candida albicans
  • C. trpicalis, C kefyr, C. glabrata, C. parapsilosis
56
Q

Types of candidal infections

A
  • Thrush in HIV infections
  • Candidasis – Perleche (edges of mouth, chronically moist area)
  • Erosio Interdigitalis Blastomycetic Chronica (finger webs
  • Candida Diaper Dermatitis
57
Q

Candidiasis – Dx

A

Clinical presentation

KOH, Gram stain, Culture (Sabouraud’s agar, Nickerson’ medium), Biopsy

58
Q

Tinea versicolor – epidemiology

A

Worldwide distribution, more common in humid/warm climates

Confined to post-pubertal pts

59
Q

Tinea versicolor – mycology

A

Malassexia furfur (Pityrosporum obiculare)

Food source: follicular lipids

60
Q

Tinea versicolor – Clinical features

A

Distribution: mostly trunk
Primary lesion: asymptomatic, tan-colored, subtly scaly macule or patch

Clinical variants: hypopigmented or folliculitis

61
Q

Diagnosis of Tinea versicolor

A

Clinical presentation

KOH (spaghetti & meatballs), Methylene blue, Biopsy, Culture = rarely done

62
Q

Scabies – epidemiology

A

Worldwide distribution, all ages, races, socioeconomic groups

Highest prevalence in children & sexually active adults

63
Q

Scabies – how to acquire

A

Spread of mites via person-to-person contact

64
Q

Scabies etiology

A

Sarcoptes scaciei var. hominis (also an animal variant, but doesn’t transmit)

Mites (.35 by .3 mm) – possible to see w/ naked eye (but usually need light microscopy)

Variable number of mites per host (usually <100)

65
Q

Scabies - distribution

A

Symmetric soft skin distribution

  • Interdigital web space
  • Flexural wrist
  • Waist
  • Axillae
  • Genitalia
  • Breast
66
Q

Scabies - symptoms

A

Pruritus (nocturnal accentuation)

Primary Lesions – erythematous papules & burrows, nodular genitalia lesions

Secondary Lesions - Excoriation, Infection

67
Q

Norwegian scabies

A

In infants or neurologically-compromised pts (no itch response)

In immunologically-compromised pts w/decreased sensory function

—> hundreds & hundreds of mites

68
Q

Diagnosis of scabies

A

Clinical presentation (burrows, genital nodules)

Mineral oil preps (mites, eggs, mite feces – scybala)

Skin biopsy (host response, burrows, mites, eggs, scybala)

69
Q

Lice infestation – epidemiology

A

Worldwide

Body lice: most common in indigent (homeless, etc.)

Head lice: 12 million new case/ year; usually in children

Crab lice: most common in homosexuals & young men

70
Q

Lice infestation – etiology

A

Pediculus human

  • – Scalp louse –var. cap
  • – Body louse – var. corporis

Pubic louse = Phthirus pubis

71
Q

Scalp lice

A

Lices – closer to scalp

Nids (egg casings) – not as close to scalp, on hair

72
Q

Body lice – morphology, location, clinical findings

A

Lice & eggs = morphologically identical to scalp lice

Location – only on clothing (eat then leave skin)

Truncal erythematous papules & macules

Intense pruritus

Secondary excoriation

73
Q

Pubic lice – distribution, symptoms, nid/lice appearance

A

Primarily genital (less commonly eyelashes, beard, axilla)

Marked pruritus of genital area

Nits similar to head/body lice

Adult: six legs, crab-like, easily found attached to base of hair follicles

74
Q

Lice infestation –Dx

A

Clinical presentation

Demonstration of louse or nit

75
Q

Treatment of scalp lice

A

Key to treatment = get rid of nids (eggs) w/comb
Less important is killing the lice w/shampoo etc.

Elimite cream (permethrin 5%)
RID shampoo & comb

Unit 3 D&D (18 decks)

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