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
Diagnosis of Impetigo
Clinical presentation | Gram stain, Biopsy of blister, Culture w/Antibiotic sensitivity test
26
Cellultis – epidemiology
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
27
Cellulitis – how to acquire
Infections occur through skin breaks
28
Bacteriology of Cellulitis - Eryiseplas
= facial variant of cellulitis | <-- Group A Beta-hemolytic streptococci
29
Bacteriology of Cellulitis – Cellulitis
``` Non-face variant of cellulitis Group A Beta-hemolytic streptococci Staph aureus Haemophilus influenza (children) Less commonly: other streptococci, Pneumococcus, Klebsiella, Yersinia, mixed flora ```
30
Erysipelas – location, incubation, appearance
Confined to face Incubates 2-5 days Bilateral facial involvement Painful, bright red, indurated, sharp border (“cliff drop border”) +/- Lymphadenopathy
31
Staphylococcal cellulitis
Primary lesion – tender, ill-defined area of painful erythema w/variable induration Lymphatic streaking is common Lymphadenopathy is variable
32
Cellulitis Diagnosis
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
Sexually transmitted disease – Risk from single sexual contact & incidence
~30% Incidence peaked in 90s, but now going up again since 2006
34
Syphilis – cause
Terponema pallidum = Spirochete w/6-14 spirals = 7-15 microns long, 0.25 micron width = can’t cultured; must ID in other ways
35
Syphilis – Clinical Classifications
Primary Secondary (early latent – 1-2 years; late latent) Tertiary Congenital
36
Primary syphilis - time & lesion type
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
Chancre in primary syphilis
Non-tender, Indurated Genital or extragenital May be unnoticeable if in hidden location Heals in 3-6 weeks Lymphadenopathy
38
Secondary syphilis – time
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
Secondary syphilis – types of skin lesions
- 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
Diagnosis of syphilis
Clinical presentation – rash + lymphadenopathy, palms & soles, etc. Darkfield microscopy Biopsy Serology - Nontreponemal (VDRL, *RPR*) tests - Treponemal (FTA-ABS, MHA-TP) tests
41
Dermatophytes
Fungi that eat keratin (skin, hair, nails)--> can’t get deep infection, rarely get septic Ex: epidermophyton (sock & jocks, no hair), trichophyton, microsporum
42
Fungal skin infections – how to acquire
Human or Animal (farm, cats) contact Water, soil Fomites, Clothing
43
Tinea capitis
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
Tinea faciei
affects face | annular placques w/some central clearing
45
Tinea barbae
- on face | - from men, barbershops, animals
46
Tinea corporis
on body
47
Tinea cruris
groin (often spares scrotum, penis)
48
Tinea pedis
- on feet - annular placques moving outward from central ring; - can be hyperkeratotic
49
Tinea manum
- on hands | - usually only affects 1 hand (--> 2-feet-1-hand syndrome)
50
Majocchi’s granuloma
- Tinea corporus w/ involvement of hair follciles | - Deeper granulomatous infection (must use systemic antifungals now)
51
Onychomycosis w/Tinea pedis/manus
Subungual (under nail) infection, lifting of nail
52
Diagnosis of tinea fungal infections
KOH test on leading edge Dermatophyte test medium Biopsy of leading edge
53
Treatment of tinea pedis
Topical naftifine | OTC topical antifungals: Tinactin>Lotrimin
54
Candidiasis – epidemiology & location
Increased prevalence in - diabetes mellitus - occlusion - corticosteroid use - broad-spectrum antibiotics Affects mucous membranes & skin Normal flora
55
Mycology – food source, most common species
Preferred food source = glucose or serum Most common pathogenic species - Candida albicans - C. trpicalis, C kefyr, C. glabrata, C. parapsilosis
56
Types of candidal infections
- Thrush in HIV infections - Candidasis – Perleche (edges of mouth, chronically moist area) - Erosio Interdigitalis Blastomycetic Chronica (finger webs - Candida Diaper Dermatitis
57
Candidiasis – Dx
Clinical presentation | KOH, Gram stain, Culture (Sabouraud’s agar, Nickerson’ medium), Biopsy
58
Tinea versicolor – epidemiology
Worldwide distribution, more common in humid/warm climates Confined to post-pubertal pts
59
Tinea versicolor – mycology
Malassexia furfur (Pityrosporum obiculare) Food source: follicular lipids
60
Tinea versicolor – Clinical features
Distribution: mostly trunk Primary lesion: asymptomatic, tan-colored, subtly scaly macule or patch Clinical variants: hypopigmented or folliculitis
61
Diagnosis of Tinea versicolor
Clinical presentation | KOH (spaghetti & meatballs), Methylene blue, Biopsy, Culture = rarely done
62
Scabies – epidemiology
Worldwide distribution, all ages, races, socioeconomic groups Highest prevalence in children & sexually active adults
63
Scabies – how to acquire
Spread of mites via person-to-person contact
64
Scabies etiology
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
Scabies - distribution
Symmetric soft skin distribution - Interdigital web space - Flexural wrist - Waist - Axillae - Genitalia - Breast
66
Scabies - symptoms
Pruritus (nocturnal accentuation) Primary Lesions – erythematous papules & burrows, nodular genitalia lesions Secondary Lesions - Excoriation, Infection
67
Norwegian scabies
In infants or neurologically-compromised pts (no itch response) In immunologically-compromised pts w/decreased sensory function ---> hundreds & hundreds of mites
68
Diagnosis of scabies
Clinical presentation (burrows, genital nodules) Mineral oil preps (mites, eggs, mite feces – scybala) Skin biopsy (host response, burrows, mites, eggs, scybala)
69
Lice infestation – epidemiology
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
Lice infestation – etiology
Pediculus human - -- Scalp louse –var. cap - -- Body louse – var. corporis Pubic louse = Phthirus pubis
71
Scalp lice
Lices – closer to scalp | Nids (egg casings) – not as close to scalp, on hair
72
Body lice – morphology, location, clinical findings
Lice & eggs = morphologically identical to scalp lice Location – only on clothing (eat then leave skin) Truncal erythematous papules & macules Intense pruritus Secondary excoriation
73
Pubic lice – distribution, symptoms, nid/lice appearance
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
Lice infestation –Dx
Clinical presentation | Demonstration of louse or nit
75
Treatment of scalp lice
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 ```