DD 03-10-14 09-10am Skin Infections and Infestations slides notes Flashcards
Human Papilloma Virus - Prevalences
Prevalence – up to 10% of children
Genital HPV infection in 20+ million in US
Human Papilloma Virus – Ways to Acquire
Breaks in skin/mucosa
Person-to-person contact
Fomites
Skin Defense mechanisms
Physical barrier
Desquamation (40,000 min)
Localized immune response (cellular & immunoglobulins)
Anti-microbial peptides (alpha-definsins)
Skin pH
HPV Virology – Family, Types, Structure
- Family Papoviridae (papovavirus)
- Many many types (over 200 at least; likely to be reinfected w/another type)
- Non-enveloped double-stranded DNA virus
Warts – how they develop & types
= 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)
Diagnosis of HPV infection
Clinical + Biopsy + In-situ hybridization
Treatment of warts
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
Herpes Simplex virus infection – Epidemiology
HSV-1 in >90% by age 2
HSV-2 seroprevalence increased with increasing sexual partners
Herpes Simplex virus infection – How to Acquire
Through breaks in skin/mucosa
Saliva, vaginal secretion, vesicular fluid, direct skin contact
Herpes Simplex Virology – Family, Location of different types, structure
Herpesvirus group
HSV-1 = lips
HSV-2 genitalia
Enveloped double-stranded DNA virus
Persistances of HSV
HSV persists in autonomic or sensory ganglia – no cure once infected
Primary & Recurrent Herpes Labialis (cold sore)
Herpes – manifestations
Group of blisters on red base, especially recurrent = Herpes until proven otherwise
- Herpetic whitlow –on fingertips
- Herpes progenitalis – on genitals
Herpes simplex infection & HIV
Serious infection quickly, may present atypically
Diagnosis of HSV infection
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
Treatment of HSV infection
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)
Varicella-Zoster Infection – Epidemiology
> 90% of adults has VZV antibodies
> 90% in susceptible household contacts
Varicella-Zoster– How to acquire
Primarily spread by respiratory route
Very communicable
Chickenpox
= 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)
Herpes Zosters
= 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)
Diagnosis of VZV infection
Clinical presentation
Tzank preparation
Biopsy, Viral culture, Serology
Direct immunofluorescence, PCR
Impetigo – epidemiology & how to acquire
Most common superficial bacterial infection of kids
Person-to-person contact
Less commonly through fomite
Predisposing factors: high humidity, cutaneous carriage, poor hygiene
Bacteria involved in Impetigo
Strep pyogenes
Staph aureus
Streptococcal Non-Bullous Impetigo (Impetigo Contagiosa)
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
Staphylococcal Non-Bullous Impetigo
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)
Diagnosis of Impetigo
Clinical presentation
Gram stain, Biopsy of blister, Culture w/Antibiotic sensitivity test
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
Cellulitis – how to acquire
Infections occur through skin breaks
Bacteriology of Cellulitis - Eryiseplas
= facial variant of cellulitis
<– Group A Beta-hemolytic streptococci
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
Erysipelas – location, incubation, appearance
Confined to face
Incubates 2-5 days
Bilateral facial involvement
Painful, bright red, indurated, sharp border (“cliff drop border”)
+/- Lymphadenopathy
Staphylococcal cellulitis
Primary lesion – tender, ill-defined area of painful erythema w/variable induration
Lymphatic streaking is common
Lymphadenopathy is variable
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%
Sexually transmitted disease – Risk from single sexual contact & incidence
~30%
Incidence peaked in 90s, but now going up again since 2006
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
Syphilis – Clinical Classifications
Primary
Secondary (early latent – 1-2 years; late latent)
Tertiary
Congenital
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
Chancre in primary syphilis
Non-tender, Indurated
Genital or extragenital
May be unnoticeable if in hidden location
Heals in 3-6 weeks
Lymphadenopathy
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
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
Diagnosis of syphilis
Clinical presentation – rash + lymphadenopathy, palms & soles, etc.
Darkfield microscopy
Biopsy
Serology
- Nontreponemal (VDRL, RPR) tests
- Treponemal (FTA-ABS, MHA-TP) tests
Dermatophytes
Fungi that eat keratin (skin, hair, nails)–> can’t get deep infection, rarely get septic
Ex: epidermophyton (sock & jocks, no hair), trichophyton, microsporum
Fungal skin infections – how to acquire
Human or Animal (farm, cats) contact
Water, soil
Fomites, Clothing
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
Tinea faciei
affects face
annular placques w/some central clearing
Tinea barbae
- on face
- from men, barbershops, animals
Tinea corporis
on body
Tinea cruris
groin (often spares scrotum, penis)
Tinea pedis
- on feet
- annular placques moving outward from central ring;
- can be hyperkeratotic
Tinea manum
- on hands
- usually only affects 1 hand (–> 2-feet-1-hand syndrome)
Majocchi’s granuloma
- Tinea corporus w/ involvement of hair follciles
- Deeper granulomatous infection (must use systemic antifungals now)
Onychomycosis w/Tinea pedis/manus
Subungual (under nail) infection, lifting of nail
Diagnosis of tinea fungal infections
KOH test on leading edge
Dermatophyte test medium
Biopsy of leading edge
Treatment of tinea pedis
Topical naftifine
OTC topical antifungals: Tinactin>Lotrimin
Candidiasis – epidemiology & location
Increased prevalence in
- diabetes mellitus
- occlusion
- corticosteroid use
- broad-spectrum antibiotics
Affects mucous membranes & skin
Normal flora
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
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
Candidiasis – Dx
Clinical presentation
KOH, Gram stain, Culture (Sabouraud’s agar, Nickerson’ medium), Biopsy
Tinea versicolor – epidemiology
Worldwide distribution, more common in humid/warm climates
Confined to post-pubertal pts
Tinea versicolor – mycology
Malassexia furfur (Pityrosporum obiculare)
Food source: follicular lipids
Tinea versicolor – Clinical features
Distribution: mostly trunk
Primary lesion: asymptomatic, tan-colored, subtly scaly macule or patch
Clinical variants: hypopigmented or folliculitis
Diagnosis of Tinea versicolor
Clinical presentation
KOH (spaghetti & meatballs), Methylene blue, Biopsy, Culture = rarely done
Scabies – epidemiology
Worldwide distribution, all ages, races, socioeconomic groups
Highest prevalence in children & sexually active adults
Scabies – how to acquire
Spread of mites via person-to-person contact
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)
Scabies - distribution
Symmetric soft skin distribution
- Interdigital web space
- Flexural wrist
- Waist
- Axillae
- Genitalia
- Breast
Scabies - symptoms
Pruritus (nocturnal accentuation)
Primary Lesions – erythematous papules & burrows, nodular genitalia lesions
Secondary Lesions - Excoriation, Infection
Norwegian scabies
In infants or neurologically-compromised pts (no itch response)
In immunologically-compromised pts w/decreased sensory function
—> hundreds & hundreds of mites
Diagnosis of scabies
Clinical presentation (burrows, genital nodules)
Mineral oil preps (mites, eggs, mite feces – scybala)
Skin biopsy (host response, burrows, mites, eggs, scybala)
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
Lice infestation – etiology
Pediculus human
- – Scalp louse –var. cap
- – Body louse – var. corporis
Pubic louse = Phthirus pubis
Scalp lice
Lices – closer to scalp
Nids (egg casings) – not as close to scalp, on hair
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
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
Lice infestation –Dx
Clinical presentation
Demonstration of louse or nit
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
