Cutaenous Infections and Infestations Flashcards
peptides involved in innate immunity of the skin
- Alpha-defensins (hNP1, hNP2)
- Beta-defensins (hBD-1, -2, -3)
- Cathelicidin (hCAP-18)
- Psoriasin
- RNase7
- Essentially these are all antibiotic to some extent.
HPV: etiology and clinical characteristics
o Etiologic: papovavirus (non-enveloped dsDNA virus).
o Clinical:
—Shows up as verrucas (warts). (fingers, hands, elbows, and knees, or palmar and plantar surfaces)
—Verrucas: hyperkeratotic papillomas with punctuate black dots that represent thrombosed capillaries
HSV: etiology and clinical characteristics
o Etiologic: dsDNA virus, acquired through breaks in skin/mucosa through saliva, vaginal secretions, vesicular fluid, etc.
o Clinical:
—Primary lesion: grouped vesicles on an erythematous base.
—Can show up on lips, gums, fingers, genitals, etc.
—Note patients with eczema can get a whole lot of outbreaks if they get herpes.
—Latent period (virus in nervous tissues) followed by recurrent re-emergence of infection.
VZV: etiology and clinical characteristics
o Etiologic: again, a herpesvirus (dsDNA).
o Clinical:
—Initially: fever, thin-walled vesicles on erythematous base
—New ‘crops’ of these vesicles for 3-5 days (“dew drops on a rose petal”– someone’s a frustrated English major).
—Like herpes simplex, lies latent; re-manifests as shingles (varicella zoster)– hurts like crazy due to inflammation in spinal nerve affected.
Impetigo: etiology and clinical characteristics
o Etiologic: caused by superficial infections with either beta-hemolytic streptococci (strep pyogenes, less common) or staph aureus (most common).
o Clinical:
-Divided into bullous and non-bullous. A bulla is a large, fluid-filled blister, thus bullous means blistering and non-bullous means non-blistering.
-Non-Bullous Impetigo (most common): “honey-colored crust that most commonly affects the face. Usually begins as a single lesion, frequently followed by other lesions adjacent to it.
-Bullous Impetigo: cleaves the skin and lives just below the stratum corneum. can show up anywhere on the body as flaccid, superficial blisters (no bleeding when they pop)..
cellulitis: etiology and clinical characteristics
o Etiologic: caused by deeper microorganism infections that get into/beneath the dermis due to microscopic or macroscopic breaks in skin (macroscopic: cuts, ulcers, surgeries, etc). More common in humid, warm areas and in the very young or very old.
o Clinical:
-Two classes of cellulitis, classified according to where they show up. They’re divided up this way because different lymphatic drainage patterns in different locations create different appearances.
—Erysipelas: cellulitis that occurs mainly in the face, mostly streptococcal (sharply demarcated)
-cellulitis: If the lesions occur mainly in the hands or extremities (lymphangitis)
syphillis: etiology and clinical characteristics
o Etiologic: Treponema pallidum spirochete, high motility, can’t be cultured. Acquired through sex.
o Clinical:
—Primary syphilis: pops up 2-6 weeks after intercourse as a papule that breaks down to produce an oval, indurated (hardened) ulcer, frequently non-tender.
—Secondary syphilis: Rash (“can look like just about anything”), lymphadenopathy, systemic malaise. Classic presentation on palms and soles. Note can produce “moth-eaten alopecia” (patchy hair loss).
dermatophyte infections: etiology and clinical characteristics
o Etiologic: Acquired through environment; attacks stratum corneum (eat keratin)
o Clinical:
—Tinea capitis: scaly plaques on head, ‘eats hair;’ can produce permanent hair loss. (Tinea = ringworm; a fungus, not a helminth.)
—Tinea barbae: same thing, but shows up on face.
—Tinea cruris: jock itch. Scaly plaques in grain. Notice that it does not affect the scrotum.
—Tinea pedis: athlete’s foot. “Likes” various toes more than others; doesn’t like the space between the big toe and second toe.
***Two-feet-one-hand: tinea pedis diagnosis.
candidiasis: etiology and clinical characteristics
o Etiologic: mainly Candida albicans.
o Clinical:
—Thrush/Oral candidiasis: white, creamy plaques in mouth
—Can show up at immobilized, moist, unaerated sites (diaper rash)
—Common cause of vaginitis (‘yeast infections’).
—Shows up as “satellite lesions”
—“Candida loves the scrotum” (as opposed to tinea).
—Without an immune response, candidiasis can get really nasty. Mainly in AIDS patients.
tinea versicolor: etiology and clinical characteristics
o Etiologic: Malassezia furfur fungus. Eats follicular lipids.
o Clinical:
—Can show up as tan, slightly scaly macules.
—Can be hypopigmented (inhibition of melanocytes).
—Can have follicular papules on trunk, arms, face
scabies: etiology and clinical characteristics
o Etiologic: Sarcoptes scabiei organism: “mites.”
o Clinical:
—Intense pruritis; show up in symmetrical pattern.
—Primary lesions: small erythematous papules, usually in soft areas of skin (bites of male mites)
—“Burrows” (female mite’s tunnels): thin lines on skin.*
—In genital regions, produce larger nodules instead of small papules.
lice: etiology and clinical characteristics
o Etiologic: bloodsucking wingless insects (Pediculus/Phthirus)
o Clinical: intense pruritis.
—Head lice: white ovals (eggs) attached to hair shafts.
—Body lice: eggs only found on trunk.
—Public (crab) lice: eggs found in genital areas.
cutaneous larva migrans: etiology and clinical characteristics
o Etiologic: found in GI tract of dogs and cats; acquired through their feces through fissured human skin. Note that they can’t get into the GI tract (or reproduce) in humans.
o Clinical:
—Can’t get through the basement membrane zone- just crawl around in the epidermis. Eventually die off by themselves. You can track the raised lesions indicating the progress of the worm.
Tzanck smear:
take blister, break it open, smear the blister base on a slide, stain. Can be used to identify herpes simplex, varicella virus
Gram Stain:
Used for bacterial classification (i.e. impetigo, cellulitis)
