The Skin Under Attack Flashcards
Describe the natural resistance properties of the skin
- physical barrier
- low pH (due to secretion of sebaceous fluid and FA)
- secretion of anti-microbial peptides
- normal flora
Describe the general mechanism of pathogenesis for bacterial skin infections
- invasion of bug through wound or pre-existing skin condition
- bacteria adheres to host cells
- bacterial evades host immune defenses
- invasion into tissues
- release of toxins
actively secreted proteins that cause tissue damage or dysfunction
exotoxins
how do exotoxins cause tissue damage?
enzymatic reactions cellular dysfunction pore formation –> cell lysis
superantigens are (exo or endo toxins)
exotoxins
MOA superantigens
bind conserved portion of TCR and therefore actives a large % of T cells –> cytokine storm
assc with severe tissue necrosis and rapid development of skin infection
superantigens
What bugs are superantigens assc with?
Staph aureus Strep pyogenes
superficial, crusting epidermal skin infection bullous and non-bullous forms usually in young chilfren usually affects the face honey colored crust
impetigo
What bugs are noted to cause impetigo?
Staph aureus Strep pyogenes
streptococcal infection of the superficial dermal lymphatics
Erysipelas
presentation of erysipelas
areas of erythema that demonstrate sharply demarcted, raised boarders
erythema with poorly demarcated boarders (infectious in nature)
cellulitis
What layers of the skin are involved in cellulitis?
deeper dermis and subcutaneous
bacterial origin of cellulitis
streptococcal
abscesses are collections of pus in the _____
dermis and subcutaneous tissue
superficial infection of the hair follicles with puss accumulation in the epidermis
folliculitis
aka boils
furuncles
how are furuncles different than folliculitis
deeper involvement of the hair follicle that extends to the subcut
term for when adjacent furuncles coalesce to form a single inflamed area
carbuncles
- Diffuse generalized erythema superficial desquamation with flexural accentuation
- Perioral and periocular crusting and radial fissuring with mild facial swelling
- Mucous membranes – uninvolved
scalded skin syndrome
*S aureus exotoxin
pathogenies of scalded skin syndrome
infection with Staph aureus EXOTOXIN which binds desmoglein-1 and cleaves it
–> loss of cell cell adhesion
–> superficial desquamation
Who usually gets scalded skin syndrome?
infants, young children, adults in renal failure (prob due to decreased clearance of toxin)
- granular layer split in epidermis
- dermis lacks inflammatory cell infiltrate
histo findings of scalded skin syndrome
insidious onset of widespread tissue necrosis
necrotizing fasciitits
how is necrotising fasciitis different than cellulitis?
it is deeper! infection spreads along fascial plane beneath subcut
pain out of proportion to clinical finding
necrotizing fasciitits **usually following minor trauma
color change seen in NF
erythema –> red-purple–> gray-blue **within 36 hrs
What are the 3 subtypes of NF and what ate the orgs assc with them?
I: polymicrobial
II: streptococcal (“flesh eating strep”)
III: clostridial myonecrosis (gas gangrene)
fever, strawberry tongue, sunburn-like erythema and sandpaper papules, later get desquamation of hands and feet
Toxic shock syndrome
What is the pathogenesis of TSS?
Staph aureus’s exotoxin TSST-1 (less commonly GAS)
Tx for TSS?
abx to remove nidus of infection
sunburn-like erythema and sandpaper papules
TSS
Pus-forming infections tend to be_____ in origin, except for periorificial abscesses, which are often______.
staphylococcal anaerobic
_____ accounts for the majority of serious bacterial SSTIs.
cellulitis
how is the Dx of a bacterial skin infection made?
usually made on the clinical presentation and historical information culture may confim dx
What layers of the skin are superficial fungal infections limited to?
- dead keratinous tissue
- epidermis
- hair follicles
What orgs cause superficial fungal infections?
- dermatophytes
- non-dermatophyte molds
- yeasts (candida and malassezia)
WHat layers of the skin do deep fungal infections involve?
all layers and can extend into the subcut
What fungi are assc with deep infections
- sporotrichosis
- mycetoma
- chromomycosis
**require direct inoculation of the skin
are fungi that digest keratin as a nutrient source
dermatocytes
Where do dermatocytes colonize?
stratum corneum,, nail plate, and hair follicles **the keratinized structures!
Are dermatocyte infections lethal?
No, they rarely invade viable tissue
What are the dermatocyte virulence factors?
enzymes that allow them to adhere to keratin and then invade keratin (secreted enzymes) **the digestive products serve as the nutrients for the fungi
What are the 3 genera of dermatophytes
trichophyton; microsporum; epidermophyton
intensely pruritic, annular lesions with peripheral scale, central clearing, and variable inflammation
tinea infection
superficial fungal infection of the foot.
tinea pedis
Fungal infection leading to nail bed deformity (onchodystrophy) with thickening (hyperkeratosis) and discoloration
tinea ungium (aka onchomycosis)
superficial fungal infection of glabrous skin occurring most commonly on the trunk and limbs
tinea corporis
superficial fungal infection of glabrous skin occurring on the face
tinea facei
erythematous patch involving the inner thigh and inguinal folds while sparing the scrotum and penis.
Tinea cruris
fungal infection of the scalp and hair.
tinea capitis
Ninety-five percent of cases of tinea capitis are caused by superficial infection with ____
T tonsurans
histo findings of superficial fungal infection
- neutrophils in stratum corenem
- fungal hyphae in stratum corneum or follicles
formation of hypopigmented or hyperpigmented patches with associated fine scale
Malassezia overgrowth (tinea versicolor)
yeast in skin, mucus membranes, nails, or gastrointestinal tract
candida albicans
spaghetti and meatballs in histo (PAS stain) = short curved hyphae and clusters of round spores
tinea versicolor
Herpes viruses are unique in their ability to…
produce latent, incurable infections
HSV1 and HSV2 establish initial infection through: What occurs following this initial infection?
mucosa or abraded skin virus travels retrograde from point of inf along sensory neuronal axons to nuclei, where they multiply and remain latent
Possible causes of HSV reactivation: Possible effects of HSV reactivation:
stress, fever, localized trauma, UV, menstruation symptomatic disease OR asymptomatic viral shedding
HSV1 infection, presents as vesicular or ulcerative lesions of oral cavity or perioral region; spread through contact with oral secretions
herpes labialis
Infection caused by HSV-2 (most of the time, but some HSV1 overlap)
herpes genitalis
HSV infections often present with:
tingling or pain in the region of subsequent disease
*note: presentation depends on immune status of host
Primary HSV1 infections? Recurrences?
–asymptomatic
–painful, grouped vesicles on erythematous base (lip) x2-3 days; ulceration crusts over and heals in 4-5days
Primary HSV2 infections? Recurrences?
- severe, painful vesicle formation and ulceration, fever, lethargy
- painful, vesicles with ulceration, but no fever/lethargy
HSV diagnosis?
**clinical.
–available: Tsanck smear, viral culture, serology, fluorescent antibodies, tissue biopsy
Digital HSV infection
herpetic whitlow
HSV superinfection of atopic dermatitis
eczema herpeticum
corporeal HSV infection related to direct skin-to-skin contact during athletics
herpes gladiatorum (get it, gladiator?)
Treatment for HSV:
acyclovir valacyclovir famciclovir foscarnet cidofovir
Reactivation of latent VZV in any DRG, contagious until crusty
herpes zoster
What are the herpes histology buzz words?
multinucleated acantholytic keratinocyte (there’s also molding, nuclear dust of neutrophils, keratinocyte necrosis)
Live, attenuated VZV vaccine
varivax
Indicated for people at least 60 y/o to prevent/lessen shingles
zostavax
Self-limting infection caused by poxvirus that usually affects children; produces smooth, dome-shaped umbilicated papules
molluscum contagiosum
Histologic molluscum findings
intracytoplasmic inclusions within keratinocytes (Henderson-Paterson bodies)
Describe the HPV structure.
icosahedral naked small circular dsDNA
Why are there few HPV anti-viral targets?
genetically simple = strong host dependence and few drug targets
HPV protein that leads to p53 degradation
E6
HPV protein that inactivates Rb
E7
What causes malignant tumors from HPV?
E6 and E7 overexpression
How is HPV transmitted, and how does it actually enter cells?
- sexually transmitted
- entry via interaction between L1/L2 proteins and cell surface receptors (access to keratinocytes)
Where does HPV replicate, and how does it spread?
nucleus (using all the host cell’s equipment)
–infected cell divides; population spreads laterally and migrates upward as the virus matures
–as top skin layer is shed, so are viruses
Causes palmoplantar warts; palm, soles, tips of fingers, etc
HPV1
Causes flat warts, “Verruca plana”; smooth or slightly keratotic, skin-colored papules on face, arms, dorsal hands
HPV3, HPV10
Causes common warts; verrucous papules on glaberous skin, like legs
HPV2, HPV4
Causes Condylomata acuminata; most distinguishable by location on penis, vulva, perianal area
HPV6, HPV11 (can also be due to HPV 16, 18, 31, 33)
Associated with an increased risk of cervical cancer
uncommon variants of genital warts-causing HPV: 16, 18, 31, 33, 51
Histology of HPV infections:
- hyperkeratosis 2. papillomatosis 3. hypergranulosis 4. vacuolated superficial keratinocytes with pyknotic nuclei (“koilocytes”)
How do HPV vaccines prevent infection?
noninfectious recombinant virus-like particles, assembled from L1 capsid proteins *these trigger an antibody response = protection
Quadrivalent HPV recombinant vaccine; protects against 6, 11, 16, 18
gardasil
Bivalent HPV recombinant vaccine; protects against 16, 18
cervarix
Causes digital squamous cell carcinoma
HPV16
Molluscipox virus
impetigo
Folliculitis
What causes this?
An exotoxin
(Staphloccal Scalded Skin Syndrome)
most common cause?
HPV-6 and 11
Tinea unguium
Herpes simplex virus 1
herpes zoster
Basal cell carcimoma
Molluscum contagiousum
Protects against both anogenital warts and cervical cancer
gardasil
herpes
furuncle
abscess
folliculitis
tinea versicolor
warts
koebner phenomenon
