Flashcards in Infectious skin diseases Deck (81):
How does the skin offer a first line of defense against microbial infection?
physical barrier; low pH, sebaceous fluid, fatty acids; normal flora deters further colonization
What is the most common means bacteria infect the skin?
penetration of the skin barrier
What are the 3 steps of bacterial pathogenesis?
bacterial adherence to host; invasion of tissue w/ evasion of host; elaboration of toxins
Which organisms are produce superantigens?
virulent S. aureus and S pyogenes
How do superantigens work?
bind conserved portions of T cell receptors and activate large numbers of T cells leading to cytokine storm and inflam response
What is impetigo
a superficial cursting of epidermal skin infections presenting in bullous and nonbullous forms
Who/What/By whom/characteristic feature of impetigo
young children; face; S. aureus and S. pyogenes; honey colored crust
streptococcal infection of superficial dermal lymphatics w/ sharply demarcated, raised borders
Define cellulitis and causative agent
infection of deeper dermis and subcutaneous tissue w/ poorly demarcated borders; majority streptococcal
collections of pus in the dermis and subcutaneous tissue
superficial infection of hair follicles w/ pus accumulation in epidermis
deeper involvement of hair follicles in which infection extends into the subcutaneous tissue
adjacent furuncles coalesce to form single inflamed area
Who/What/By whom of Staphyloccal scalded skin syndrome
infants/kids, adults w/ renal failure, immsprsd;
granular layer split of epidermis;
exotoxin producing S. aureus
What are the clinical features of Staph scalded skin syndrome?
diffuse generalized erythema, superficial desquamation w/ flural accentuation; **uninvolved mucous membranes**; perioral, periocular crusting, radial fissures
What is staph scalded skin syndrome Tx?
Antibiotics and supportive care
What is the pathogenesis of staph scalded skin syndrome?
exotoxin bind to desmoglein 1 and cleave leading to loss of cell-cell adhesion
define necrotizing fasciitis
insidious and deadly soft tissue infections associated w/ widespread tissue necrosis
Who is subject to necrotizing fasciitis?
patients after minor trauma and surgical wounds; most are immunocompromised, diabetic, alcoholic, or obese
What is an early warning sign of necrotizing fasciitis? What happens if it is ignored?
**pain out of proportion to clinical findings**; ignoring leads to rapid progression and delay may be fatal (red to purple skin w/in 36 hours)
What type of emergency is necrotizing fasciitis?
surgical emergency associated with debridement
What is toxic shock syndrome?
S. aureus caused disease that produces TSST-1 toxin classically from tampons, surgery or deep abscesses
How does toxic shock syndrome present?
sunburn-like erythema and sandpaper papules progressing to desquamation of hands and feet
Toxic shock syndrome Treatment
antibiotics and remove agent
What are general features of bacterial skin diseases?
pus forming infections: staphylococcal except in periorifical abscesses that are anaerobic
What accounts for the majority of serous bacterial SSTIs?
How is a diagnosis made in bacterial skin diseases?
clinical presentation and Hx; culture to confirm and base Tx from
In fungal diseases, where are superficial infections?
confined to dead keratinous tissue, epidermis and hair follicles
What causes superficial fungal diseases?
dermatophytes; nondermatophyte molds; yeasts (candida)
in fungal diseases, where are deep infections?
all skin layers and some extend into the subcutaneous tissue
How do deep infections typically occur?
direct inoculation of skin such as sporotrichosis, mycetoma, chromomycosis
Where are systemic fungal infections typically found?
since inhaled, least common cutaneous and have pulmonary focus even though a skin lesion may tip the infection
What does the most common cause of superficial fungal infections feed on?
dermatophytes digest keratin as nutrient source
Where will dermatophytes likely colonize?
stratum corneum; nail plate; hair follicles
What are the dermatophytes virulence factors?
enzymes: adherence to keratin; invasion of keratin by secretized enzymes
What are the dermatophyte genera that cause superficial fungal infections?
Trichophyton (most common); microsporum; epidermophyton
How is a tinea infection characterized?
intensely pruritic, annular lesions with peripheral scale, central clearing and variable inflammation
What is the most common cause of tinea pedis?
95% dermatophytes due to occlusive footwear
What is the result of tinea unguium/onchomycosis?
infection of nail plate/bed leading to deformity with thickening and discoloration (onchodystrophy and hyperkeratosis)
Where is tinea corporis located?
trunk and limbs
Where is tinea cruris? clinical presentation?
jock itch of groin: erythematous patch of inner thigh and inguinal folds **spares scrotum and penis**
What is the common cause of tinea capitis?
infection of scalp and hair from superficial infection w/ T. tonsurans
What are 3 distinctive features of superficial fungal diseases regarding histopathology?
neutrophils present in stratum corneum;
hyphae in corneum visible on PAS stain (pink-red);
culture material scraped from area for ID
Where does candidiasis typically present?
skin, mucus membranes, nails or GI tract
Who is candidiasis more common in?
women (vulvovaginal candidiasis); immunosuppressed
What is a typical presentation of tinea versicolor?
recent tropical visit; Malassezia overgrowth causing harmless hypo/hyper pigmented patches with fine scaling
What disease presents as off-white/pink macules and papules with a spaghetti and meatball appearance?
What is significant about most viruses affecting the skin?
produce chronic/life long infection
Describe the infection and reactivation of HSV 1,2 infections
initial via mucosa or abraded skin; travel retrograde along sensory neuronal axons to nuclei during latency; reactivate at previous primary infection site
HSV reactivations lead to what?
shedding of viral particles w/o symptomatic disease contributing to disease spread
What causes herpes labialis? how is it spread?
HSV-1 and spread through contact with oral secretions
What causes herpes genitalis?
HSV-2 (increasing overlap from HSV-1)
What is the typical presentation of HSV infection?
variable depending on immune status of host with prodrome tingling or pain in diseases region
How could HSV-1 and HSV-2 infections be differentiated other than location?
HSV-2: severe, painful vesicle form, ulceration, fever, lethargy
How does HSV-1 reactivations typically present?
grouped vesicles on erythematous base for 2-3 days; lesions develop ulceration w/ crusting then heal in 4-5 days
How are HSV infections diagnosed?
**most clinical eval alone**; Tsanck smear, viral culture, direct fluorescnt Ab study; serologic testing
What are the dermatologic disease manifestations of HSV infections?
eczema herpeticum (atopic dermatitis); herpetic whitlow (digital infection); herpes gladiatorum (corporeal)
How should a HSV infection be treated?
Acyclovir; valacyclovir; famciclovir; foscarnet; cidofovir
What is the MOA of acyclovir?
inhibits viral DNA polymerase after phosphorylation by herpes specific thymidine kinase
How does resistance arise to acyclovir?
viral thymidine kinase deficiency
How is VZV transmitted and incubation period?
very contagious airborne or direct contact with incubation 11-20 days
What describes the primary infection of VZV?
pruritic eruption spreading from face/scalp to trunk/ to extremities resembling drops on a rose petal
VZV under histology has what characteristic finding?
multinucleated acanthoytic keratinocyte
What are the vaccines for VZV?
varivax (live attenuated prevents/decreases risk)
Zostavax (persons at least 60y/o)
What causes molluscum contagiosum? What does it look like?
DNA poxvirus of the molluscipox genus;
smooth, dome-shaped, umbilicated papules
What does molluscum contagiosum look like on histologic exam?
Henderson-Patterson bodies => intracytoplasmic inclusions within keratinocytes
How does molluscum contagiosum progress?
self limited disease in healthy patients
What is the genome of HPV?
icosahedral, naked, circular ds DNA
HPV are very genetically simple. How does this help the virus?
implies strong host dependence and few targets for anti-virals
What are the 3 domains of the HPV genome?
upstream regulatory region; early and late regions;
What proteins of HPV may lead to cancer? How?
E6 protein leads to degradation of p53; E7 inactivates Rb protein
How does HPV infect a person?
through basal keratinocytes through minor abrasions in skin/mucosa => direct contact; cell entry L1/L2 proteins and cell surface receptors
How does the virus replicate and divide?
replicates in nucleus; divides and spreads laterally and migrates upward to suprabasal cell layers
What does HPV-1 cause?
palmoplantar warts on volar aspect of palms/soles and fingers/toes
What does HPV-2, 4 cause?
common warts => verrucous papules on glaberous skin
What does HPV-3, 10 cause?
flat warts=> slightly elevated flesh colored papules that are smooth or hyperkeratotic
What does HPV-6, 11 cause?
genital warts=> scaly and papular to smooth and flesh colored
How will the histology of the HPV-6, 11 be viewed?
hyperkeratosis; papillomatosis; hypergranulosis
koilocytes: vacuolated superficial keratinocytes w/ pyknotic raisin like nuclei
How should warts from HPV be treated?
most are self limited in healthy patients but Tx tailored to site involved
What causes an increase risk in cervical cancer?
condylomata associated with HPV will increase cervical cancer risk