Epidermis/Dermis Layers Flashcards
Most common agents in Tinea pedis
- Trichophyton mentagrophytes
- Trichophyton rubrum
- Epidermophyton floccosum
Most common agent in Tinea manuum
- Trichophyton rubrum
- Trichophyton mentagrophytes
- Epidermophyton floccosum
nails lose luster, become opaque/white, brittle, and have a crumbling consistency - commonly caused by?
White Superficial Onychomycosis (Leukonychia mycotica) is commonly caused by T. rubrum and T. metagrophytes
Most common agent in Tinea cruris
- Epidermophyton floccosum
- Trichophyton mentagrophytes
- Trichophyton rubrum
Most common agent in Tinea unguium
T. rubrum and T. metagrophytes
Most common fungal nail infection; nail thickens and often discolors
Distal Subungual Onychomycosis
Most common fungal nail infection in HIV pts; begins in nail fold
Proximal Subungual Onychomycosis
Nails hardened, thickened, brownish-green discoloration, w/ striated ridges or grooves; generally w/ cuticle involvement w/ or w/o pus
Paronychial or Onychomycotic Candidosis: AKA onychomycosis caused by Candida albicans
“weeping” or “scaled skin” lesion
Intertriginous Candidosis
Nonspecific febrile illness followed by rash w/ “slapped cheek” appearance
Erythema Infectiosum/Fifth Disease caused by HPV B19
HPV B19 - describe the genome and virus
ssDNA, non-enveloped virus w/ 1 serotype
socks and gloves maculopapular rash
Erythema Infectiosum/Fifth Disease caused by HPV B19
bone marrow biopsy reveals: presence of large pink or lilac colored inclusions in giant pronormoblasts
HPV B19 infection
HHV-6 uses __________ as a cellular receptor
CD46 - found on ALL human nucleated cells
Measles virus - describe the genome and virus
ssRNA, enveloped w/ 1 serotype
Which virus causes Giant cell formation
Measles virus
Complication of HPV B19
Aplastic Crisis
Rash and Fever
Measles
Measles rash is due to
immune system - T cell (HLA I and II on endothelial cells)
Describe a “Morbilliform rash” and what disease it exists with
symmetrical, non-pruritic, bright red maculopapular rash; Measles
Describe the rash appearance and disappearance with Measles
Begins on face and descends, ~1-2days later rash rapidly fades from top to bottom by fine briny desquamation
Giant Cell Pneumonia
Measles
Describe the genome and virus of VZV
Alpha herpesvirus: large, dsDNA virus, enveloped, encodes its own thymidine kinase w/ 1 serotype
VZV travels down nerves via
reverse axoplasmic flow
Primary infection with VZV, viral replication occurs
URT -> lymph nodes -> lymphoid tissue, liver, spleen, etc
Exfoliatin exotoxin mechanism
glutamate specific serine proteases highly specific to the cadherin desmoglein I
Exfoliatin exotoxin is produced by
Staph aureus
Exfoliatin exotoxin may cause
Bullous impetigo, SSSS, Ritter’s disease
dsDNA virus that replicates in the nucleus
Herpes
dsDNA virus that replicates in the cytoplasm
Variola major (Orthopox)
Candida pathogenic form
yeast, pseudohyphae, and hyphae
Risk Factors for Cutaneous Candidiasis
Female, young/old, diabetes, obesity (skin folds), pregnancy
Intertriginous Candidosis lesions
“weeping” or “scaled skin - Pruritic, erythematous w/ macerated edges
Paronychial or Onychomycotic Candidosis lesions
Chronic - Nails hardened, thickened, brownish-green discoloration, w/ striated ridges or grooves
Culture Candida on?
Sabouraud-Glucose agar
Definitive diagnosis for Candida?
Germ Tube Test
Cutaneous Candidosis Treatment
1% Crystal Violet
Paronychial Candidosis Treatment
Nystatin, Amphotericin B, Ketoconazole
HPV B19 has a predilection for
bone marrow and erythrocyte precursors
Is HPV B19 present in the rash?
No - immune-mediated
Biphasic course of HPV B19 is
-initial phase/prodrome caused by viremia at day8
FEVER BREAKS…
- Immune-mediated Rash (face->limbs/trunk->palms/soles)
Rash of Erythema Infectiosum is due to
Type III HSN rxn
Prodrome of Erythema Infectiosum begins on Day __ and lasts _____
Day 8 and lasts 2-3 days
Describe the course of the rash with Erythema Infectiosum
FEVER BREAKS….initially on the face as “slapped cheek” appearance w/ relative circumoral (around the mouth) sparing. Maculopapular rash may appear later on limbs, trunk, palms and soles (socks and gloves)… lasts 2-3 days
Does anything make the rash of Erythema Infectiosum worse?
exacerbated by exercise, emotion, hot baths, sunlight
Typical pt w/ Erythema Infectiosum
Late winter, early spring, endemic in 4-15 y/o, school or daycare outbreak
Erythema Infectiosum In Seronegative Adults causes
Prodrome: flu-like symptoms lasting 3-4 days
symmetric polyarthralgia of the hands and wrists, occasionally ankles and knees for 2-3 weeks
Erythema Infectiosum exposure in Pregnant female…
Treat w/ IVIG to prevent abortion
Complication of Erythema Infectiosum
Aplastic crisis (esp in anemic pts) for 7-10d
Immunity in Erythema Infectiosum
Humoral - Type III HSN
For Erythema Infectiosum, Bone marrow biopsy would reveal
large pink or lilac colored inclusions in giant pronormoblasts and absence of erythroid progenitor cells
Treatment for Erythema Infectiosum
Supportive – antipyretics, analgesics, NSAIDs
IVIG for immunocompromised/pregnant females
How does HHV-6 enter cells?
uses CD46 as a cellular receptor, glycoprotein expressed on the surface of all human nucleated cells
Clinically important serotype of HHV in Exanthem Subitum?
HHV-6B
HHV-6 - Life-long, active infection in
Salivary glands
HHV-6 - Persistent, latent infection in
macrophages and monocytes
Exanthem Subitum is biphasic, describe
Initial prodrome w/ HIGH fever
FEVER BREAKS…
Immune-mediated rash
Typical Patient w/ Exanthem Subitum
6mo - 3yrs
The prodrome of Exanthem Subitum begins ____ and lasts _____
4-7 days after exposure; lasts 4-6 days; characterized by HIGH fever
Exanthem Subitum Sx In Adults
Mononucleosis-like Sx: Fever, pharyngitis, cervical lymphadenopathy
Diagnosis of Exanthem Subitum
EIA IgM, but it cross-reacts w/ CMV
Treatment for Exanthem Subitum
Supportive
Measles virus initially replicates in
URT and draining lymph nodes
Measles in primarily controlled by what type of immunity
CMI
Is the rash of Measles infectious?
Yes
How does Measles cause malnutrition?
Desquamation of epithelium - GIT -> bloody diarrhea
Communicability of Measles?
Begins at prodrome and lasts until 4-5 after rash onset
Typical patient with Measles?
Winter/spring, nonvaccinated, 5-9
INcubation period of Measles
10-12 days
Prodromal Sx of Measles
High fever, coryza, conjunctivitis, brassy cough, cervical LAD, Koplik spots (secondary viremia)
Describe the rash of Measles
Fever and prodrome continue w/ rash appearance
“Morbilliform rash” symmetrical, non-pruritic, bright red maculopapular rash on face, confluent and descends to LE
Measles Rash clears by
desquamation from head –> toe
Atypical Measles patient population
people vaccinated b/w 1963-1967 w/ killed vaccine - vesicular and purpuric and starts on limbs
Complications of Measles
Otitis Media, Primary Viral Giant Cell Pneumonia, Diarrhea, encephalitis, Subacute Sclerosing Panencephalitis
Subacute Sclerosing Panencephalitis is caused by
defective measles virus
Subacute Sclerosing Panencephalitis is a condition where
fatal, slowly progressive, inflammatory, demyelinating disease of the CNS
Congenital Measles results in
stillbirth or fetal malformation
Lab diagnosis of Measles
giant cell formation, FAT
Treatment for Measles
Supportive, Vitamin A, Gamma globulin (IgG) for immunocompromised or unvaccinated pts w/in 6 days of exposure
MMR live attenuated vaccine is administered
o Dose 1: 15-18 mo
o Dose 2: 4-6 years or 11-13 years
lymph node enlargement (postauricular, suboccipital, and cervical) indicates
Rubella, German Measles, 3-day Measles
Forschheimer Spots
enanthem, small red spots on soft palate associated w/ Rubella
Incubation period for Rubella
14-21 days
Communicability of Rubella begins and lasts?
Begins 5 days before rash and 5 days after appearance of rash
Typical Rubella patient
Unvaccinated, older child/adolescent, winter/spring
Describe the prodrome of Rubella
Minimal or Absent (low fever, lymph node enlargement)
Describe the rash of Rubella
Discrete pink-red maculopapular rash lasting 3-5 days, initially on face -> trunk -> extremities; Forschheimer spots on soft palate
Congenital Rubella Syndrome
first trimester -> teratogenic effects -> abortion
If survival -> isolate due to prolonged shedding, PDA, cataracts, hearing loss, CNS; recommend abortion
Diagnosis for Congenital Rubella Syndrome is made by
STORCH - IgM in cord blood
Treatment for Rubella
Supportive
Post-exposre prophylaxis for pregnant female refusing abortion
IG w/in 72hr of exposure
Scarlet fever is caused by
S. pyogenes, beta-hemolytic, lysogenized w/ a phage producing exotoxin, catalase negative
Scarlet fever is mediated by S. pyogenes
SPE exotoxin - superantigen
Virulence factors of S. progenes of Scarlet fever
M protein - antiphagocytic
SPE exotoxin
Scarlet fever is preceded by
pharyngitis or impetigo
Scarlet fever Sx
o Enanthem: hyperemia of the entire pharynx w/ petechial lesions; white strawberry -> red strawberry -> raspberry tongue
o Exanthem: diffuse macular erythroderma -> blanching scarlitiniform rash: fine, red, punctate, “sandpaper” like rash spreads from trunk -> periphery
Pastia Lines
Scarlet Fever - petechiae in skin folds
Scarlet Fever rash resolves by
desquamation 1-2 weeks after onset
Fever and rash in summer/fall
Non-polio enterovirus
Kaposi Sarcoma agent
HHV-8
Site of latency for HHV-8
B cells
Risk Factors for Kaposi Sarcoma
> 60, Male, Mediterranean and Middle Eastern descent, AIDS
Kaposi Sarcoma lesions
Bluish-red or purple bumps (tumors) on the skin
Treatment for Kaposi Sarcoma
Surgical excision, Radiation, Chemotherapy
Describe the VZV genome
dsDNA virus, enveloped, encodes its own thymidine kinase w/ 1 serotype
Latency of VZV occurs in
DRG or CN (CNV ganglia) after primary infection
Communicability of VZV
Person is infectious 1-2d before rash and 4-5d after; once scabbed over, pt is no longer infectious
Incubation period of VZV
14-16days
Describe the prodrome of VZV
absent in young, 1-2days before rash in older
Describe rash of VZV varicella
mild-high fever, fatigue, anorexia, HA, n/v, rash, centripetal pattern: more severe on head/trunk, thin-walled vesicle on a maculopapular base
Describe the stages of VZV varicella
All stages seen bc new lesions appear each time the fever spikes 3-6d: vesicular, pustular, crusted, and scab
Adult varicella infection typically has 1 or more:
Interstitial pneumonia, hepatitis, meningoencephalitis, thrombocytopenia
Neonatal Varicella lesion
hemorrhagic lesion -> fatal
Zoster Sx
Initially, tingling or pin-prick sensation
Followed by severe pain in dermatome
Complications of Zoster
Opthalmic zoster or zoster oticus (Emerg)
Postherpetic Neuralgia, Facial palsy, Ramsey-Hunt Syndrome
Lab Findings of VZV
Multinucleated giant cells w/ Cowdry type A
Treatment of VZV
Supportive
Treatment of VZV in Immunocompromised/Pregnant:
VZIG w/in 3-4 days
Anergy occurs with
Measles and MMR vaccine
Child vaccine for VZV
Varivax
Adult vaccine for VZV Zoster
Zostavax
Treatment for Zoster
acyclovir, famciclovir, valacyclovir given w/in 3 days of onset of rash
Treatment for Postherpetic Neuralgia
Nortiptyline, Lidocain, Gabapentin, Opioid, Acyclovir
Exfoliatin Exotoxin is produced by
S. aureus + phage
Exfoliatin Exotoxin causes which diseases
Bullous impetigo, SSSS, Ritter’s Disease
Exfoliatin Exotoxin mechanism
glutamate specific serine proteases highly specific to the cadherin desmoglein I: adhesion protein is the desmosomes of the stratum granulosum
Clefts form in which layers in bullous impetigo
cleft formation b/w the stratum corneum and spinosum
Bullous impetigo lesions
flaccid, paper-thin, white, serous fluid-filled sacks that rupture -> painful, moist, denuded erythematous lesions that dry in 1-2d the thin ”varnish-like” light-brown crusted lesions
Is organism present in Bullous impetigo lesions?
Yes
SSSS
Single, focal infection -> hematogenous dissemination of EXOTOXIN -> fever and sterile bullae
SSSS lesions
Widespread, diffuse (scarlitiniform rash) that progresses in 1-3 days to extensive size, w/ spontaneous exfoliation of skin; w/in 5 days desquamation of total body
Nikolsy Sign is positive in
SSSS
Diagnosis of bullous impetigo and SSSS
CIE or gel diffusion assay for elevated anti-teichoic acid Ab’s
Treatment for bullous impetigo
Mupirocin
Treatment for SSSS
Cephalosporin
Black piedra agent
piedra hortai
White piedra agent
Trichosporon beigelii
White piedra Sx
white nodules on the hair shaft
Black piedra Sx
brown/black collar around the hair shaft; decreases hair luster and shine
Treatment for White or Black Piedra
Cut/Shave hair, oral azole antifungals
Tinea capitis etiologic agents
- Microsporum
2. Trichophyton
Microsporum
Ectothrix
Trichophyton
Endothrix
In the US, Tinea capitis is caused primarily by
Microsporum audouinii and M. canis
Tinea capitis due to Microsporum Sx
itchy, scaly, papules on scalp
Hair becomes dull and brittle breaking off 3-4mm above the scalp
Tinea capitis due to Trichophyton Sx
Hair breaks off at scalp “black dot”
Tinea capitis common Sx
scalp scaling, scalp pruritis, occipital LAD, patchy or diffuse alopecia
Diagnosis of Tinea Capitis
Wood’s Lamp: Microsporum – ectothrix fluorescence
P. acnes
GPR, non-motile, obligate anaerobic, diptheroid/pleomorphic rod (lacks catalase)
Virulence Factors of P. acnes
Extracellular Lipase
Inflammatory acne due to P. acnes infection
Inflammatory mediators: fatty acids resulting from microbial lipase breakdown of sebaceous gland products
Treatment for Inflammatory acne due to P. acnes infection
Salicyclic Acid, Retinoid Acid, Azelaic Acid: antikeratinizing and decreased sebum production; Antibiotics, Benzoyl Peroxide
Impetigo etiologic agents
S. aureus and S. pyogenes
Impetigo lesions
Thickened honey-colored adhesive crust, purulent discharge on top of lesions resolves in a couple weeks w/o scarring
Impetigo Treatment
Retapamulin: topical abx for MRSA
Mupirocin: topical abx
Tinea favosa etiologic agent
Trichophyton schoenleinii
Tinea favosa lesions
Formation of yellow crusts w/in the hair follicles (scutula) and cicatricial alopecia and scarring, w/ Mousey or cheesy odor present
Tinea favosa
Chronic mycotic infection of the scalp or glaborous skin
Tinea favosa Treatment
Oral antifungals
Hot tub folliculitis agent
P. aeruginosa
Refractory folliculitis agent
Malassezia furfur
Folliculitis agent
S. aureus
Tinea barbae agents
T. rubrum (anthropophilic)
T. mentagrophytes (zoophilic)
T. verrucosum (zoophilic)
Hair removal is ___________ in tinea barbae, but _________ in bacterial infections
painless; painful
Foruncle and carbuncle agent
S. aureus
Foruncle lesion
boil/deep folliculitis are firm, painful, tender, discrete, red nodules
Carbuncle lesion
several hair follicles, lesion is larger, deeper, indurated, erythematous, edematous, painful + SYSTEMIC SIGNS
Treatment of Foruncle and carbuncle
Moist heat, incision/drainage
Ecthyma common etiologic agent
S. pyogenes
Ecthyma
nonbullous impetigo extending into dermis
Ecthyma lesions
“punched out” ulcers w/ greenish-yellow crust and violaceous margin; scarring
largest, dsDNA, replicates in cytoplasm of infected cell
Smallpox
Smallpox incubation period
7-17days
Prodrome of Smallpox Sx include
high fever (104 F) w/ chills, severe HA, back pain, delirium, prostration for 2-4 day
Rash of Smallpox
Enanthem -> Exanthem on face -> extremities
Macules -> Papules -> Vesicles -> Pustules (umbilicate) -> Scabs (SAME SATGE)
Smallpox Rash lasts
8 – 13 days before scabbing occurs
Guarnieri bodies:
Smallpox - eosinophilic intracytoplasmic inclusions on smears or biopsies
Diagnosis of Smallpox
CALL CDC
Treatment of Smallpox
Cidofovir: nucleoside phosphonate - DNA polymerase inhibitor
Smallpox lesions are located in what layer
deep dermis
Normal reaction to Dryvax Vaccinia for Smallpox
pustular lesion at the injection site leaving a depigmented scar, flu-like Sx, regional LAD, satellite lesions
Erysipelas agent
S. pyogenes
Ersipelas location of infection
extremities (leg, feet) and face (cheeks, bridge of nose “butterfly” distribution)
Recurrent erysipelas due to
lymphatic obstruction
Ersipelas lesion
Burning, itching at site of infection w/ rapid spread (minutes/hours) -> bright red erythema
SHARPLY DEMARCATED
Erysipelas
Involves the upper dermis and superficial lymphatics - lymphatic tracking
Cellulitis lesion
Systemic S/S: fever, chills, malaise, leukocytosis
Inflammation: pain, erythema, edema, warmth, Rapidly advancing edge +/- elevation, Diffuse, NOT sharply demarcated
Subcutaneous tissues palpation in Cellulitis
can be palpated
Diagnosis of cellulitis
Xray, CT, MRI for gas presence
Treatment for cellulitis
Cefazolin-probenecid, Nafcillin, Ceftriaxone, Clindamycin
MRSA: Vancomycin, Linezolid, Daptomycin
Treatment for complicated cellulitis
Levofloxacin