front 1 What part of the body does HSV-1 affect? (generally) | back 1 HSV-1 causes oral-labial infections
58% of US population seropositive |
front 2 What part of the body does HSV-2 affect? (generally) | back 2 HSV-2 causes 90% of genital herpes infection
16% of US population seropositive |
front 3 What does herpes simplex look like? | back 3 Infection occurs at mucosal surfaces or sites of abraded skin
High rate of transmission
Characteristic small, grouped, painful, vesicles |
front 4 How does herpes simplex travel in the body? | back 4 Virus infects sensory and autonomic nerve endings
Virus is transported to nucleus of nerve cells where it may become dormant to reactivate later
Trauma, UV exposure, systemic illness
Contiguous spread and autoinoculation can occur |
| back 5 Acute Herpetic Gingivostomatitis
First infection with HSV
Only seen in approx 1% of infected people
Generally seen in children or young adults
Crops of painful, grouped, vesicles
May rupture to form erosions with crusts
Oral mucosa, hard/soft palate, tongue, lips
Fever, malaise, lymphadenopathy
Resolves in 2 weeks |
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| back 9 Recurrent Herpes Labialis
Recurrence of infection
Fever blisters and cold sores
Outer portions of lips (usually spares oral cavity)
Can occur on hard palate
Prodrome: stinging, burning, tingling
Heal completely within 10 days
Viral shedding stops after crusts form
40% have recurrences (average 2/year)
Treatment: Antivirals (acyclovir, valacylovir, etc)
Can be taken at prodrome onset, or daily for suppressive therapy |
| back 10 Primary Herpes Genitalis
Predominantly HSV-2
Multiple erosions on external genitalia
Occur one week after exposure
Viral shedding ends around 11 days
Pain, itching, dysuria, inguinal adenopathy
90% women have cervical lesions
Healing complete in 2 to 3 weeks
Only 57% of primary infections are symptomatic |
| back 11 Primary Herpes Genitalis
Predominantly HSV-2
Multiple erosions on external genitalia
Occur one week after exposure
Viral shedding ends around 11 days
Pain, itching, dysuria, inguinal adenopathy
90% women have cervical lesions
Healing complete in 2 to 3 weeks
Only 57% of primary infections are symptomatic |
| back 12 Primary Herpes Genitalis
Predominantly HSV-2
Multiple erosions on external genitalia
Occur one week after exposure
Viral shedding ends around 11 days
Pain, itching, dysuria, inguinal adenopathy
90% women have cervical lesions
Healing complete in 2 to 3 weeks
Only 57% of primary infections are symptomatic |
| back 13 Recurrent Herpes Genitalis
Mild to moderate pain for 1 week
Decreased local symptoms
Lesions cover 10% of original area
Cervical lesions are uncommon (12%)
Average recurrence rate: 4 per year
Clears by 10 days
Like oral-facial disease, can be treated with antivirals (intermittent or suppressive therapy) |
| back 14 Recurrent Herpes Genitalis
Mild to moderate pain for 1 week
Decreased local symptoms
Lesions cover 10% of original area
Cervical lesions are uncommon (12%)
Average recurrence rate: 4 per year
Clears by 10 days
Like oral-facial disease, can be treated with antivirals (intermittent or suppressive therapy) |
| back 15 Herpetic Whitlow
HSV infection of fingers or hands
Medical or dental personnel traditionally
Most cases now seen in persons with HSV elsewhere
HSV-1 in children
About 75% in adults caused by HSV-2
Inoculation on abraded or broken skin
Wear gloves!!! |
| back 16 Herpetic Whitlow
HSV infection of fingers or hands
Medical or dental personnel traditionally
Most cases now seen in persons with HSV elsewhere
HSV-1 in children
About 75% in adults caused by HSV-2
Inoculation on abraded or broken skin
Wear gloves!!! |
| back 17 Herpetic Whitlow
HSV infection of fingers or hands
Medical or dental personnel traditionally
Most cases now seen in persons with HSV elsewhere
HSV-1 in children
About 75% in adults caused by HSV-2
Inoculation on abraded or broken skin
Wear gloves!!! |
| back 18 Herpes Gladiatorum
Cutaneous and ocular HSV-1 infection
Seen in wrestlers, contact sport players
Head (75%) > trunk > extremities
Direct skin-to-skin contact
Saliva is not major source of transmission |
| back 19 Eczema Herpeticum
Secondary HSV infection in patients with atopic dermatitis or other disorders of skin barrier
Widely spread eruption
Punched out erosions in areas of previously abnormal skin
Associated with fever, malaise and lymphadenopathy |
| back 20 Eczema Herpeticum
Secondary HSV infection in patients with atopic dermatitis or other disorders of skin barrier
Widely spread eruption
Punched out erosions in areas of previously abnormal skin
Associated with fever, malaise and lymphadenopathy |
| back 21 Eczema Herpeticum
Secondary HSV infection in patients with atopic dermatitis or other disorders of skin barrier
Widely spread eruption
Punched out erosions in areas of previously abnormal skin
Associated with fever, malaise and lymphadenopathy |
front 22 How is herpes simplex diagnosed? | back 22 Diagnosis by history and clinical features
Tissue culture: most sensitive test
Tzanck prep: rapid confirmation
Fluorescent Antibodies (88% correlation with tissue culture) |
front 23 Treatment for herpes simplex | back 23 Treatment
Acyclovir
Valacyclovir
Famciclovir
Topical therapy is generally ineffective |
front 24 Chickenpox- caused by which virus. How can you get it? | back 24 PRIMARY infection
Caused by varicella-zoster virus (VZV)
Highly contagious
Contact with lesions or respiratory route
Majority in children < 10 years of age
Incubation around 14 days
Infectious 2 to 3 days before exanthem and for 5 days thereafter (until crusting occurs) |
front 25 Varicella- What is the prodrome, what is its appearance? | back 25 Prodrome: fever, chills, malaise, headache
Rash begins on face and spreads to trunk
Thin-walled vesicles surrounded by erythema – “dew drops on rose petal”
Appear in crops; vesicles soon crust
Lesions in various stages of development
May affect mucous membranes |
front 26 Complications to varicella | back 26 Secondary bacterial infection
Secondary bacterial pneumonia, otitis media, suppurative meningitis (rare)
More complications in adult patients, pregnant females and immunocompromised
Congenital and neonatal varicella |
| back 27 Treatment
Healthy children: calamine lotion, antihistamines, oatmeal baths, +/- acyclovir
Adults: Acyclovir because of high risk of complications
Immunosuppressed: IV acyclovir, VZ immune globulin
Prevention: VZV vaccine |
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| back 31 Herpes Zoster
Reactivation of VZV (from primary infection or vaccine) from latent form
Pain often precedes lesions
Unilateral, dermatomal, grouped vesicles
Does not cross midline
50% occur in thoracic region
Crusting occurs in 7-10 days |
| back 32 Herpes Zoster
Reactivation of VZV (from primary infection or vaccine) from latent form
Pain often precedes lesions
Unilateral, dermatomal, grouped vesicles
Does not cross midline
50% occur in thoracic region
Crusting occurs in 7-10 days |
| back 33 Herpes Zoster
Reactivation of VZV (from primary infection or vaccine) from latent form
Pain often precedes lesions
Unilateral, dermatomal, grouped vesicles
Does not cross midline
50% occur in thoracic region
Crusting occurs in 7-10 days |
| back 34 Herpes Zoster
10% affect ophthalmic division of the trigeminal nerve
Rash affecting nasal tip occurs in 40% with ophthalmic involvement -Hutchinson’s sign. Need to be evaluated for herpes keratitis which is potentially blinding
Ramsey-Hunt: involves facial and auditory nerves, facial nerve palsy, tinnitus, vertigo, deafness |
front 35 Complications for Herpes Zoster | back 35 Complications
Post-herpetic neuralgia (15%)
Dissemination occurs in 2 to 10% (immunosuppressed, HIV, malignancy)
Visual impairment (ophthalmic zoster)
Meningoencephalitis |
front 36 Diagnosis and Treatment for Herpes Zoster | back 36 Diagnosis: clinical, Tzanck, culture, immunofluorescence
Treatment: acyclovir, valacyclovir, famciclovir
IV acyclovir for immunocompromised |
| back 37 Hand-Foot-Mouth Disease **
Benign, self-limited viral disease
Highly contagious; coxsackievirus A16, enterovirus 71
Spreads by direct contact with mucous, saliva, feces
Thin-walled, gray vesicles
Tongue, palate, buccal mucosa, fingers, toes, palms, soles
Resolves in 10 to 14 days; no treatment needed |
| back 38 Hand-Foot-Mouth Disease **
Benign, self-limited viral disease
Highly contagious; coxsackievirus A16, enterovirus 71
Spreads by direct contact with mucous, saliva, feces
Thin-walled, gray vesicles
Tongue, palate, buccal mucosa, fingers, toes, palms, soles
Resolves in 10 to 14 days; no treatment needed |
| back 39 Hand-Foot-Mouth Disease **
Benign, self-limited viral disease
Highly contagious; coxsackievirus A16, enterovirus 71
Spreads by direct contact with mucous, saliva, feces
Thin-walled, gray vesicles
Tongue, palate, buccal mucosa, fingers, toes, palms, soles
Resolves in 10 to 14 days; no treatment needed |
| back 40 Herpangia
Benign, self-limited viral disease
Highly contagious, caused by Coxsackieviruses A, B and echoviruses
Spread via oral-fecal or respiratory routes
Painful and vesicular erosions of SOFT PALATE, uvula, pharnyx, tonsils and buccal mucosa
Resolves over one to two weeks, no treatment |
front 41 How would you diagnose and treat this? | back 41 Dermatitis Herpetiformis
Diagnosis: skin biopsy and direct immunofluorescence
Treatment: gluten-free diet, dapsone, colchicine |
| back 42 Dermatitis Herpetiformis
Autoimmune vesicular dermatitis with epidermal transglutaminase as likely autoantigen
Related to gluten-sensitive enteropathy
Gluten – protein found in wheat, barley, rye
Grouped vesicles on elbows, knees, buttocks, shoulders, scalp (symmetric appearance)
Extremely itchy
Occasionally associated with other AI diseases: lupus, thyroid disease, and lymphoma |
front 43 What can be the differential diagnosis for Dermatitis Herpetiformis? | back 43 Differential dx (includes):
Linear IgA bullous dermatosis
Bullous pemphigoid
Scabies
Contact dermatitis
Neurotic excoriations |
| back 44 Pemphigus Vulgaris
Autoimmune disease
Body produces antibodies to desmoglein 3 and 1, proteins that helps hold epithelial cells together
Flaccid blisters
Widespread erosions, crusts, scarring
Oral mucosa is frequently involved
May have electrolyte imbalance, low albumin, or secondary bacterial infections
Mortality as high as 50% before discovery of oral steroids |
front 45 What is the differential dx? | back 45 Pemphigus Vulgaris
Differential dx includes:
Bullous dermatoses
TEN |
front 46 How would you diagnose and treat? | back 46 Pemphigus Vulgaris
Diagnosis: skin biopsy, direct immunofluorescence
Treatment: high dose prednisone, azathioprine, cyclophosphamide, plasmapheresis, IVIG |
| back 47 Bullous Pemphigoid
Common autoimmune disease, usually of elderly
Body produces antibodies to bullous pemphigoid antigens 1 and 2 (BPAG), proteins that hold epidermis to dermis
Tense blisters in flexural areas
Mucous membranes usually spared |
front 48 How would you treat this? | back 48 Bullous Pemphigoid-
Prednisone
Azathioprine, cyclophosphamide, mycophenylate mofetil, dapsone, tetracycline, nicotinamide
Topical steroids in mild, localized cases |
front 49 How would you diagnose this? | back 49 Bullous Pemphigoid-
Diagnosis: biopsy, DIF |
front 50 What are the differential dx? | back 50 Bullous Pemphigoid-
Differential dx: Bullous dermatoses, arthropod bite |
| back 51 Erythema Multiforme **
Spectrum of disease from self-limited (EM minor) to large areas of cutaneous and mucosal involvement (EM major)
EM major’s relationship to SJS/TEN controversial
Usually self-limited
Usually associated with infectious agents
HSV, mycoplasma
May involve oral mucous membranes
Young adults |
| back 52 Erythema Multiforme **
Usually resolves in 2 to 4 weeks
Acyclovir or valacyclovir if related to HSV infection |
| back 53 Stevens-Johnson & Toxic Epidermal Necrolysis **
Severe, rapid, widespread blistering dermatosis
Up to 10% BSA – SJS
10-30% BSA – SJS/TEN overlap
30% BSA -- TEN
90% of cases mucosa involved: eyes, airways/GI, GU tract
>95% cases are drug-induced
Usually develops within 1-3 weeks of starting offending medication |
front 54 What kinds of drugs usually cause this? | back 54 SJS and TEN
Drugs: sulfa, anticonvulsants, NSAIDS
Bactrim, dilantin, allopurinol |
front 55 How to diagnose and treat? | back 55 High mortality rate
SJS – 5%
TEN – 30+%
Diagnosis: history, clinical, biopsy
Treatment: admit to burn unit or MICU; supportive care, IVIG (in select cases), eye/respiratory care, steroids (in select cases) |
