What part of the body does HSV-1 affect? (generally)
HSV-1 causes oral-labial infections
58% of US population seropositive
What part of the body does HSV-2 affect? (generally)
HSV-2 causes 90% of genital herpes infection
16% of US population seropositive
What does herpes simplex look like?
Infection occurs at mucosal surfaces or sites of abraded skin
High rate of transmission
Characteristic small, grouped, painful, vesicles
How does herpes simplex travel in the body?
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
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
HERPES SIMPLEX
HERPES SIMPLEX
HERPES SIMPLEX
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
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
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
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
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)
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)
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!!!
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!!!
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!!!
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
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
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
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
How is herpes simplex diagnosed?
Diagnosis by history and clinical features
Tissue culture: most sensitive test
Tzanck prep: rapid confirmation
Fluorescent Antibodies (88% correlation with tissue culture)
Treatment for herpes simplex
Treatment
Acyclovir
Valacyclovir
Famciclovir
Topical therapy is generally ineffective
Chickenpox- caused by which virus. How can you get it?
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)
Varicella- What is the prodrome, what is its appearance?
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
Complications to varicella
Secondary bacterial infection
Secondary bacterial pneumonia, otitis media, suppurative meningitis (rare)
More complications in adult patients, pregnant females and immunocompromised
Congenital and neonatal varicella
Treatment for Varicella
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
varicella
varicella
smallpox
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
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
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
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
Complications for Herpes Zoster
Complications
Post-herpetic neuralgia (15%)
Dissemination occurs in 2 to 10% (immunosuppressed, HIV, malignancy)
Visual impairment (ophthalmic zoster)
Meningoencephalitis
Diagnosis and Treatment for Herpes Zoster
Diagnosis: clinical, Tzanck, culture, immunofluorescence
Treatment: acyclovir, valacyclovir, famciclovir
IV acyclovir for immunocompromised
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
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
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
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
How would you diagnose and treat this?
Dermatitis Herpetiformis
Diagnosis: skin biopsy and direct immunofluorescence
Treatment: gluten-free diet, dapsone, colchicine
What is this?
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
What can be the differential diagnosis for Dermatitis Herpetiformis?
Differential dx (includes):
Linear IgA bullous dermatosis
Bullous pemphigoid
Scabies
Contact dermatitis
Neurotic excoriations
What is this?
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
What is the differential dx?
Pemphigus Vulgaris
Differential dx includes:
Bullous dermatoses
TEN
How would you diagnose and treat?
Pemphigus Vulgaris
Diagnosis: skin biopsy, direct immunofluorescence
Treatment: high dose prednisone, azathioprine, cyclophosphamide, plasmapheresis, IVIG
What is this?
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
How would you treat this?
Bullous Pemphigoid-
Prednisone
Azathioprine, cyclophosphamide, mycophenylate mofetil, dapsone, tetracycline, nicotinamide
Topical steroids in mild, localized cases
How would you diagnose this?
Bullous Pemphigoid-
Diagnosis: biopsy, DIF
What are the differential dx?
Bullous Pemphigoid-
Differential dx: Bullous dermatoses, arthropod bite
What is this?
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
How would you treat?
Erythema Multiforme **
Usually resolves in 2 to 4 weeks
Acyclovir or valacyclovir if related to HSV infection
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
What kinds of drugs usually cause this?
SJS and TEN
Drugs: sulfa, anticonvulsants, NSAIDS
Bactrim, dilantin, allopurinol
How to diagnose and treat?
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)