Viral Skin Infections ICM I Summer 2009 Rich Callahan MSPA, PA-C.
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Transcript of Viral Skin Infections ICM I Summer 2009 Rich Callahan MSPA, PA-C.
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Viral Skin Infections
ICM I
Summer 2009
Rich Callahan MSPA, PA-C
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Overview
• Viral Warts
• Molluscum Contagiosum
• Herpes Simplex
• Varicella
• Herpes Zoster
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Viral Warts
• Caused by Human Papilloma Virus (HPV)• Wide variety of presentations from
subclinical infection to benign epithelial tumors of skin and mucosa
• 150+ subtypes of HPV identified• Several subtypes associated with cancer
pathogenesis – Squamous Cell Carcinoma (SCC) of skin, mucosa, cervix, etc
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Viral Warts - Pathogenesis
• Virus ubiquitous in the environment – it is around us all the time
• Spread by skin-to-skin contact or by contaminated surfaces.
• Virus needs break in skin surface to enter and infect epidermis.
• Virus occupies skin cells in an intracellular fashion, making immune recognition and response more difficult.
• Compromised immune status (HIV, organ transplant) generally results in more widespread, significant infection.
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Genital Warts (Condyloma Acuminata)
• Generally an STD, but not always
• When seen in children, may or may not indicate sexual abuse
• When seen around orifices (anus;vagina) important to investigate further as infection in rectum/vagina more likely to lead to squamous dysplasia and SCC
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Treatment of Warts
• Most cases resolve spontaneously in 1-3 years.• Patient expectations prior to treatment extremely
important – cutting, burning and freezing of warts does not guarantee a cure – visible warts can disappear and reappear as infection becomes subclinical
• I never treat warts without discussing appropriate expectations first – warts can be one of the most stubborn diseases to treat!
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Treatment of Warts
• Destructive treatment: Aim is to destroy skin cells occupied by virus in hopes of stimulation an immune response:
• Liquid nitrogen cryotherapy
• Electrodessication
• Surgical removal
• Canthacur/Podophyllin/Topical retinoids
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Treatment of Warts
• Topical Chemotherapy:• 5-FU (5-Fluorouracil) – compound more
rapidly absorbed by abnormally dividing infected keratinocytes causing premature cell death and clearance of warts
• Treatment generally used for AK (pre-cancers) but occasionally used on viral warts
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Treatment of Warts
• Topical Immunotherapy: Geared towards stimulating a more pronounced immune response
• Aldara (imiquimod)• DNCB and SADBE: Induce allergic reaction in
skin (type IV delayed hypersensitivity) which summons lymphocytes to treated area in hopes of stimulation immune recognition and response
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Molluscum Contagiosum
• Pox Virus• Red, pink or flesh-colored papules or
nodules with characteristic central umbilication
• Can be transmitted by direct skin-to-skin contact, fomites or autoinoculation
• Adults/children who pick at them can literally spread hundreds around the body
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Molluscum Contagiosum
• Generally seen in children or as sexually transmitted disease in adults
• Ranges from classic presentation to mimicry of other diseases – can look a lot like acne if on the face.
• Black dot sign: When lightly frozen by cryotherapy, lesions of molluscum exhibit characteristic black dot on superior aspect
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Molluscum Contagiosum - Treatment
• Physical Destruction – Electrocautery, curettage, cryotherapy, manipulation
• Chemical destruction – cantharadin, topical retinoids• Immunotherapy – Aldara (imiquimod) • Unlike warts, treatment of molluscum stimulates
brisk immune response with spontaneous resolution of all lesions in 4-6 weeks. In really stubborn/widespread cases must suspect immune compromise such as HIV disease
• In rare cased, Cidofovir IV.
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Herpes Simplex Virus (HSV)
• Where does the name come from?• Herpes – “creeping” or snake-like eruption• Simplex – uncomplicated compared to other
blistering eruptions as generally confined to and recurrent in one area of body.
• Two Strains of HSV: HSV 1 and HSV 2• HSV 1 generally face/lips and HSV 2 generally
genitals/anal area.• Virus doesn’t follow any rules: HSV 1 can appear
on genital and HSV 2 can appear on face
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Herpes Simplex Virus (HSV)
• On lips, also known as herpes labialis, cold sore or “fever blister”
• On fingers, called herpetic whitlow• On wrestlers and other athletes, called herpes
gladiatorum• Inside mouth, called herpes gingivostomatitis• Ocular HSV/Herpes facial paralysis• Remember, can occur anywhere!
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Herpes Simplex Virus (HSV)
• HSV is a recurrent disease, which after initial exposure and infection, ascends peripheral sensory nerves to the nerve ganglion, where it then resides in a latent fashion
• Virus contagious skin-to-skin contact or exposure to fluid from active blisters.
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Initial infection generally subclinical; asymptomatic
• Virus then tracks down cutaneous nerves innervating affected area and becomes latent in nerve roots for indeterminate period of time, waiting for right set of circumstances (immune compromise) to reactivate
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HSV – Clinical Presentation
• Great majority of HSV cases are recurrent, and present with symptoms localized to affected area.
• In the rare case of a true symptomatic primary infection: Patient will have vesicles at inoculation site, with regional lymphadenopathy.
• +/- malaise, fever, fatigue, myalgias, headache
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HSV – Clinical Presentation
• Symptomatic infection starts with burning/tingling sensation in affected area
• 12-24 hours later, erythematous macules/patches appear, soon followed by rapid development of painful, yellow, fluid-filled vesicles
• Vesicles rupture 24-48 hours later leaving painful, crusted ulcerations and erosions.
• Eruption usually clears in 7-10 days and re-enters period of asymptomatic latency. In some cases, can take up to 4 weeks for it to clear entirely
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HSV – Clinical Presentation
• Most contagious in active phase when blister fluid present.
• Small number of individuals asymptomatically shed virus from normal appearing skin in small quantities
• Be careful about playing blame game: First clinical eruption can be preceded by 10+ years of subclinical infection, as is rare for primary infection to be symptomatic
• Some studies of general population have shown that up to 75% of us carry antibodies to HSV!
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HSV – Clinical Presentation
• Wide range in severity of eruption – not always classic, full-blown vesicular eruption
• Can present as pruritic red macules and patches, or red papules mimicking acne vulgaris.
• Majority of patients with HSV are asymptomatic carriers
• Trigger factors for eruption: Physical/emotional stress, sunburn, trauma, concurrent skin disease, fever, menstruation
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HSV – Clinical Presentation
• Remember: Location of clinical eruption doesn’t always correspond to that of primary infection.
• For example: 1st symptomatic episode on buttocks – could be preceded by primary anogenital infection, as any skin innervated by a lumbrosacral ganglion is fair game.
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HSV - Diagnosis
• Often a clinical diagnosis• Viral Culture for HSV 1/HSV 2• Tzanck Smear (not used in my community that
often)• Dermatopathology• Serology (takes 2 to 6 weeks to seroconvert HSV
antibodies after primary infection)• Antigen detection/PCR: Expensive, but has just
replaced Viral Cx at our institution as gold-standard diagnostic test.
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HSV – Treatment
• Topicals: Acyclovir 5% ointment, Penciclovir 1% cream
• Oral meds: Acyclovir, valcyclovir (valtrex), famciclovir (famvir)
• For severe, disseminated infections: IV acyclovir, foscarnet
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HSV – Viral Shedding
• Active HSV lesions shed virus into environment – highest viral counts in vesicle fluid
• Areas of skin infected by HSV continue to shed virus even after infection clinically resolved
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HSV – Viral Shedding
• Viral shedding rates highest in:
• First year after acquisition of HSV and patients with frequent outbreaks
• Duration of shedding longer in primary episode as compared with recurrences
• Primary infection: ~12 days
• Recurrence: ~2-5 days
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HSV – Viral Shedding
• Treatment with oral antivirals greatly reduces amount/duration of viral shedding both after symptomatic episode and in patients prone to frequent outbreaks who shed more virus
• It’s called daily suppressive therapy:• Valacyclovir (Valtrex) 500/1000mg daily• Famciclovir (Famvir) 250mg daily
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Varicella – “Chicken Pox”
• VZV – Varicella Zoster Virus, What is it?• Common herpes virus infecting ~98% of human
populations by adulthood• As primary infection resolves (chicken pox,) virus
retreats to sensory nerve ganglia and enters period of latency.
• VZV immunity declines with age, concurrent disease/malignancy, immune compromise – this allows VZV to re-activate as localized dermatomal infection called “shingles” or herpes zoster
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Varicella – “Chicken Pox”
• ~90% of cases occur in children 10 y/o or younger.
• Unusual in adults• Transmitted by respiratory contact with
airborne droplets and direct skin-to-skin contact – highly contagious!
• Incubation period 10-23 days• Epidemics in schools usually winter/spring
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VSV – Clinical Presentation
• Presents as evolving rash composed of successive crops of papules and wheals which quickly evolve into yellow vesicles on an erythematous base – the so-called “dew drop on a rose petal.”
• Lesions then evolve into pustules and crusts 12-24 later.
• Crusts resolve in 1-3 weeks, can leave scars.
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VSV – Clinical Presentation
• Distribution: Rash usually starts on face/scalp, then progress downwards to trunk/extremities.
• Often affects mucous membranes• Often accompanied by mild fever and malaise• Infection can be more severe in adults, with potential
severe prodrome and complication by Varicella pneumonia
• Extremely pruritic = scratching = secondary bacterial infection
• Greater age of patient = greater severity of primary infection
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VSV – Treatment
• VSV vaccine: ~80% effective. Should be used in VSV negative adults, patients with immune compromise, childhood cancers.
• In healthy children, symptomatic treatment with antipruritics and rest appropriate
• In select cases: Oral/IV antivirals• Occasionally VSV secondarily infected
with bacteria – treat accordingly
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Herpes Zoster
• Commonly known as “shingles”• Reactivation of latent VSV in dorsal root or
cranial nerve ganglion cells• ~66% of patients are > 40 years old• Lesions appear over several days, usually
resolve in 2-4 weeks• Disease more severe/longer duration in
immunocompromised patients
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Herpes Zoster
• Severe HZ can be first sign of HIV of underlying malignancy (often Hodgkin’s disease)
• Average adult has one episode over lifetime
• Patients with multiple episodes over a short period of time indicate further investigation
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HZ - Presentation
• Lesions often preceded by pruritis, tenderness and pain and/or neurologic changes such as hyperesthesia, dysesthesia and hypoesthesia
• This pain often confused with Sciatica, renal/urinary stones, cholecystitis (gallbladder disease,) and pleural/cardiac disease
• Neurologic symptoms can precede the eruption by 3-10 days
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HZ - Presentation
• Lesions appear posteriorly, the progress in anterior direction, then to peripheral locations
• Presents as grouped papules, vesicles, pustules and crusts on erythematous base
• Lesions spontaneously heal in 1-2 weeks
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HZ - Presentation
• 50% of cases involve thoracic nerves
• 15-20% cervical or lumbar nerves
• Remainder involve sacral and cranial nerve roots
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HZ - Presentation
• Be wary of lesions presenting on nasal tip as this defines involvement of nasociliary branch of ophthalmic division of trigeminal nerve (CN V1)
• ~33% of cases of ophthalmic zoster involve CN V1
• Ophthalmic Zoster can be extremely destructive to eyeball apparatus
• Zoster with nasal tip involvement indicates immediate referral to ophthalmology for further investigation!
• May need IV antivirals – let ophthalmology make that call!
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HZ - Diagnosis
• Usually a clinical diagnosis based on characteristic prodromal symptoms and appearance
• When it’s Zoster it usually looks/acts like zoster…..but when in doubt….
• Usually do viral culture for VSV• Can also do skin biopsy for histopathology,
Tzanck smear, Antibody studies, etc.
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HZ - Treatment
• Immunization ~80% effective (Zostavax)• Symptomatic treatment with lotions and
antihistamines• Oral/IV antiviral treatments – the sooner initiated
in course of illness the more effective they are!• Treatment of full-blown HZ rash won’t alter
course that much• May occassionally need to treat secondary
bacterial infection with oral/topical antibiotics
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PHN – Post Herpetic Neuralgia
• Syndrome defined by pain and/or other neurologic symptoms within affected dermatome persisting beyond 4 of onset of skin lesions of HZ
• Can last months to years beyond the illness itself
• Severe pain during prodrome/onset of skin lesions highly predictive for PHN