Transcript Viral Skin Infections

Viral Skin Infections
ICM I
Summer 2009
Rich Callahan MSPA, PA-C
Overview
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Viral Warts
Molluscum Contagiosum
Herpes Simplex
Varicella
Herpes Zoster
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
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.
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
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!
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
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 (precancers) but occasionally used on viral
warts
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
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
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
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.
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
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!
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.
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
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
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
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!
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
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.
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 goldstandard diagnostic test.
HSV – Treatment
• Topicals: Acyclovir 5% ointment,
Penciclovir 1% cream
• Oral meds: Acyclovir, valcyclovir
(valtrex), famciclovir (famvir)
• For severe, disseminated infections: IV
acyclovir, foscarnet
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
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
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
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
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
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.
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
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
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
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
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
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
HZ - Presentation
• 50% of cases involve thoracic nerves
• 15-20% cervical or lumbar nerves
• Remainder involve sacral and cranial
nerve roots
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!
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.
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
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