Viral Skin Infections

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					Viral Skin Infections

          ICM I
      Summer 2009
Rich Callahan MSPA, PA-C
•   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
• Virus needs break in skin surface to enter and infect
• 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
• 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
• 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 (pre-
  cancers) but occasionally used on viral
          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
• 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 -
• Physical Destruction – Electrocautery, curettage,
  cryotherapy, manipulation
• Chemical destruction – cantharadin, topical
• 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
• 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
• Virus contagious skin-to-skin contact or
  exposure to fluid from active blisters.
   Initial infection generally subclinical;

• 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
• Small number of individuals asymptomatically
  shed virus from normal appearing skin in small
• 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
• 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
• 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.
          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
• 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
• 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
• 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
• 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
• 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
• 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
• Severe pain during prodrome/onset of skin
  lesions highly predictive for PHN

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