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Shingles, Awakening of a Dormant Disease

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Shingles, Awakening of a Dormant Disease. Kievers L. Cunningham, MD. Overview ... zoster (commonly referred to as 'shingles') and post herpetic neuralgia result ... – PowerPoint PPT presentation

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Title: Shingles, Awakening of a Dormant Disease


1
Shingles, Awakening of a Dormant Disease
  • Kievers L. Cunningham, MD

2
Overview
  • Herpes zoster (commonly referred to as
    "shingles") and post herpetic neuralgia result
    from reactivation of the varicella-zoster virus
    acquired during the primary varicella infection,
    or chickenpox.
  • Varicella is generally a disease of childhood.
  • Herpes zoster and post herpetic neuralgia become
    more common with increasing age.

3
Overview
  • Factors that decrease immune function may also
    increase the risk of developing herpes zoster.
  • E.g.- human immunodeficiency virus infection,
    chemotherapy, malignancies, chronic
    corticosteroid use, and aging.

4
Epidemiology
  • Sporadic disease- lifetime incidence of 10 to 20
    percent.
  • The incidence of herpes zoster increases sharply
    with advancing age, roughly doubling in each
    decade past the age of 50 years.
  • Herpes zoster is uncommon in persons less than 15
    years old.

5
Epidemiology
  • The incidence of herpes zoster is up to 15 times
    higher in HIV-infected patients than in
    uninfected persons, and as many as 25 percent of
    patients with Hodgkin's lymphoma develop herpes
    zoster.
  • Herpes zoster in HIV-infected patients does not
    appear to increase the risk of acquired
    immunodeficiency syndrome (AIDS

6
Epidemiology
  • No clinically significant differences between
    race.
  • Although herpes zoster is not as contagious as
    the primary varicella infection, persons with
    reactivated infection can transmit
    varicella-zoster virus to nonimmune contacts.
  • The most established risk factor is age this
    complication occurs nearly 15 times more often in
    patients more than 50 years of age.

7
Pathophysiology
  • Varicella-zoster virus is a highly contagious DNA
    virus.
  • Varicella represents the primary infection in the
    nonimmune or incompletely immune person.
  • During the primary infection, the virus gains
    entry into the sensory dorsal root ganglia.
  • How the virus enters the sensory dorsal root
    ganglia and whether it resides in neurons or
    supporting cells are not completely understood.

8
Pathophysiology
  • The virus remains latent for decades because of
    varicella-zoster virusspecific cell-mediated
    immunity acquired during the primary infection.
  • Reactivation of the virus occurs following a
    decrease in virus-specific cell-mediated
    immunity.
  • The reactivated virus travels down the sensory
    nerve and is the cause for the dermatomal
    distribution of pain and skin lesions.

9
Pathophysiology
  • The pathophysiology of postherpetic neuralgia
    remains unclear.
  • Pathologic studies - damage to the sensory
    nerves, the sensory dorsal root ganglia and the
    dorsal horns of the spinal cord.

10
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11
Clinical Presentation- Symptoms
  • Malaise
  • Headache
  • Acute, knife-like pain (with tingling and
    itching) that occurs 3-5 days before the rash in
    the dermatome where the rash will appear
  • Weakness
  • Fever
  • Acute loss of hearing, vertigo, and paralysis of
    the affected side of the face may occur in herpes
    zoster of the facial nerve (Ramsay Hunt syndrome)

12
Clinical Presentation- Signs
  • Closely grouped red papules, which rapidly become
    vesicular, appear in a continuous, uninterrupted
    band, generally in a single dermatome
  • A few patients have some vesicles outside the
    affected dermatome
  • Rash is almost always unilateral
  • Appearance of the rash may be the first sign in
    children

13
Clinical Presentation- Signs
  • Lymph nodes draining the affected area may be
    enlarged and tender
  • Vesicles become papular and/or hemorrhagic in 1-4
    days
  • Vesicles have a red base and are cloudy in
    appearance
  • Vesicles are of different sizes
  • Vesicles become umbilicated and then form crusts
    that fall off in about 3 weeks, generally leaving
    some scarring

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17
Differential Diagnosis- Rash
  • Herpes simplex virus infection
  • Disseminated coxsackievirus infection
  • Contact dermatitis
  • Autoimmune bullous skin diseases
  • Blistering bacterial infection

18
Differential Diagnosis- Pain
  • Cholecystitis
  • Pleuritic chest pain
  • Myocardial infarction
  • Pericarditis
  • Renal colic
  • Prolapsed disc

19
Treatment- Acute Infection
  • Antiviral Therapy- Acyclovir (Zovirax),
    Valcyclovir(Valtrex), Famciclovir(Famvir) and
    Foscarnet.
  • Acyclovir- moderately active against zoster/most
    clinical data cost (inexpensive) multiple time
    daily(5x)
  • Treatment should be initiated 48-72 hour after
    onset of symptoms- ? post-herpetic neuralgia and
    healing time.

20
Treatment- Acute Infection
  • Newer Antivirals-Valcyclovir and Famciclovir
  • Valcyclovir- 1st line- rapid resolution of
    neuritis, pain and post-herpetic neuralgia (1
    gram TID PO x 7 days85)
  • Famvir- more expensive than Valtrex(140) better
    bioavailability

21
Treatment- Acute Infection
  • Prednisone (steroids)-may improve healing and
    healing time in severe cases when added to
    antiviral.
  • Should not be given alone or extended beyond
    antiviral regimen,
  • Do not give to HIV/AIDS patients.
  • Should be given in reducing-dose or taper
    regimen.
  • Treatment of choice for Ramsay Hunt Syndrome
    (facial nerve).

22
Treatment- Acute Infection
  • Pain relief can be obtained by any of the
    following
  • Acetaminophen
  • Opioid analgesics
  • NSAIDs arent recommended.
  • Capsaicin (once lesions have crusted over)
  • Calamine lotion
  • Topical lidocaine/xylocaine
  • Nerve blocks

23
Treatment- Post-Herpetic Neuralgia
  • Anticonvulsants- gabapentin, phenytoin,
    carbamazapine
  • Tricyclic Antidepressants amitriptyline,
    nortriptyline, imipramine etc.
  • Topical- Capsaicin, lidocaine patch

24
Immunization
  • Zostavax
  • FDA approved in 2006
  • Only licensed for prevention of zoster in patient
    60 years.
  • Live attenuated virus
  • Side effects- headache and injection site
    reaction
  • Contraindicated- immunosuppression, pregnancy and
    hypersensitivity (anaphylactic reaction to
    gelatin or neomycin).

25
Immunization
  • Shingles Prevention Study
  • Followed for median of 3.1 years
  • RRR 51
  • ARR5.7
  • NNT17
  • ? Chicken Pox Vaccine

26
References
  • 1. Donahue JG, Choo PW, Manson JE, Platt R. The
    incidence of herpes zoster. Arch Intern Med
    19951551605-9.
  • 2. Dubinsky RM, Kabbani H, El-Chami Z, et al.
    Practice Parameter treatment of post-herpetic
    neuralgia an evidence-based report of the Quality
    Standards Subcommittee of the American Academy of
    Neurology. Neurology 200463959-65
  • 3. Mounsey AL, Matthew LG, Slawson DC. Herpes
    Zoster and Post-Herpetic Neuralgia Prevention
    and Managment. Am Fam Physician 2005721075-80
  • 4. Dworkin RH, Johnson RW, Breuer J, et al.
    Recommendations for the management of herpes
    zoster. Clin Infect Dis 200744 Suppl 1S1-26.

27
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