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HERPES ZOSTER

DERMATOLOGY LECTURE NOTES

DEBABRATA BANDYOPADHYAY
PROFESSOR & HEAD, DEPT. OF DERMATOLOGY,
R. G. KAR MEDICAL COLLEGE, CALCUTTA, INDIA

 

 

Herpes zoster (HZ), also known as shingles, is an acute viral infection of the skin caused by varicella zoster virus (VZV). Latent infection in nerve root ganglions follows  an attack of chicken pox; reactivation of latent VZV infection  leads to a blistering disease limited to a single or adjacent dermatomes. This self-limited disease often leads to severe pain in the affected region long after the lesions are healed.

 

 

ETIOLOGY & PATHOGENESIS

  • During an attack of chicken pox, the varicella-zoster virus travels along the sensory nerve fiber centripetally to the spinal and cranial sensory ganglia where the virus establishes a life-long latent infection.
  • On a later date, reactivation of the virus occurs in the ganglia where the virus is most numerous and is triggered by diminished immunity associated with advancing age, immunosuppression due to drugs or diseases like HIV infection or lymphoma, radiation or trauma.
  • Viral proliferation leads to traveling down of virus along nerve fibers to skin and mucosa where it causes degenerative and inflammatory changes producing characteristic lesions at the corresponding dermatome.

CLINICAL FEATURES

  • Herpes zoster affects both sexes equally.
  • Occurrence is sporadic, without any seasonal variation.
  • About 10-20% of people are expected to develop HZ in their lifetime.
  • People of all ages may be affected. Frequency increases with advancing age. Two-thirds of patients are over forty years of age.
  • Prodromal phase: is dominated by constitutional symptoms like headache, photophobia, fever, and pain.
  • The pre-eruptive pain may be of varying severity and may be deep aching, sharp neuralgic or there may be allodynia (pain produced by minor stimuli like touching). The pain may mimic acute abdomen, migraine, or myocardial ischemia.
  • The pain is soon followed by a rash limited to one side of the body in the distribution of a single or 2-3 adjacent dermatomes.. Redness, papules and plaques appear, may be associated with itching or burning sensation.
  • Grouped vesicles develop on the area, umbilication, pustulation follows. The lesions gets crusted and gradually heal over 2-4 weeks.
  • Thoracic segments are most commonly involved (>50%) followed by cervical, trigeminal, lumbosacral dermatomes. Mucosa in the affected dermatome are also involved.



  • Viraemia occur during the course of the illness and a few outlying vesicles may be found elsewhere on the body away from the involved dermatome.
  • Tender, regional lymph node enlargement is common.
  • Ophthalmic zoster: Involvement of the tip and side of the nose (Huchinson's sign) portends severe ocular involvement . Ocular involvement may be manifested by conjuntivitis, keratitis, uveitis, lid edema and severe pain.
  • Herpes zoster in HIV infection: Non-adjacent multiple dermatomes may be affected. HZ is a sign of early immunosuppression in HIV infection. Lesions may be severe, ulcerated or hemorrhagic, and long-lasting.
  • Ramsay-Hunt syndrome: infection of geniculate ganglion leads to involvement of motor and sensory portion of facial nerve. There may be unilateral loss of sensation on anterior two-third of tongue, facial palsy, and vesicles on tympanic membrane, external ear or ear canal.
  • Complications:
        
    Post-herpetic neuralgia (PHN)
    is the dominant cause of morbidity in HZ.   This is defined as pain persisting after 30 days of onset of rash. The incidence of PHN increases with advancing age. About 75% of patients above 70 years of age may develop this. PHN is limited to the site of the rash and can be extremely disabling, persisting for months to years. The degree of pain is not related to the extent or severity of vesicles or inflammation.

     

    COMPLICATIONS OF HERPES ZOSTER

    Post-herpetic neuralgia
    Secondary bacterial infection
    Pigmentary changes
    Scarring and keloids
    Encephalitis
    Myelitis

    Cutaneous dissemination
    Visceral involvement
    Blindness
    Acute retinal necrosis
    Motor palsies: Facial, ocular, bladder
    Delayed contraleral hemiplegia

 

 

 

 

 

DIFFERENTIAL DIAGNOSIS

  •  Prodromal pain: Migraine, pleurisy, myocardial ischemia, or acute abdomen.

  •  Rash: Herpes simplex
              Phytophotodermatitis
              Contact dermatitis
              Impetigo
              Erysepelas

 

 

DIAGNOSIS

 
 
  • Typical clinical features of grouped vesicles on an erythematous base in a dermatomal distribution is highly diagnostic.

  • Tzank smear (smear from base of ruptured vesicle stained with Giemsa) reveals multinucleated giant cells.

  • Direct immunofluorescence of cellular material to detect viral antigen.

  • Culture or PCR for viral DNA

 

 
 

COURSE AND PROGNOSIS

 
 
  • Herpes zoster is a self-limiting disease. Complete, spontaneous recovery within 2 to 4 weeks is the rule. Some residual sensory change and post-inflammatory dyspigmentation, however, may remain in some.
  • In immunocompromized individuals, severe affection with prolonged disease course and scarring may occur.
  • Second attack of herpes is rare, but in HIV-infected individuals, frequent recurrences may occur.

 
 

TREATMENT

 
 

     Acute attack:
                       Cool compresses.

                       Analgesics and sedatives

                       Antiviral therapy: acts best if initiated within 48 hours of onset.
                       Acyclovir (800mg 5 times a day x 7-10 days), valacyclovir (100mg
                       tid x 7 days), or famciclovir (500 mg tid x 7 days) . Antiviral therapy
                       reduces acute pain and inflammation, reduce duration of disease and
                       viral shedding and may reduce frequency of PHN.
                       Topical antiviral therapy has no role in the treatment of HZ.

                       Concurrent therapy with systemic steroid may reduce acute pain and
                       inflammation, but has no role in prevention of PHN.  

     Post-herpetic neuralgia:
                      Analgesics

                      Topical lidocaine patch, capsaicin

                      Tricyclic antidepressants ( amitryptiline 75mg/day), gapapentin 300 mg
                       tid    

 
 

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