A 14-year-old boy presents with deep burning pain and a vesicular eruption in a band starting at the left chest and ending just across the midline of the back (Figure 109-1). The varicella-zoster virus (VZV) leaves the dorsal root ganglion to travel down the spinal nerves to the cutaneous nerves of the skin. The vesicles do cross the midline by a few centimeters because the posterior primary ramus of the spinal nerve includes a small cutaneous medial branch that reaches across the midline.¹ The boy was treated with analgesics and an antiviral medication. The zoster healed with scarring.

Herpes zoster (shingles) is a syndrome characterized by a painful, usually unilateral vesicular eruption that develops in a restricted dermatomal distribution (Figures 109-1 and 109-2).^2,3

Shingles.

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  According to the Centers for Disease Control and Prevention (CDC), 32 percent of persons in the US will experience zoster during their lifetimes accounting for about 1 million cases annually.⁴ Older age groups account for the highest incidence of zoster. Approximately 4 percent of patients will experience a second episode of herpes zoster.⁵

  
  
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  Herpes zoster is uncommon in healthy children; most cases are seen in immunocompromised patients, including children who have received solid organ and hematologic transplants.

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  After primary infection with either chickenpox or vaccine-type VZV, a latent infection is established in the sensory dorsal root ganglia. Reactivation of this latent VZV infection results in herpes zoster (shingles).

  
  
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  Both sensory ganglia neurons and satellite cells surrounding the neurons serve as sites of VZV latent infection. During latency, the virus only expresses a small number of viral proteins.

  
  
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  How the virus emerges from latency is not clearly understood. Once reactivated, virus spreads to other cells within the ganglion. The dermatomal distribution of the rash corresponds to the sensory fields of the infected neurons within the specific ganglion.³

  
  
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  Loss of VZV-specific cell-mediated immune response is responsible for reactivation.³

  
  
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  The pain associated with zoster infections and postherpetic neuralgia (PHN) is thought to result from injury to the peripheral nerves and altered central nervous system processing.

  
  
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  The most common complication is bacterial superinfection that can delay healing and cause scarring of the zoster lesions.

  
  
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  Complications may include:⁶

  
  
  
  
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    PHN—Uncommon in the pediatric population.

    
    
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    Ocular complications, including uveitis and keratitis (see Chapter 110, Zoster Ophthalmicus).

    
    
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    Bell palsy and other motor nerve plastic.

    
    
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    Bacterial skin infection.

    
    
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    Meningitis caused by central extension of the infection.

    
    
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    Herpes zoster oticus (Ramsay Hunt syndrome; Figure 109-3) includes the triad of ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal and auricle.⁸ Disturbances in taste perception, hearing (tinnitus or hyperacusis), lacrimation, and vestibular function (vertigo) may occur.

    
    
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    Other rare complications may include acute retinal necrosis, transverse myelitis, encephalitis, leukoencephalitis, contralateral thrombotic stroke syndrome, and granulomatous vasculitis.⁷

  
  
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  Immunosuppressed patients are at increased risk for complications, including severe complications such as broader dermatomal involvement (Figure 109-4), disseminated infection, visceral involvement, pneumonitis, and/or meningoencephalitis.

  
  
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  PHN is the persistence of pain, numbness, and/or dysesthesias precipitated by movement or in response to non-noxious stimuli in the affected dermatome for more than 1 month after the onset of zoster. The incidence of PHN in the general population is 1.38 per 1000 person-years, and it occurs more commonly in individuals older than age 60 years and in immunosuppressed individuals.³ This is rare in the pediatric population.