Herpes Zoster, also known as shingles, is caused by the reactivation of the varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox). After the primary infection, chickenpox, is cured, the virus becomes inactive, and retreats to an individual’s nerve tissues located near the brain or spinal cord (Nair & Bhimji, 2017). The virus can be reactivated with aging, immune insufficiency, illness, and/or stress; however, the exact cause of the reactivation of varicella zoster virus causing shingles is not known.
The varicella-zoster virus will destroy the neurons in the ganglion nerve to replicate and spread causing pain (Dunphy, Winland-Brown, Porter, Thomas, 2015). The pain from the destruction of ganglion nerves is often the first symptom of shingles before a rash occurs. Vesicular lesions appear from the virus spreading through nerves to dermatome (Dunphy et al., 2015). Shingles typically occur in one nerve at a time. Thus, shingles presents itself as a rash that appears on only one side of the body with accompanying pain, headaches, fever, and blisters. Prior to these symptoms, one may experience pain in the area where the blisters have yet to appear about 3 to 5 days beforehand (Ferri, 2018). These blisters are contagious because they contain the actual virus and will remain contagious upon contact until they are scabbed and healed over. Patients may experience what is called post-herpetic neuralgia, or pain at the site after the breakout, for months or maybe even years after the disease (Ferri, 2018).