Shingles is a reactivation of the viral infection in the nerves. After a patient has contracted the varicella zoster virus, the virus lays dormant in the dorsal root ganglia in the central nervous system. Host immunologic mechanisms control the replication of the varicella zoster virus. Many stressors can affect the host mechanisms from controlling the replication of the virus including stress, age, nerve injury or weakening of the immune system. Once the virus has been reactivated, it becomes herpes zoster and the dorsal root ganglia becomes inflamed and passes through the dorsal root neurons, this inflammation obstructs the dorsal horn cellular metabolism. The virus travels from dorsal root ganglia to peripheral nerves where the herpes zoster virus can cause damage to the myelin sheath, or demyelination. It travels to the surface of the skin in small clusters or band in a localized area and creates a rash with vesicles. The vesicles break open exposing the virus. At this stage the virus can be spread by