Herpes zoster is an infection resulting from reactivation of the varicella-zoster virus (VZV) that affects peripheral or cranial nerves and usually occurs years after primary infection with the varicella (chickenpox) virus or receipt of the live, attenuated varicella vaccine
The disease manifests as painful cutaneous eruptions over a single dermatome or two or more contiguous dermatomes; they are invariably unilateral and do not cross the midline. These eruptions are most commonly distributed on the thorax but can appear anywhere on the body. In some cases, cranial nerves supplying the eyes, ears, and face are involved, resulting in complicated presentations with potentially severe sequelae
The herpes zoster vaccine reduces the risk of developing the infection and reduces the severity and duration of the disease, as well as its most common complication, postherpetic neuralgia
Antiviral therapy hastens resolution of the disease and can prevent associated complications; pain medications lessen disability
Herpes zoster, also known as shingles or zoster, is a reactivated VZV infection of the sensory nerve ganglion and the peripheral nerve and its branches. Inflammation of the nerve axons results in a painful, burning sensation on the affected dermatome(s) being supplied by the peripheral nerve. Vesicular eruptions on skin of the involved dermatome are also present.
The causative agent of herpes zoster, VZV, is a linear, double-stranded deoxyribonucleic acid (DNA) genome enclosed in a protein envelope. After a bout of illness with the primary infection (chickenpox), the virus lies dormant in the sensory nerve ganglion until reactivated. The process of reactivation is not entirely understood, but some of the associated risk factors are listed below.
Advanced age (the older the patient, the higher the risk)
In elderly patients or when cellular immunity becomes compromised, the level of T-cell function decreases until it falls below a threshold that is associated with inadequate containment of VZV reactivation and the subsequent development of herpes zoster
Immunocompromise due to disease or use of immunosuppressive medications
Cancer, human immunodeficiency virus (HIV) infection, organ or bone marrow transplantation, and chronic intake of immunosuppressive medications predispose patients to have poor cell-mediated immunity and, thus, develop herpes zoster
Immunocompromised patients are 20 times more likely to develop herpes zoster than immunocompetent patients. They are also more likely to have more diffuse involvement, severe skin lesions, increased severity and duration of pain, and atypical manifestations
Emotional and psychological stress
Emotional stress, such as bereavement, may be associated with the development of herpes zoster within 6 months after the stressful life event
Long-term stress may alter the immune system, and specific VZV cellular immunity is lower among adults with major depression
Believed to stimulate the nervous system, thus triggering reactivation of dormant VZV in the dorsal root ganglion