Thursday, December 4, 2008 - 10:02PM EST

Introduction to Shingles

Shingles, also called Herpes Zoster, is an outbreak of rash or blisters on the skin that is caused by the same virus that causes chickenpox - the varicella-zoster virus (VZV). The varicella-zoster virus is now recognized as one of the eight herpes viruses that infect humans. The varicella-zoster virus is closely related to herpes simplex virus (HSV) types 1 and 2, however, it has become clear that the varicella-zoster virus is distinct from the herpes simplex virus both in its biology and in its clinical behavior.

Shingles results from reactivation of the varicella-zoster virus that was acquired during a primary varicella infection (chickenpox) - which usually occurs in childhood after exposure to the airborne virus. Therefore, anyone who has had chickenpox is at risk for shingles later in their life, and, whereas varicella is generally a disease of childhood, shingles becomes more common with increasing age.

It is thought that during the initial chickenpox outbreak, some of the virus invades the nervous system. The virus remains inactive (latent) for decades, living in the nerves. For reasons that are as yet unknown, the virus may reactivate in later years, then travels down the sensory nerve and erupts as a painful rash on the skin (shingles).

A dermatome is the area of skin that is supplied by a single nerve branching off the spine. The spinal nerves supply the entire body in slice-like sections (8 cervical sections, 12 thoracic sections, 5 lumbar sections, and 5 sacral sections). The varicella-zoster virus usually lives and erupts within one of these dermatomes only and does not cross the midline of the body. The most frequently affected are the thoracic (torso) and cranial (face/head) dermatomes. When the virus erupts in more than one dermatome, it is said to be disseminated.

Dissemination is defined as more than 20 vesicles outside the primary and immediately adjacent dermatomes. In persons with compromised immune systems, the risk of dissemination is approximately 40%. Dissemination on the skin is followed by involvement of the lungs, liver, or brain in 10% of these high-risk persons.

Although shingles is not as contagious as chickenpox, people with reactivated infection can transmit varicella-zoster virus to non-immune contacts. Therefore, patients with shingles should avoid contact with those who have never had chickenpox and women who are pregnant until the rash is resolved.

Primary infection with varicella-zoster virus has traditionally caused about 4 million cases of chickenpox each year (mostly in children). Reactivation occurs in 15% of cases causing shingles later in life. It is unusual for people with competent immune systems to develop shingles more than once, which suggests that the first reactivation provides further immunological protection.

Nearly every adult in the United States today has experienced chickenpox in their past, although this will change over time following the introduction of a vaccine in 1995. Although the complication rate in healthy children is low, the previous high rate of disease accounted for significant varicella-related mortality and morbidity. In the pre-vaccine era, there were about 4 million cases of varicella annually in the United States, with 100 deaths (mostly in otherwise healthy individuals, and despite the availability of antiviral therapy) and 11,000 hospitalizations. Most varicella-zoster virus infection results in a clinical illness, but about 5% of primary infections are subclinical (no detectable symptoms).