A 75-year-old woman presented with a severely painful case of herpes zoster in a lower abdominal/lower extremity distribution. Groups of vesicles were becoming bullae and leading to erosions (Figure 130-1). The woman was treated with oral analgesics and an oral antiviral medication. Her primary care physician treated her zoster aggressively in an attempt to prevent postherpetic neuralgia (PHN).
A 75-year-old woman with severe case of herpes zoster in a lower abdominal/lower extremity distribution. A. Note the erosions on the upper thighs in addition to the vesicles and bullae. B. Close-up of the zoster lesions showing grouped vesicles and bullae on a red base. (Reproduced with permission from Richard P. Usatine, MD.)
Herpes zoster (shingles) is a syndrome characterized by a painful, usually unilateral vesicular eruption that develops in a restricted dermatomal distribution (Figures 130-1 and 130-2).1-3
Herpes zoster on the back of a young woman. Note the grouped vesicles on a red base. Some of the vesicles cross the midline as there is some cross-innervation of the spinal sensory nerves on the back. (Reproduced with permission from Richard P. Usatine, MD.)
According to the Centers for Disease Control and Prevention (CDC), 32% of persons in the United States 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% of patients will experience a second episode of herpes zoster.5
More zoster cases have been observed among women, even when controlling for age.6
Herpes zoster occurs more frequently and more severely in immunosuppressed patients, including transplantation patients.
ETIOLOGY AND PATHOPHYSIOLOGY
After primary infection with either chickenpox or vaccine-type varicella-zoster virus (VZV), a latent infection is established in the sensory dorsal root ganglia. Reactivation of this latent VZV infection results in herpes zoster (shingles).
Both sensory ganglia neurons and satellite cells surrounding the neurons serve as sites of VZV latent infection. During latency, the virus expresses only a small number of viral proteins.
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
Loss of VZV-specific cell-mediated immune response is responsible for reactivation.3
The pain associated with zoster infections and PHN is thought to result from injury to the peripheral nerves and altered central nervous system processing.
The most common complications are PHN and bacterial superinfection that can delay ...