Herpes zoster is a painful, blistering skin eruption in a dermatomal distribution. After primary infection with varicella (ie, chicken pox), the virus persists asymptomatically in the ganglia of sensory cranial nerves and spinal dorsal root ganglia. As cellular immunity to VZV decreases with age or because of immunosuppression, the virus reactivates and travels along the sensory nerves to the skin, causing the distinctive prodromal pain followed by eruption of the rash. It is estimated that approximately 1 in 3 people will develop HZ during their lifetime, resulting in an estimated 1 million episodes in the United States annually.2
Herpes zoster can occur at any age but is generally less severe in children and young adults, with the greatest morbidity and mortality seen in older adults and in immunocompromised patients. A recent population-based study in Olmsted County, Minnesota, found that the incidence of HZ was 3.6 per 1000 patient-years. 3
In that study, the incidence of HZ and the rate of HZ-associated complications increased with age, with 68% of cases occurring in those aged 50 years and older. Prodromal symptoms that herald HZ include pruritus, dysesthesia, and pain along the distribution of the involved dermatome. This pre-eruptive pain may precede the rash by several days and may be mistaken for myocardial infarction, biliary or renal colic, pleurisy, dental pain, glaucoma, duodenal ulcer, or appendicitis, leading to misdiagnosis and potentially mistreatment. In rare instances, the nerve pain is not accompanied by a skin eruption, a condition known as zoster sine herpete
. The classic skin findings are grouped vesicles on a red base in a unilateral, dermatomal distribution (). However, the lesions of HZ progress through stages, beginning as red macules and papules that, in the course of 7 to 10 days, evolve into vesicles and form pustules and crusts (scabs) (). Complete healing may take more than 4 weeks.
The classic skin findings of herpes zoster are grouped vesicles on a red base in a unilateral, dermatomal distribution.
FIGURE 2. The lesions of herpes zoster progress through stages, beginning as red macules and papules that, in the course of 7-10 days, evolve into vesicles and form pustules and crusts (scabs). A common site is the distribution of the ophthalmic division of the (more ...)
The localization and distribution of the skin findings are distinctive. Typically, HZ is unilateral, does not cross the midline, and is localized to a single dermatome of a single sensory ganglion (adjacent dermatomes are involved in 20% of cases).4
The most common sites are the thoracic nerves and the ophthalmic division of the trigeminal nerve. Herpes zoster ophthalmicus, which occurs in 10% to 20% of HZ episodes,5
can involve the entire eye, causing keratitis, scarring, and vision loss. An early sign of this condition is vesicles on the tip, side, or root of the nose (Hutchinson sign). Herpes zoster of the second and third divisions of the trigeminal nerve may produce symptoms and lesions in the
mouth, ears, pharynx, or larynx. Ramsay Hunt syndrome, ie, facial paralysis and lesions of the ear (zoster oticus) that are often accompanied by tinnitus, vertigo, and deafness, results from involvement of the facial and auditory nerves. Some cases of Bell palsy may be a form of zoster sine herpete.
Disseminated HZ occurs primarily in immunocompromised patients; it usually presents with a dermatomal eruption followed by dissemination but may also present with a diffuse varicella-like eruption. Systemic dissemination may accompany the skin changes with involvement of the lung, liver, and brain. Visceral dissemination is associated with a mortality rate of 5% to 15%, with most deaths attributable to pneumonia.6,7
The neurologic complications of HZ may include acute or chronic encephalitis, myelitis, aseptic meningitis, polyradiculitis, retinitis, autonomic dysfunction, motor neuropathies, Guillain-Barré syndrome, hemiparesis, and cranial or peripheral nerve palsies.8,9
More common complications include bacterial superinfection by Staphylococcus aureus
or Streptococcus pyogenes
, scarring, and hyperpigmentation.
Herpes zoster is usually diagnosed clinically by the prodromal pain, characteristic rash, and distinctive distribution. However, a group of vesicles, especially if located by the mouth or genitals, can represent other possibilities. The differential diagnosis for HZ includes herpes simplex virus, impetigo, candidiasis, contact dermatitis, insect bites, autoimmune blistering disease, dermatitis herpetiformis, and drug eruptions. Although shell vial viral culture remains the criterion standard test with which other diagnostic tests are compared, detection of viral DNA by polymerase chain reaction, when available, is the most useful test because it is sensitive and specific and results can be obtained within a few hours.10
Other tests that can be used to support the diagnosis are direct fluorescent antibody staining, immunoperoxidase staining, histopathology, and Tzanck smear.
Herpes zoster lesions contain high concentrations of VZV, which can be spread by contact and by the airborne route and which can cause primary varicella in exposed, susceptible persons. Less contagious than primary varicella, HZ is only contagious after the rash appears and until the lesions crust.11
Risk of transmission is reduced further if lesions are covered.