A 67-year-old man who has been in generally good health begins to experience fever, headache, and malaise, along with persistent pain in the area of his left thorax. Four days later, a rash consisting of a broad band of erythematous maculopapules develops along the center of his left thorax. The maculopapules evolve into vesicles and pustules over the next 36 hrs. The vesicles have an erythematous base, are cloudy, and vary in size. The man continues to experience severe pain in the area where the rash is occurring, so he comes to your office to seek advice.

Question 9.1: What should you ask this man?

This looks to be a classic case of herpes zoster, commonly known as shingles, which is basically a localized recurrence of chicken pox. Therefore, you want to know if the man had chicken pox when he was younger. In this case, it turns out that, like most people in his age group, the patient did have chicken pox when he was a young child.

Question 9.2: What is the causative agent?

The causative agent of shingles is the varicella zoster virus (VZV), which causes chicken pox the first time it infect a particular individual. VZV is a member of the herpesvirus family. Like the other members of this family, it has a double-stranded DNA genome, a glycoprotein-containing envelope, and an icosadeltahedral capsid.

Question 9.3: How does the disease develop?

Following the initial infection that results in chicken pox, VZV becomes latent in the dorsal root or cranial nerve ganglia. The virus can be reactivated in older adults (highest incidence in individuals in the sixth through the eighth decades of life) or in patients with impaired cellular immunity (e.g., AIDS victims). The factors responsible for reactivation of the virus are not known. On reactivation, the virus replicates and is released along the neural pathways to the skin, where the characteristic rash is produced (generally affecting one dermatome) as the virus replicates in the cutaneous tissue. The dermatomes from T3 to L3 are most frequently involved. The continuum of pain from onset to resolution of the infection is known as zoster-associated pain.

Question 9.4: Are there any specialized forms of this disease?

When branches of the trigeminal nerve are involved, lesions may appear on the face, in the eyes, in the mouth, or on the tongue. Involvement of the ophthalmic branch of the trigeminal nerve results in zoster ophthalmicus. Involvement of the geniculate ganglion of the sensory branch of the facial nerve leads to Ramsay Hunt syndrome, in which pain and vesicles develop in the external auditory canal, and patients lose their sense of taste in the anterior two-thirds of the tongue while developing ipsilateral facial palsy. Tinnitus, hearing loss, and/or vertigo may also occur. Recurrent shingle is possible, but it is exceedingly rare, except in immunocompromised patients (especially AIDS victims).

Question 9.5: How is the diagnosis confirmed?

Laboratory tests usually aren't required for diagnosis of shingles. Unilateral vesicular lesions in a dermatomal pattern almost always indicate a case of shingles. The differential includes rashes caused by herpes simplex virus and a couple of other viruses, but the lesions in those diseases are typically more uniform in size. If deemed necessary, the diagnosis can usually be confirmed by fluorescent staining of skin scrapings with monoclonal antibodies.

Question 9.6: How should you treat this case?

Victims of herpes zoster benefit from oral antiviral therapy, as evidenced by accelerated healing of lesions and resolution of zoster-associated pain with acyclovir, valacyclovir, and famciclovir. Acyclovir, which is now off patent, is administered at a dosage of 800 mg five times daily for 7-10 days. Famciclovir is at least as effective as acyclovir (possibly more so). The dose is 500 mg orally three times daily for 7 days. Valcyclovir accelerates healing and resolution of pain noticeably more promptly than acyclovir. The dose is 1 g orally three times daily for 5-7 days.