CE/CME

Herpes Zoster Infection

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Herpes zoster (HZ) infection, commonly called shingles, represents a reactivation of the chickenpox virus. Persons older than 50 and those with compromised immune systems are at greatest risk. Most cases resolve spontaneously, but about one-third of patients develop postherpetic neuralgia or other complications, and 1% to 4% require hospitalization. Treatment involves antiviral medications and 
pain management. Vaccination against HZ, which is recommended for adults 60 and older, 
incurs benefits and risks that the clinician must be prepared to explain to eligible patients.

Infection with herpes zoster (HZ) affects approximately one million individuals in the United States each year.1-3 The disease is caused by a reactivation of the varicella zoster virus (VZV), which causes chickenpox. Once chickenpox has resolved, VZV remains dormant in the dorsal (spinal) root ganglia, trigeminal nerve, and autonomic ganglia of the nervous system.4 At some later time, VZV may reactivate, causing an extremely painful vesicular rash along the distribution of one or more sensory dermatomes; the rash (as well as the condition in general) is commonly referred to as shingles.

It has been estimated that 90% or more of US adults older than 40 are infected with VZV.1,3 Because the virus is so ubiquitous, virtually anyone may be at risk for the reactivation of VZV in the form of shingles. It is estimated that 10% to 20% of the US population will develop HZ in their lifetime,3 with age and immune status the most significant determinants of persons to be affected.3-6

About half of all cases of shingles in the US occur in persons age 50 or older. Incidence among those older than 75 is approximately 10 cases per 1,000 individuals, compared with about two cases per 1,000 individuals in those younger than 50.3

In addition to age, the integrity of an individual’s immune system plays a key role in the development of shingles. Reactivation of VZV is usually suppressed by the host’s cell-mediated immune response, particularly the T cells.3,5 Thus, if the cell-mediated immune system is compromised, reactivation and widespread dissemination are more likely to occur. Adults with cancer or HIV infection and those taking immunosuppressive drugs have a significantly increased risk for HZ. Psychological or physical stress and trauma have also been shown to play a role in the development of HZ.5 In contrast to chickenpox, HZ has no seasonal predilection.7

Since 1995, with the licensing of Varivax (the vaccination to prevent varicella), the incidence of wild-type varicella infection is now quite low in the US. From 2000 to 2010, varicella wild-type infection declined by 82%.8 Efforts to further quantify the incidence of varicella have been hampered by the absence of reporting requirements for this infection.

Due to the live nature of the Varivax vaccine, patients who have received it remain at risk for HZ infection by way of reactivation of vaccine-type VZV. A population-based surveillance study conducted in California from 2000 to 2006 showed that the incidence of HZ infection decreased by 55% in children 10 years or younger who were vaccinated against varicella.9 This finding, along with similar results in other, older research in immunocompromised hosts, supports the notion that the risk for HZ is substantially reduced among children who have been vaccinated against varicella.10

Incidence of HZ infection seems to be on the rise, both in the US and worldwide1; however, the causes for this are a point of controversy. Fears have been expressed that incidence of HZ infection in adults would increase once varicella vaccination in children became commonplace, based on reasoning that exposure to the virus (which is thought to boost cell-mediated immunity and keep the virus from reactivating) would decline. This concern has put a halt to vaccination against varicella in some European countries.11 At least one US researcher considers the evidence strong for a causal link between the increase in incidence of HZ and the widespread implementation of varicella vaccination.12

Other research has led to different conclusions. Authors of a nationwide, retrospective review of claims data noted an increase in HZ prior to Varivax licensure but did not find any association between vaccination rates and HZ rates geographically.13 Similarly, researchers conducting a case-control study in a Wisconsin clinic found no relationship between HZ and exposure to VZV in the previous 10 years.14

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