Clinical Overview

Cause

Herpes zoster, also known as shingles, is caused by reactivation of varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox).

Primary infection with VZV causes varicella. After a person has varicella, the virus remains latent in the dorsal root ganglia. VZV can reactivate later in a person’s life and cause herpes zoster, a painful maculopapular and then vesicular rash.

Clinical Features

People with herpes zoster most commonly have a rash in one or two adjacent dermatomes. The rash most commonly appears on the trunk along a thoracic dermatome or on the face and it usually does not cross the body’s midline.

The rash is usually painful, itchy, or tingly. A person can experience the following symptoms several days before the rash appears:

• Headache
• Photophobia (sensitivity to bright light)
• Malaise

The rash develops into clusters of vesicles. New vesicles continue to form over 3 to 5 days, and the rash progressively dries and scabs over. The rash usually heals in 2 to 4 weeks. Permanent skin discoloration and scarring can occur.

Complications

Postherpetic neuralgia (PHN)

PHN is the most common complication of herpes zoster. PHN is pain that persists in the area where the rash once was located and continues more than 90 days after rash onset. PHN can last for months or even years.

A person’s risk of having PHN after herpes zoster increases with age. Older adults are more likely to have longer lasting, more severe pain. Approximately 10% to 18% of people with herpes zoster will have PHN. PHN is rare in people younger than 40 years old. The likelihood of PHN is also higher in people who experience more pain with the rash or have a large rash.

Herpes zoster ophthalmicus

Herpes zoster that affects the ophthalmic division of the trigeminal nerve is called herpes zoster ophthalmicus. This can result in acute or chronic ocular sequelae, including vision loss.

Disseminated zoster

Disseminated zoster can include generalized skin eruptions where the lesions occur outside of the primary or adjacent dermatomes. It can be difficult to distinguish from varicella. Visceral involvement of the central nervous system (meningoencephalitis), lungs (pneumonitis), and liver (hepatitis) can also occur. Disseminated zoster generally occurs in people with compromised or suppressed immune systems.

People with compromised or suppressed immune systems are more likely to have a severe, long-lasting rash and experience more severe complications from herpes zoster.

Vaccination

Recombinant zoster vaccine (RZV, Shingrix) is the recommended vaccine to prevent shingles and related complications. For information about vaccination recommendations see Shingles Vaccination.

Transmission

People with active herpes zoster lesions can spread VZV , which causes varicella in people who never had varicella or never received varicella vaccine. Once varicella resolves, these people would be at risk for herpes zoster.

Active herpes zoster lesions are infectious through direct contact with vesicular fluid or through breathing in virus particles from the blisters until they dry and scab over. People with active herpes zoster lesions should cover their lesions and avoid contact with susceptible people in their household and in occupational settings until their lesions are dry and scabbed.

Also see Managing People at High Risk for Severe Varicella and Preventing VZV Transmission from Herpes Zoster in Healthcare Settings

 Top of Page

Epidemiology

Risk Factors

Anyone who had varicella can develop herpes zoster. Approximately 99.5% of people born before 1980 in the United States were infected with wild-type VZV. Children who receive varicella vaccine have a lower risk of herpes zoster compared with children who were infected with wild-type VZV.

Approximately 1 in 3 people in the United States will develop herpes zoster during their lifetime. Most people have only one episode; however, herpes zoster can recur.

A person’s risk for herpes zoster and related complications sharply increases after 50 years of age. The reasons why VZV reactivates and causes herpes zoster are not well understood. However, a person’s risk for herpes zoster increases as their VZV-specific cell-mediated immunity declines. This decline in immunity can result from increasing age and medical conditions or medications that suppress a person’s immune system. People with the following conditions that compromise or suppress their immune system have an increased risk for herpes zoster:

• Bone marrow or solid organ (renal, cardiac, liver, and lung) transplant recipients
• Cancer, especially leukemia and lymphoma
• Human immunodeficiency virus (HIV)
• Taking immunosuppressive medications, including steroids, such as for treatment of autoimmune diseases and other immune system deficiencies

Other potential risk factors for herpes zoster have been identified, but the findings are either inconsistent or unexplained. For example:

• More women than men develop herpes zoster.
• Herpes zoster is less common in Blacks than in Whites.

Disease Rates

An estimated one million cases of herpes zoster occur annually in the United States.

• The incidence of herpes zoster varies by age and is approximately 2–9 cases per 1,000 US population annually.

The precise incidence of recurrence is not known.

Complications

• Approximately 10% to 18% of people with herpes zoster will have PHN.
• Approximately 1% to 4% of people with herpes zoster are hospitalized for complications.
• Older adults and people with compromised or suppressed immune systems are more likely to be hospitalized. About 30% of people hospitalized with herpes zoster have compromised or suppressed immune systems.

Deaths

One study estimated 96 deaths occur each year where herpes zoster was the underlying cause (0.28 to 0.69 per 1 million population). Almost all the deaths occurred in older adults or those with compromised or suppressed immune systems.

Trends

Herpes zoster rates among adults in the United States gradually increased over a long period of time. We do not know the reason for this increase. However, the rates across age groups have recently plateaued or declined.

CDC studies have found that herpes zoster rates started increasing before varicella vaccine was introduced in the U.S. and did not accelerate after the routine varicella vaccination program started.

Herpes Zoster in People Who Received Varicella Vaccine

Varicella vaccines contain live attenuated VZV, which results in latent infection. Although herpes zoster has always been uncommon among children, the rate of herpes zoster in U.S. children has declined since the routine varicella vaccination program started in 1996.

• Children (healthy and immunocompromised) vaccinated against varicella have lower rates of herpes zoster compared to children who had natural infection with varicella.
  • Vaccinated children are less likely to become infected with wild-type VZV.
  • The risk of reactivation of vaccine-strain VZV in children is lower compared with reactivation of wild-type VZV.
• Few older adults have received the varicella vaccine since it was licensed in 1995. There is very little information on the risk of herpes zoster in people who got varicella vaccine as adults.

CDC continues to monitor the impacts of the U.S. varicella and herpes zoster vaccination programs among adults and children.

References

1. CDC. Use of Recombinant Zoster Vaccine in Immunocompromised Adults Aged ≥19 Years: Recommendations of the Advisory Committee on Immunization Practices — United States, 2022. MMWR Recomm Rep. 2022;71(3):80-84.
2. Leung et al. The Impact of Universal Varicella Vaccination on Herpes Zoster Incidence in the United States: Comparison of Birth Cohorts Preceding and Following Varicella Vaccination Program Launch. Journal of Infection Diseases. 2022.
3. Harpaz and Leung. The Epidemiology of Herpes Zoster in the United States During the Era of Varicella and Herpes Zoster Vaccines: Changing Patterns Among Older Adults. Clin Infect Dis.2019;69(2):341-344.
4. CDC. Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP) Recommendations for use of Herpes Zoster Vaccines. MMWR Recomm Rep. 2018;67(03):103-108.
5. Thomas SL, Hall AJ. What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis. 2004;4(1):26-33.
6. Tseng HF, Smith N, Harpaz R, et al. Herpes zoster vaccine in older adults and the risk of subsequent herpes zoster disease. JAMA. 2011;305(2):160-6.
7. Mahamud A, Marin M, Nickell SP, et al. Herpes zoster-related deaths in the United States: validity of death certificates and mortality rates, 1979-2007. Clin Infect Dis.2012;55(7):960-6.
8. Leung J, Harpaz R, Molinari NA, et al. Herpes zoster incidence among insured persons in the United States, 1993-2006: evaluation of impact of varicella vaccination. Clinical Infectious Diseases. 2011;52(3):332-340.
9. Yih W, Brooks D, Lett S, et al. The Incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage. BMC Public Health. 2005;5(68).
10. Jumaan AO, Yu O, Jackson LA, et al. Incidence of herpes zoster, before and after varicella vaccination-associated decreases in the incidence of varicella. Journal of Infectious Diseases. 2005;191:2002-7.
11. Hales CM, Harpaz R, Joesoef MR, Bialek SR. Examination of links between herpes zoster incidence and childhood varicella vaccination. Annals of Internal Medicine. 2013;159(11):739-45.
12. Russell ML, Dover DC, Simmonds KA, Svenson LW. Shingles in Alberta: before and after publicly funded varicella vaccination. Vaccine. 2014;32(47):6319-24.
13. Weinmann S, Chun C, Schmid DS, et al. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, 2005–2009. Journal of Infection Diseases. 2013;208(11):1859-68.
14. Hardy I, Gershon AA, Steinberg SP, LaRussa P. The incidence of zoster after immunization with live attenuated varicella vaccine. A study in children with leukemia. Varicella Vaccine Collaborative Study Group. N Engl J Med. 1991;325(22):1545-50.

 Top of Page