Shingles: a disease on the rise

My lovely shingles rash
My lovely shingles rash

I caught the chickenpox when I was in elementary school. It was circa 1980. There was not yet a vaccine against chickenpox, and the disease was spreading through my school classroom at a fast pace. I remember sitting in the gym for an assembly, and my friend next to me was picking at a blister-like lesion on her leg. Days later similar lesions began popping up on my skin and I was diagnosed with chickenpox. I earned a week off of school. I had a very mild case, ten lesions total, if that. I can almost remember exactly where each one was located. I didn’t have a fever or feel sick, I just knew that the blisters meant that I was contagious and so I sat home. Unfortunately, I infected my younger sister, and a week later she came down with chickenpox… BAD. They covered her entire body: in her hair, down her throat, under her arm pits, in the creases of skin between her legs and hips. She was a miserable, sore, itchy mess. Even though we caught the same virus, our experiences were light years apart.

Three decades later, this minor inconvenience of a virus resurfaced with a much bigger impact: shingles (also called herpes zoster). I was at work when my left shoulder suddenly felt like it was on fire, like I had developed a really bad sunburn. Three days later I noticed small, red marks on my shoulder. The next morning these spots had gotten bigger and spread to my neck, chest, and back. It was now obvious that I had shingles.

The culprit behind both chickenpox and shingles is a human herpesvirus called varicella zoster virus (VZV). [Side note: there are 8 human herpesviruses. When most people hear the word “herpes” they immediately think of herpes simplex virus (HSV) types 1 or 2, which cause oral cold sores and genital lesions, respectively. However, the other 6 human herpesviruses are VZV, Epstein-Barr virus (which causes mononucleosis), human cytomegalovirus, human herpesvirus-6 (HHV-6), HHV-7, and Kaposi’s sarcoma-associated herpesvirus.] When a person is first infected with VZV, the disease manifests as chickenpox, causing a blister-like rash, itching, tiredness, and fever. It spreads easily from person-to-person through the air by coughing or sneezing; it can also be spread by touching the chickenpox blisters. A person is infectious from a few days before the appearance of the rash until all the blisters have developed scabs.

However, once the disease has run its course, that is not the end of the virus. Like all herpesviruses, VZV remains within its host for life. The virus sets up a latent (dormant) infection in nerve cells. During this time of latency, there are no clinical symptoms. Due to as-yet-undetermined factors (stress, old age, and weakened immune systems are thought to play roles), years later the virus becomes activated once more and manifests as shingles. New viral particles are produced and travel along the nerves to the skin and once again form blister-like lesions. Unlike chickenpox lesions, shingles lesions are confined to the area of the infected nerve cells. Usually they appear in a swath along a person’s abdomen, shoulder, leg, neck, or face. In some cases VZV even infects an eye. The lesions appear only on one side of the body (following the path of the affected nerve).

My own shingles rash was on my left shoulder and the left side of my neck, up into my hairline (see photo). One of my symptoms was a terrible earache from the lesions surrounding my left ear. A few lesions also appeared down my left arm towards my elbow. A person suffering through a case of shingles cannot pass shingles on to someone else – what they can pass on is chickenpox to someone who either 1) was not vaccinated, or 2) never had chickenpox themselves. VZV produced from shingles is usually not airborne and requires contact with virus released from the blisters to pass the infection from person-to-person. Like chickenpox, once the lesions scab over the person is considered non-infectious.

Because the virus is emerging from nerve cells, shingles rashes are much more painful than those from chickenpox. Treatments for those with shingles include antiviral medicines (acyclovir, famciclovir, valacyclovir) to reduce the pain and the duration of the disease. Over-the-counter medicines such as acetaminophen or ibuprofen, or even prescription medicines such as Vicodin or Percocet, can also be used to manage the pain. It is important to begin treating shingles with antivirals as soon as it is diagnosed, as these medicines also decrease the chances of shingles-related complications.1

One such complication is post-herpetic neuralgia, pain due to nerve damage by the virus. Typically, this pain lasts only for a few weeks, but for an unlucky few it can last months or years. For me, even though I started taking antivirals as soon as my rash appeared, I still developed post-herpetic neuralgia. It’s been two years since my shingles outbreak and I still get periodic numbness in my left shoulder, as well as a tingling sensation that is more annoying than painful. For some people with post-herpetic neuralgia, the pain is much more intense and their quality of life can suffer. Other complications from shingles include scarring, loss of vision (if an eye is infected), palsy, and secondary bacterial infections.

Roughly 1/3 of those who had previously had chickenpox will develop shingles later in life. However, over the past few decades there has been a steady rise in the number of shingles cases in the United States and other countries.2 When Medicare claims data from 1992-2010 (which included 2.8 million people over the age of 65) were analyzed, it was found that the annual rate of shingles increased 39% over the 18-year study period.3 In fact, shingles is increasing for all age groups except one: people 17 and younger. This group is most likely to have been immunized against chickenpox, and are nearly 5x less likely to get shingles than those who have contracted wild-type chickenpox.4 However, because the chickenpox vaccine has only been available in the USA for about 20 years, it remains to be seen if the vaccine will protect young people from shingles as they age.

Still, is the chickenpox vaccine indirectly responsible for the increase in shingles cases? Maybe the reason we are seeing an increase in shingles is because we have greatly decreased wild-type chickenpox through our childhood vaccination program. Perhaps exposure to wild-type chickenpox in the pre-vaccine era (parents and grandparents coming into contact with pox-y kids) “reminded” our immune systems of the virus lurking within and helped to keep it at bay… like a natural booster shot. Although this is a popular hypothesis, the data seems to disprove it. The increase in the rate of shingles started prior to the introduction of the vaccine, and did not vary between states where there were different rates of chickenpox vaccine uptake.3,5

So, continue to get your kids vaccinated against chickenpox. Eventually, as these vaccinated kids get older, there will be less and less shingles cases and hopefully shingles will become a thing of the past. Until then, adults who are aged 60 and older should receive the shingles vaccine (this vaccine is a more potent form of the chickenpox vaccine, and is recommended even if one doesn’t remember getting chickenpox as a child).6 The shingles vaccine reduces the risk of shingles by about 50% and the risk of post-herpetic neuralgia by 67%. Although most health insurance plans cover the vaccine for people 60 years of age or older, the vaccine has been approved by the Food and Drug Administration for anyone over age 50. Personally, I hope that this age restriction is eventually lifted; the shingles vaccine might have saved me from a week of pain, ongoing shoulder numbness and increased risk of stroke.7

References/ Further Reading
1. http://www.cdc.gov/shingles/about/prevention-treatment.html

2. Kawai K, Gebremeskel BG, Acosta CJ. 2014. Systematic review of incidence and complications of herpes zoster: towards a global perspective. BMJ. Published online: DOI: 10.1136/bmjopen-2014-004833.

3. Hales CM, Harpaz R, Joesoef MR, Bialek SR. 2013. Examination of links between herpes zoster incidence and childhood varicella vaccination. Ann Intern Med. 159:739-745.

4. Weinmann S, et al. 2013. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, 2005-2009. J Infect Dis. 208:1859-1868.

5. http://consumer.healthday.com/senior-citizen-information-31/misc-aging-news-10/chickenpox-vaccine-isn-t-responsible-for-rise-in-shingles-study-sayse-682609.html

6. http://www.cdc.gov/vaccines/vpd-vac/shingles/vacc-need-know.htm1

7. Breuer J, et al. 2014. Herpes zoster as a risk factor for stroke and TIA: a retrospective cohort study in the UK. Neurology. Published online: DOI: 10.1212/WNL.0000000000000038.

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