Chickenpox, herpes zoster, and understanding the shingles vaccine

Chickenpox was all the rage back in the day.  Oatmeal baths with your siblings, unexplained weekday sleep-overs with pox-laden, peripheral childhood friends.  Even the sweet but short-lived relief of itching and scratching made the week-long infectious endeavor, if anything, a pleasant respite from the doldrums of early childhood.

Unfortunately for a handful of us unsuspecting chickenpox veterans, the infection that we so fondly include in our potpourri of childhood nostalgia will someday shape-shift into our most evil adulthood nemesis: shingles.

Whereas chickenpox is a household concept to many of us (at least to those of us who missed out on the varicella vaccine introduced to the U.S. in 1995), shingles occur much less frequently and often much later in life.

That being said, it’s worth covering the topic of shingles, not only because of it’s fascinating clinical presentation, but also because of the fact that diagnosing it and thus treating the condition earlier can shorten its duration and help prevent its potential complications.

Varicella zoster virus

To understand shingles, one must understand the virus that causes it.

Both chickenpox (varicella) and shingles (herpes zoster) are both manifested from a single virus: the varicella zoster virus (VZV).  This virus is unique in that it has the capacity to cause two very distinct forms of clinical disease in the same infected person throughout his or her lifetime.

VZV is a highly contagious virus and transmission occurs both via indirect contact with aerosolized droplets and by direct contact with someone experiencing chickenpox.

According to the NIH Conference on VZV some years ago, an individual without prior exposure to VZV has over a 90% chance of becoming infected with the virus if they live in the same household with someone with active chickenpox.

Chickenpox is the hallmark disease that occurs as a result of a primary infection of VZV.  While this predominantly childhood condition is an interesting subject in itself, the remarkable part of the evolution of a VZV infection really occurs in the events that follow.

From chickenpox to shingles

Although the memory of having chickenpox was not an unpleasant one, the actual skin findings of chickenpox are pretty nasty; red, fluid-filled mini-blisters from head-to-toe that itch like crazy.  What’s worse is knowing that the fluids in these vesicles are chock-full of replicating VZV.  From these vesicles, the virus makes way to the skin’s nerve endings, travels down deep into the body’s nervous system, and settles there for the duration of the infected host’s lifetime.  Admittedly, a foul and unsettling notion.

This asymptomatic stage of the infection is called the latent stage, where the virus remains relatively dormant for years and years without producing any clinical signs of disease.  Fortunately, the majority of VZV-infected individuals out there will live the rest of their lives unperturbed by this uninvited live-in guest.

Nevertheless, as is the potential for any unscreened roommate to wreak havoc at the homestead, a good percentage of us will experience quite the falling out with this virus once it reactivates into an active infection known as shingles.

You have shingles

Once fully expressed, the clinical characteristics of a classic case of shingles are so identifiable that often no lab test is needed to make the diagnosis.

Here’s a quick summary of the most common presentation of shingles:

  • Most patients with reactivated VZV will experience days to weeks of burning pain in the area of affected skin prior to the typical rash.
  • Within 3-4 days, a blistery, infectious and painful rash emerges in a very unique distribution on the skin.  The rash typically presents itself on only one of half of the body, and these streaky patches correspond with discreet areas of skin that are often innervated by a single infected nerve root. Commonly, these rashes form on the chest and/or back but can present anywhere on the body.
  • After a week or so of this angry-looking rash, the vesicles begin to crust over, become less painful, and are no longer infectious

Sounds awful.

So are all of us with a history of chickenpox at risk for shingles?

Don’t shoot the messenger, but yes.

According to a 2006 report conducted by the Advisory Committee on Immunization Practices (ACIP), up to 32% of us will experience shingles at some point within our lifetimes.

Although anyone at any age with a post-primary VZV infection can get shingles, individuals that suffer from immune problems are at a much higher risk for VZV reactivation.  This is due to the fact that their immune systems have more trouble suppressing the infection than those with normal immune function.

Along this same line of reasoning, the geriatric population is also at a higher risk for reactivation due to the physiologic waning of VZV-specific immunity.

Take home point

Most episodes of shingles, albeit painful and less than pleasing to the eye, are self-limiting.  Nevertheless, complications (prolonged pain syndromes, secondary bacterial infections, even loss of vision if the rash extends to the eye) are not uncommon, and practitioners should be quick to treat shingles with at least a solid week of antiviral therapy to help prevent these complications from occurring.

For those of you 50 years and older, I will end this pseudo-public awareness piece with some good news: A herpes zoster vaccination is currently available that, when administered appropriately, can significantly reduce your chances of getting shingles.

Trust me, it’s worth a shot.

Brian J. Secemsky is an internal medicine resident who blogs at The Huffington Post.  He can be reached on Twitter @BrianSecemskyMD.

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