Herpes Zoster

Herpes zoster (or simply zoster), commonly known as shingle and also known as zona, is a viral
disease characterized by a painful skin rash with blisters in a limited area on one side of the body,
often in a stripe. The initial infection with varicella zoster virus (VZV) causes the acute (short-lived)
illness chicken pox, which generally occurs children and young people. Once an episode of
chickenpox resolved, the virus is not eliminated from the body but can go on cause shingles- an
illness with very different symptoms-often may years after the initial infection. Herpes zoster is not
the same disease as herpes simplex virus despite the name similarity (both the varicella zoster virus
and herpes simplex virus belong to the same viral subfamily Alphaherpesvirinae).

Varicella zoster virus can become latent in the nerve cell bodies and less frequently in non-neuronal
satellite cells of dorsal root, cranial nerve or autonomic ganglion, without causing any symptoms.
Years or decades after a chickenpox infection, the virus may break of nerve cell bodies and travel
down nerve axons to cause viral infection of the skin in the region of the nerve. The virus may
spread from one or more ganglia along nerves of an affected segment and infect the corresponding
dermatome (an area of the skin supplied by one spinal nerve) causing a painful rash. Although the
rash usually heals within two to four weeks, some sufferers experience residual nerve pain for
months or years, a condition called postherpetic neuralgia.

Clinical Presentation

The earliest symptoms of herpes zoster, which include headache fever, and malaise, are nonspecific,
and may result in an incorrect diagnosis. These symptoms are commonly followed by sensations of
burning pain, itching, hyperesthesia (oversensitivity), or paresthesia ("pins and needles": tingling,
pricking, or numbness). The pain may range mild to extreme in the affected dermatome, with
sensations that are often described as stinging, tingling, aching, numbing or throbbing, and can be
interspersed with quick stabs of agonizing pain. Herpes zoster in children is often painless, but older
people are more likely to get zoster as they age, and the disease tends to be more severe. In most
cases after 1-2 days, but sometimes as long as 3 weeks, the initial phase is followed by the
appearance of a characteristic skin rash. The pain and rash most commonly occurs on the torso, but
can appear on the face, eyes or other parts of the body. At first the rash herpes zoster causes skin
changes limited to a dermatome, normally resulting in a stripe or belt-like pattern that is limited to
one side of the appears similar to the first appearance of hives; however, unlike hives, body and
does not cross the midline. "Zoster without herpes" describes a patient who has all of the symptoms
of herpes zoster except this characteristic rash.

Later the rash becomes vesicular, forming small blisters filled with a serous exudate, as the fever and
general malaise continue. The painful vesicles eventually become cloudy or darkened as they fill
with blood, crust over within seven to ten days; usually the crusts fall off and the skin heals, but
sometimes, after severe blistering, scarring and discolored skin remain. Herpes zoster may have
additional symptoms, depending on the dermatome involved. Herpes zoster ophthalmicus involves
the orbit of the eye and occurs in approximately 10-25% of cases. The virus reactivating in the
ophthalmic division of the trigeminal nerve causes it. In a few patients, symptoms may include
conjunctivitis, keratitis, uveitis, and optic nerve palsies that can sometimes cause chronic ocular
inflammation, loss of vision, and debilitating pain. Herpes zoster oticus, also known as Ramsay Hunt
syndrome type II, involves the ear. It has thought to result from the virus spreading from the facial
nerve to the vestibulocochlear nerve. Symptoms include hearing loss and vertigo (rotational
dizziness).
 Pathophysiology

The causative agent for herpes zoster is varicella zoster virus, a double stranded DNA virus related to
the herpes simplex virus group. most people are affected with this virus as children and suffer from
an episode of chicken pox the immune system eventually eliminates the virus from most location but
it remains dormant (or latent) in the ganglia adjacent to the spinal cord called the (dorsal root
ganglion) or the ganglion semilunar (ganglion Gasseri) in the base of the skull. Repeated attacks of
herpes zoster are rare, and it is extremely rare for patients to suffer more than three recurrences.
Herpes zoster occurs only in people who have been previously infected with VZV; although it can
occur at any age, approximately half of the cases in the USA occur in those aged 50 years or older.
The disease results from the virus reactivating in a single sensory ganglion. In contrast to Herpes
simplex virus, the latency of VZV is poorly understood. The virus has not been recovered from
human nerve by cell culture and the location and structure of the viral DNA is not known. Virus-
specific proteins continue to be made by the infected cells during the latent period, so true latency,
as opposed to a chronic low-level infection, has not been proven. Although VZV has been detected
in autopsies of nervous tissue, there are no methods to find dormant virus in the ganglia in living
people. Unless the immune system is compromised, it suppresses reactivation of the virus and
prevents herpes zoster. Why this suppression sometimes fails is poorly understood, but herpes
zoster is more likely to occur in people whose immune system is impaired due to aging,
immunosuppressive therapy, psychological stress, or other factors. Upon reactivation, the virus
replicates in the nerve cells, and virions are shed from the cells and carried down the axons to the
areas of skin served by that ganglion. In the skin, the virus causes local inflammation and blisters.
The short- and long-term pain caused by herpes zoster comes from the widespread growth of the
virus in the infected nerves, which causes inflammation. As with chickenpox and / or other forms of
herpes, direct contact with an active rash can spread VZV to a person who has no immunity to the
virus. This newly infected individual may then develop chickenpox, but will not immediately develop
shingles. Until the rash has developed crusts, a person is extremely contagious. A person also not
infectious before blisters appear, or during postherpetic neuralgia (pain after the rash relieves).

Diagnosis

If the rash has appeared, identifying this disease (making differential diagnosis) requires only a visual
examination, since very few diseases produce a rash in a dermatomal pattern. However, herpes
simplex virus (HSV) can occasionally produce a rash in such pattern. The Tsanck smear is helpful for
diagnosing acute infection with herpes virus, but does not distinguish between HSV and VZV. When
the rash is absent (early or late in the disease, or in the case of zoster sine herpete), herpes zoster
can be difficult to diagnose. Apart from the rash, most symptoms can occur also in other conditions.
Laboratory tests are available to diagnose herpes zoster. The most popular test detects VZV-specific
IgM antibody in blood; this appears only during chickenpox or herpes zoster and not while the virus
is dormant. In larger laboratories, lymph collected from a blister is tested by polymerase chain
reaction for VZV DNA, or examined with an In a recent study, samples of lesions on the skin, eyes,
and lung from 182 patients with presumed herpes simplex or herpes zoster were tested with real-
time PCR or with viral culture. In this comparison, viral culture detected VZV with only 14.3%
sensitivity, although the test was highly specific (specificity-D100%). By comparison, real-time
electron microscope for virus particles. PCR resulted in 100% sensitivity and specificity. Overall
testing for herpes simplex and herpes zoster using PCR showed 60.4% improvement over viral
culture.
 Treatment

The aims of treatment are to limit the severity and duration of pain, shorten the duration of a
shingles episode, and reduce complications. Symptomatic treatment is often needed for the
complication of postherpetic neuralgia. However, a study on untreated herpes zoster shows that,
once the rash has cleared, postherpetic neuralgia is very rare in people under 50 and wears off in
time; in older people the pain wore off more slowly, but even in people over Treatment 70, 85%
were pain free one year after their shingles outbreak.

Analgesics

People with mild to moderate pain can be treated with over-the- counter analgesics. Topical lotions
containing calamine can be used on the rash or blisters and may be soothing. Occasionally, severe
pain may require an opioid medication, such as morphine. Once the lesions have crusted over,
capsaicin cream (Zostrix) can be used. Topical lidocaine and nerve blocks may also reduce pain.
Administering gabapentin along with antivirals may offer relief of postherpetic neuralgia.

Antivirals

Antiviral drugs inhibit VZV replication and reduce the severity and duration of herpes zoster with
minimal side effects, but do not reliably prevent postherpetic neuralgia. Of these drugs, acyclovir has
been the standard treatment, but the new drugs valaciclovir and famciclovir demonstrate similar or
superior efficacy and good safety and tolerability. The drugs are used both as prophylaxis (for
example in AIDS patients) and as therapy during the acute phase. Antiviral treatment is
recommended for all immunocompetent individuals with herpes zoster over 50 years old, preferably
given within 72 hours of the appearance of the rash. Complications in immunocompromised
individuals with herpes zoster may be reduced with intravenous acyclovir. In people who are at a
high risk for repeated attacks of shingles, five daily oral doses of acyclovir are usually effective.

Steroids

Orally administered corticosteroids are frequently used in treatment of the infection, despite clinical
trials of this treatment being unconvincing. Nevertheless, one trial studying immunocompetent
patients older than 50 years of age with localized herpes zoster, suggested that administration of
prednisone with acyclovir improved healing time and quality of life. Upon one-month evaluation,
acyclovir with prednisone increased the likelihood of crusting and healing of lesions by about
twofold, when compared to placebo. This trial also evaluated the effects of this drug combination
on quality of life at one month, showing that patients had less pain, and were more likely stop the
use of analgesic agents, return to usual activities and ha uninterrupted sleep. However, when
comparing cessation of her zoster-associated pain or post herpetic neuralgia, there was the
difference between acyclovir plus prednisone and acyclovir. Because of the risks of corticosteroid
treatment, it is recommended that this combination of drugs only be used in people more than 50
years of age, due to their greater risk of postherpetic neuralgia.