Herpes zoster
Herpes zoster
DEF:
Herpes zoster (or simply zoster), commonly known as shingles and also known as
zona, is a viral disease caused by varicella zoster virus (VZV) affecting
mainly the nerves characterized by a painful skin rash with blisters in a
limited area on one side of the body, often in a stripe.
v
It is an acute unilateral and segmental
inflammation of the dorsal root ganglia caused by a virus varicella zoster
virus characterized by localized vesicular skin lesions and severe neuralgic
pain in the area bordering the inflamed nerve.
CAUSE
-
Varicella zoster virus a herpes virus
PATHOPHYSIOLOGY
•
The initial infection with varicella zoster
virus (VZV) causes the acute (short-lived) illness chickenpox which generally
occurs in children and young people. Once an episode of chickenpox has
resolved, the virus is not eliminated from the body but can go on to cause
shingles—an illness with very different symptoms—often many years after the
initial infection.
•
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
out 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 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
post-herpetic neuralgia. Exactly how the virus remains latent in the body, and
subsequently re-activates is not understood.
Signs
and symptoms
•
headache
•
fever
•
malaise
•
Sensations of burning pain, itching,
hyperesthesia (oversensitivity), or paresthesia ("pins and needles":
tingling, pricking, or numbness).
•
The pain may be 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.
•
In most cases, after 1–2 days (but
sometimes as long as 3 weeks) the initial phase is followed by the appearance
of the 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 appears similar to
the first appearance of hives; however, unlike hives, 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 body and does not cross the midline.
Zoster sine herpete 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, and usually the
crusts fall off and the skin heals: but sometimes, after severe blistering,
scarring and discolored skin remain.
•
Development of the shingles rash Day 1 Day 2 Day
5 Day 6
•
ShinglesDay1.JPG ShinglesDay2 ed.JPG ShinglesDay5 ed.JPG ShinglesDay6 ed.JPG
•
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. It
is caused by the virus reactivating in the ophthalmic division of the
trigeminal nerve. 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 is
thought to result from the virus spreading from the facial nerve to the
vestibulocochlear nerve. Symptoms include hearing loss and vertigo (rotational
dizziness).
Pathophysiology
•
Progression of herpes zoster. A cluster
of small bumps turns into blisters. The blisters fill with lymph, break open,
crust over, and finally disappear. Post-herpetic neuralgia can sometimes occur
due to nerve damage,
•
The causative agent for herpes zoster
is varicella zoster virus (VZV), a double-stranded DNA virus related to the
Herpes simplex virus group. Most people are infected with this virus as
children, and suffer from an episode of chickenpox. The immune system
eventually eliminates the virus from most locations, but it remains dormant (or
latent) in the ganglia adjacent to the spinal cord (called the dorsal root
ganglion) or the ganglion semilunare (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 had chickenpox, and although it can occur at any age, the majority of
sufferers are more than 50 years old. 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
cells 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 area 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. The
symptoms of herpes zoster cannot be transmitted to another person. However,
during the blister phase, direct contact with the 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 is also
not infectious before blisters appear, or during post-herpetic neuralgia (pain
after the rash is gone). The person is no longer contagious after the rash has
disappeared.
Diagnosis
•
Herpes zoster on the chest
•
If the rash has appeared, identifying
this disease (making a differential diagnosis) only requires a visual
examination, since very few diseases produce a rash in a dermatomal pattern
(see map).
•
The T-sanck smear is helpful for
diagnosing acute infection with a 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: The most popular test
detects VZV-specific IgM antibody in blood; this only appears during chickenpox
or herpes zoster and not while the virus is dormant.
•
Lymph collected from a blister is
tested by the polymerase chain reaction for VZV DNA, or examined with an
electron microscope for virus particles.
•
Real-time PCR or with viral culture -
In this comparison, viral culture detected VZV with only a 14.3% sensitivity,
although the test was highly specific (specificity=100%).
Treatment
•
Herpes zoster on lower back
•
The aims of treatment are to;
-
limit the severity and duration of pain,
-
shorten the duration of a shingles
episode,
-
Reduce complications.
·
Symptomatic treatment is often needed
for the complication of post-herpetic neuralgia.
Analgesics
•
Patients 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.
•
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 post-herpetic 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 post-herpetic neuralgia.
•
Acyclovir has been the standard
treatment, but the new drugs valacyclovir and famciclovir demonstrate similar
or superior efficacy and good safety and tolerability.
•
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.
•
Prednisone
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