HERPES ZOSTER (SHINGLES)
The varicella zoster virus (VZV) is responsible for causing varicella (chickenpox) as well as herpes zoster (shingles). Herpes zoster is caused by reactivation of dormant VZV. Only hosts who have previously been infected with VZV can develop herpes zoster. The incidence of herpes zoster is sure to decrease in the future, because the zoster vaccine has good efficacy in increasing immunity against the virus. The live attenuated vaccine is currently recommended for those individuals 60 years of age and older who fulfill the criteria for receiving a live vaccine. This age was chosen because the incidence of herpes zoster increases after age 60, possibly related to a waning immune response and anti-body titer remaining from the patient’s original VZV infection. Whether the VZV vaccine protects against herpes zoster will take years to determine. The United States introduced widespread childhood immunization against VZV in 1995, and none of these children have yet reached the age of 60. Whether future booster vaccinations or VZV revaccination will be required is yet to be determined.
Clinical
Findings: Herpes zoster is caused by reactivation of VZV, as acquired previously,
that has been lying dormant in the dorsal root ganglia of the spinal cord or
the ganglia of the cranial nerves. Patients are typically older individuals.
The incidence increases with each decade of life and peaks at about 75 years of
age. Herpes zoster is infrequently encountered in children. Men and women are
equally affected. The initial symptom typically is a vague pain, tingling, or
itching sensation. This may precede the rash by 1 or 2 days. Constitutional
symptoms are commonly seen in older patients. After this prodrome, the
characteristic vesicular rash develops in a dermatomal distribution. The
location most frequently affected is the thoracic spine region; however, the
trigeminal nerve is the most frequently involved nerve. The vesicles spread out
to involve almost the entire dermatome of the nerve that has been infected. The
rash does not cross the midline, and this is a clue to the diagnosis. Bilateral
herpes zoster is very rare and is seen more frequently in immunosuppressed
individuals.
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| CLINICAL PRESENTATION OF HERPES ZOSTER |
The rash is
exquisitely tender and can lead to significant sleep disturbances and
significant morbidity. With healing, which usually occurs within 1 to 2 weeks,
scarring is common. Pain typically dissipates over time, but a small subset
of individuals, usually older than 50 years of age, develop postherpetic
neuralgia. Postherpetic neuralgia can be a life-altering condition of abnormal
sensation within the region affected by the herpes zoster outbreak. Patients
often describe pain and paresthesias. Clothing or bedding rubbing against the
skin can cause severe discomfort and pain. Postherpetic neuralgia can last for
weeks to months or even years and can be devastating.
Although the
thoracic dorsal ganglia, taken as a whole, are responsible for the most cases
of herpes zoster, the trigeminal nerve is the most frequently involved single
nerve. The severity of the infection depends on the branch or branches
involved. Herpes zoster infections on the face are typically more severe than
those on the trunk or extremities. Infections on the face can affect the eye
and ear and can lead to blindness or to hearing loss in severe cases. If the
vesicles of herpes zoster affect the
tip of the nose, the eye is likely to be involved. The nasociliary branch of
the ophthalmic division of the trigeminal nerve innervates the nasal tip, and
involvement of this region indicates that the infection is within the ophthalmic
nerve. This involvement of the nasal tip with subsequent involvement of the
globe is termed Hutchinson’s sign. VZV infection of the eye is a medical
emergency, and the patient must be evaluated by an ophthalmologist as soon as
possible.
Simultaneous
involvement of the facial and vestibular nerves is not infrequent and has been
termed the Ramsay Hunt syndrome. These two nerves originate in close proximity
to each other, and reactivation of VZV within the geniculate ganglion may
involve both these nerves. This can lead to hearing loss and motor nerve loss
due to involvement of the vestibular and the facial nerve, respectively. The
ear and the anterior tongue develop the vesiculation seen in routine VZV
infections. The motor loss may mimic Bell’s palsy, and hearing loss may be
permanent. Other cranial nerves have been reported to be affected in Ramsay
Hunt syndrome, but the seventh and eighth nerves are those most frequently
affected by far.
Scarring may
be a severe sequela of this infection, and it can be made worse by bacterial
superinfection. The presence of any honey-colored crusting or expanding
erythema outside the dermatome should suggest the possibility of secondary
impetigo or cellulitis. Prompt recognition and therapy are required to help
prevent serious, disfiguring scarring.
The
diagnosis is made clinically, and the Tzanck test can confirm the diagnosis.
The presence of multinucleated giant cells on a Tzanck preparation taken from a
vesicular rash in a dermatomal distribution confirms the diagnosis. Viral
culture can be performed, but is not cost-effective. Direct immunofluorescent
antibody testing (DFA) is a rapid method to determine the viral cause, but it
is expensive and is rarely needed in these cases.
Histology:
Skin
biopsies are not needed for diagnosis of this infection. If one were to biopsy
a vesicle, ballooning degeneration of the keratinocytes would be present. This
ballooning degeneration leads to the vesiculation and bulla formation.
Multinucleated giant cells can be seen at the base of the blister. A mixed
dermal inflammatory infiltrate is present.
Pathogenesis:
Any
individual previously infected with VZV in the form of chickenpox is
predisposed to develop herpes zoster later in life. Most cases occur with
advancing age, as cell-mediated immunity tends to wane with time. The virus
remains latent in the nerve ganglia until it reactivates. The ability to
reactivate and the exact signal for reactivation are unknown. Once the virus
reactivates, it begins to replicate and to cause necrosis of the affected nerve
cells. The virus travels along the cutaneous sensory nerves and eventually
affects the skin that is innervated by the nerve root where the virus became
reactivated.
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| VARICELLA ZOSTER WITH KERATITIS |
Treatment:
Treatment
with antiviral medications from the acyclovir family should be instituted
immediately. The sooner therapy is started, the better is the chance of
decreasing the length of disease. Therapy may also decrease the incidence of
postherpetic neuralgia. The use of oral corticosteroids in conjunction with the
antiviral medication has been advocated to help decrease the risk of postherpetic neuralgia, but large
studies have thus far shown inconclusive data to support this approach. The
therapy has the best chance of changing the course of the disease if given within
the first 72 hours after the onset of disease symptoms.
A live
attenuated zoster vaccine for the prevention of herpes zoster is being given to
patients older than 60
years of age. This vaccine has been shown to boost natural immunity against VZV
and to decrease the
number of cases of herpes zoster and the frequency of postherpetic neuralgia in
those who do develop herpes zoster after vaccination. As with all live
vaccines, its use in immunosuppressed patients is contraindicated.
Currently,
the treatment of postherpetic neuralgia is not optimal. Amitriptyline,
gabapentin, lidocaine patches, pregabalin, antico vulsants, and opioids are all used with varying
success.
