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.
|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.
|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.