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INTRODUCTION

Herpes zoster is a viral infection because the reactivated of latent Varicella

Zoster viral in cranial-nerve or dorsal-root ganglia, with spread of the virus along the

sensory nerve to the dermatome.1

The incidence of zoster increases with age. Below the age of 45, the annual

incidence is less than 1 in 1000 persons. Among patients older than 75 years of age,

the rate is more than four time greater. For white persons older than 80 years of age,

the lifetime risk of developing zoster is 10-30%. There are more than 1 million cases

of herpes zoster in the United States each year, with an annual rate of 3 to 4 cases per

1000 persons.1,2

Varicella- zoster virus, also known as human herpes virus 3 (HHV3) belongs

to the herpes virus family ( Herpesviridae). VZV is highly contagious and spread both

 by respiratory droplets and direct contact. Infection with VZV occurs when the virus

comes into contact with the mucosa of the upper respiratory tract or the conjunctiva

of the eye. The virus travels in the bloodstream via mononuclear cells to the skin,

resulting in the generalized rash of chickenpox. The virus also infects human cells in

the dorsal root ganglia of the spinal column and cranial nerve ganglia, where it

 become latent. Essentially protected from the human immune system, VZV typically

remains dormant in the ganglia for decades.3

The mechanisms involved in re-activation of latent VZV are unclear, but re-

activation has been associated with immunosuppression, emotional stress, irradiation

of the spinal column, tumor involvement of the cord, dorsal root ganglion or adjacent

structures, local trauma, and surgical manipulation of the spine. When VZV specific

cellular immunity falls below some critical level, virus can no longer be contained,

makes it multiplies and spreads within the ganglion, causing neuronal necrosis and

intense inflammation. Infectious VZV then spreads antidromically down the sensory

nerve, causing intense neuritis, and released from the sensory nerve endings in the

skin, where it produces the characteristic cluster of zoster vesicles.4 

 

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Herpes zoster usually begins with a prodromal, such as pain, itching or

tingling in the area that becomes affected. This may precede the characteristic rash by

days or even weeks but is rarely the only clinical manifestation of varicella zoster

virus reactivation (sometimes referred to as zoster sine herpete ). Typically, patients

experience headache, malaise and sometimes photophobia. Abnormal sensation or

 pain, often described as burning, throbbing or stabbing, occurs in approximately 75%

of patients and may be the first noticeable feature. Often pruritus in the affected

region is the most prominent feature.4

The rash of herpes zoster is dermatomal and does not cross the midline, a

feature that is consistent with reactivation from a single dorsal-root or cranial-nerve

ganglion. In nonimmunocompromised persons, a few scattered lesions outside the

affected dermatome are not unexpected. The rash is often preceded by tingling,

itching, or pain (or a combination of these) for 2 to 3 days, and these symptoms can

 be continuous or episodic. The rash begins as macules and papules, which evolve into

vesicles and then pustules. New lesions appear over a period of 3 to 5 days,often with

filling in of the dermatome despite antiviral treatment. The rash usually dries with

crusting in 7 to 10 days. Immunocompromised patients may have disseminated rashes

with viremia and new lesions occurring for up to 2 weeks.1

The clinical picture of herpes zoster is almost always distinctive enough for

diagnosis. Laboratory tests reserved for more atypical cases. The Polymerase Chain

Reaction (PCR) is a useful method to detect VZV-DNA in fluids and in tissues.4,5

The mayor goals of therapy in patients with herpes zoster are to (1) limit the

extent, duration and severity of pain and rash in the primary dermatome: (2) prevent

disease elsewhere: and (3) prevent PHN. Three oral nucleoside analogues  –  

valaciclovir, famciclovir and aciclovir  –   are available for the treatment of herpes

zoster. They reduce the severity and duration of the illness if started within 72 hours

of onset of the rash.1,4,5