HERPES ZOSTER (SHINGLES)

Guided by :- Dr. Alpesh Patel Dr. Uday Patel

Produced by :- Nancy Hirpara Bhakti Jivani Monali Joshi

INTRODUCTION Herpes zoster is an acute infectious viral

disease. It is extremely painful and having

incapacitating nature. It is characterised by inflammation of dorsal

root ganglia or extra-medullary cranial nerve ganglia , associated with vesicular eruptions of the skin or mucous membrane in areas supplied by sensory nerves.

VIRICELLA-ZOSTER VIRUS ( VZV ; HHV-3 )

Viricella zoster virus is simillar to herpes simplex virus(HSV) in many respects.

Chicken pox represents the primary infection with VZV latency ensures and recurrence is possible as HERPES ZOSTER

This disease is most common in adult life and affects male and female with equal frequency.

Although rare it does occur in children. The infection period is 10 – 21 days with

an average of 15 days.

PREDISPOSING FACTORS FOR REACTIVATION

HIV infection Cytotoxic or treatment with immuno-

suppressive drugs Radiation Presence of malignancies Old age Alcohol abuse Stress ( emotional and physical ) Dental manipulation

PATHOGENESIS After the initial infection with VZV

( chicken pox ) , the virus is transported up the sensory nerves and presumably establishes latency in dorsal spinal ganglia.

Simillar eosinophilic intra-nuclear inclusion bodies , indicative of viral infection occur in both the cases.

Herpes zoster rash has healed , a debilitating complications known as post herpatic neuralgia(PHN).

The incidense and severity of herpes zoster and PHN increase with age in association with an age related decline in cell-mediated immunity to VZV

CINICAL FEATURES It can be grouped into three phases - prodrome - acute - chronic During initial viral replication , active

ganglionitis develops with resultant neuronal necrosis and sever neuralgia

As the virus travels down the nerve, pain intensifies and has been described as burning, tingling, itching, boring, prickly, or knifelike.

Approximately 10% of affected individuals will exhibit no pro-dermal pain.

The pain may be -sensitive teeth -otitis media -migraine headache - myocardial infraction or appendicitis, depending upon which dermatome is

affected

ZOSTER SINE Conversely on occasion there may be

recurrence in the absence of vesiculation of the skin or mucosa.

This pattern is called zoster sine (zoster with out rash).

The acute phase begins as the involved skin develops clusters of vesicles set on an erythmatous base.

within 3 to 4 days the vesicles becomes pustular and ulcerate with crusts developing after 7 to 10 days.

ORAL LESIONS Oral lesions occur with trigeminal nerve

involvement and may be present on the movable or bound mucosa.

The lesions often extend to the mid-line and frequently are present on conjuction with involvement of skin overlying the affected quardant.

Individual lesions manifest as 1 to 4 mm, white, opaque vesicles that rupture to form shallow ulcerations.

Involvement of maxilla may be associated with devitalization of the teeth in the affected area.

Several reports have documented significant bone necrosis with loss of teeth in areas involved with herpes zoster.

It is postulated that the gnathic osteo-necrosis may be secondary to damage of the blood vessels supplying the alveolar ridges and teeth, leading to focal ischemic necrosis.

Of the reported cases there is almost an equal distribution between maxilla and mandible with both sexes similarly.

Ocular involvement is not unusual and can be the source of significant morbidity, including permanent blindness.

JAMES RAMSAY HUNT’S SYNDROME A special form of zoster infection of the geniculate

ganglion, with the involvement of the external ear and oral mucosa, has been termed hunte’s syndrome.

Clinical manifestation :- - facial paralysis - pain of external auditory meatus and pinna of ear. - vesicular eruption occur in oral cavity and

oropharynx with hoarseness,tinnitus,vertigo and occasional oter dtsterbences.

ORAL MANIFESTATION Herpes zoster may involve the face by

infection of trigeminal nerve. This usually consist of unilateral

involvement of skin areas supplied by either the opthalmic , maxillary or mandibular nerves.

Lesions of the oral mucosa are fairly common , and extremely painful vesicles may be found on the buccal mucosa , tongue, uvula, pharynx and larynx.

This generally rupture to leave areas of erosion.

One of the characteristics clinical features of the disease involving the face and oral cavity is the unilaterality of the lesions.

Typically, when large, the lesions will extend upto the midline and stop abruptly.

HISTOPATHOLOGIC FEATURES

The virus causes acantholysis, the formation of numerous free-floating tzanck cells which exhibit nuclear margination of chromatin and occational multinucleation.

DIAGNOSIS Viral cultural can confirm the clinical

impression but takes atleast 24 hours. A rapid diagnosis can be obtain through the

use of direct staining of cytologic smears with fluorescent monoclonal antibodies for VZV.

This technique gives positive results in almost 80% of cases.

Molecular techniques such as dotblot hybridization and PCR also can be used to detect VZV.

TREATMENT & PROGNOSIS

Fever should be treated with antipyretics that do not contain aspirin.

Antipruritics such as diphenhydramine can be administrated to reduce etching.

Early therapy with appropriate antiviral medications such as acyclovir, valacyclovir and famciclovir has been found to accelarate healing of the cutaneous and mucosal lesions.

This medications are most effective if initiated within 72 hours after development of first vesicle.

One topical treatment, capsaicin has had significant success with 80% of patients.

A live attenuated VZV vaccine has been approved for use in adults, 60 years of age or older.

Zostavax is 14 times more potent than varivax.

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