Bahir Dar University

CMHS-TGSH
Department of Dermatovenereology
varicella and herpes zoster
presenter DR. Meriniya
moderator DR. Debas
03/10/14
outline
Introduction
Etiology
Epidemiology
Pathogenesis
Clinical manifestations
Complications
Laboratory findings
Treatment
Prevention
Introduction

• Varicella (chickenpox) and herpes zoster (shingles, zoster) are distinct

clinical entities
• Caused by a single member of the herpesvirus family, varicella-zoster virus
(VZV).
• The different clinical manifestations of these 2 diseases are the result of
• differences in the host immune response and
• in the pathogenesis of the VZV infection
Con’t...
• The VZV genome encodes about 70 unique genes

• Immediate early (IE) gene products regulate VZV replication

• Early gene products(the virus-specific

thymidine kinase and the viral DNA polymerase) –support viral replication

• Late genes encode virus structural proteins that serve as targets for
neutralizing antibodies and cellular immune responses
Con’t...
 Varicella,
• A highly contagious vesicular exanthem that occurs most often in
childhood
• Is the result of exogenous primary infection
herpes zoster
• Results from reactivation of endogenous virus that persists in
latent form within ganglionic neurons following an earlier attack of
varicella.
• Localized dermatomal disease characterized by unilateral radicular
pain and a vesicular dermatomal eruption.
varicella
Epidemiology
• Distributed worldwide, but its age-specific incidence differs in
 temperate versus tropical climates
 vaccinated vs unvaccinated

• In temperate climates in the absence of varicella vaccination

 endemic
 Infection occurs at a younger age
 Regularly recurring seasonal prevalence in winter and spring
 Periodic epidemics that depend upon the accumulation of susceptible
persons
Con’t...

• In tropical and semitropical countries

 the mean age of varicella is higher
 susceptibility among adults to primary VZV infection is
significantly greater than in temperate climates
Con’t...
• Varicella is highly contagious with attack rates of

 87% among susceptible siblings in households

 70% among susceptible patients on hospital wards

• More than 95% of cases of varicella are clinically apparent

• Over half of primary infections occur before the age of 5 and 85%
before puberty
Con’t...
• A typical patient is infectious for 1–2 days before the exanthem appears

• For 4 or 5 days thereafter, that is until the last crop of vesicles has
crusted

• immunocompromised patient is infectious for a longer period of time

• The mean incubation period of varicella is 14 or 17 days, with a range of

10–23 days
• The major route by which varicella is acquired & transmitted is from the
respiratory tract by airborne droplets or aerosols
• Infection also may be spread by direct contact. Varicella crusts are not
infectious

Natural varicella
• varicella caused by wild type VZV
• Generally confers life-long immunity to the disease
• With severe immunocompromise, reinfections manifested as
varicella have been observed
Con’t...
 Modified varicella
 Infected early in infancy in the presence of maternal antibody
 following postexposure prophylaxis with VZ-IgG or varicella vaccine

 Breakthrough varicella
 occurs when vaccinated individuals are reinfected following exposure to
wildtype VZV
 Approximately 10% to 15% of vaccinees immunized with a single dose of
varicella vaccine
 lesions few in number(< 60)
 maculopapular, few vesicles
 severity of fever is less & ,less contagious
Pathogenesis
• Entry of VZV is through the mucosa of the URT & oropharynx
• Infects tonsillar T cells that disseminate virus via the blood and lymphatics
(the primary viremia).

• Infected T cells carry virus to

• the reticuloendothelial system, the major site of virus replication
during the remainder of the incubation period,
• and to the skin.
Con’t...
• Viremia occurs early in the incubation period
• but VZV replication and rash formation are delayed by
• Innate immune responses,( interferon and natural killer cells)
• By developing VZV-specific immune responses.

• Virus replication eventually overcomes these host defenses

• 10 to 14 days after infection a much larger (secondary) viremia occurs
• resulting in systemic symptoms and skin lesions.
Con’t...
• Skin lesions appear in successive crops, reflecting a cyclic viremia

• In the normal host is terminated after about 3 to 5 days by VZV-specific immune

responses
• primarily VZV-specific T cell–mediated immune responses.

• Virus circulates in mononuclear leukocytes, primarily lymphocytes

• Even in uncomplicated varicella, the secondary viremia results in the subclinical

infection of many organs in addition to the skin
Con’t...
• Humeral immunity to VZV protects against varicella

• Cell-mediated immunity to VZV also develops, persists for many years, and
protects against severe infection
Clinical feature
Prodrome

• In young children, prodromal symptoms are uncommon.

• In older children and adults, the rash is often preceded by 2 to 3 days of
• mild fever, chills, malaise, headache
• anorexia, backache and, in some patients
• sore throat and dry cough.
Con’t...
RASH
• In unvaccinated persons, the rash usually begins on the face and scalp and
• spreads rapidly to the trunk, with relative sparing of the extremities.

• New lesions appear in successive crops, and are mainly distributed

centrally
• The rash tends to be denser on the back between the shoulder blades
than on the scapulae and buttocks

• more profuse on the medial than on the lateral aspects of the limbs.
• It is not uncommon to have a few lesions on the palms and soles
Con’t...

• A characteristic feature of varicella lesions is their rapid progression, over

as little as 12 hours, from rose colored macules to papules, and then to
vesicles, pustules, and crusts.

• The typical vesicle is 2 to 3 mm in diameter and elliptical, with its long axis
parallel to the folds of the skin.

• The early vesicle is superficial and thin-walled, and surrounded by an

irregular area of erythema which gives the lesions the appearance of a
“dewdrop on a rose petal.”
 Con’t...
• The vesicular fluid soon becomes cloudy with the influx of inflammatory cells
that converts the vesicle to a pustule,
• then dries, beginning in the center, producing an umbilicated pustule and
then a crust.

• Crusts fall off spontaneously in 1 to 3 weeks, leaving shallow pink

depressions that gradually disappear.

• Scarring is rare unless the lesions were traumatized by the patient or

superinfected with bacteria.
Con’t...
• Healing lesions may leave hypopigmented macules that persist for weeks
to months

• Inimmunocompromised patients, lesions may lack surrounding erythema,

and progression of vesicles to pustules may be delayed or absent

• vesicles also develop in the mucous membraneof mouth, nose, conjuctiva,

pharynx, larynx, trachea, GIT, UT & vagina
Con’t...
• A distinctive feature of varicella is the simultaneous presence of lesions in
all stages of development in any one area of skin.

• The average number of lesions in healthy children is 250 to 500

• After 4 days, no new lesions appear & existing vesicles dry & crust
Con’t...
FEVER
• Fever usually persists as long as new lesions continue to appear, and
• Its height is generally proportional to the severity of the rash.

• It may be absent in mild cases or rise to 40.5°C (105°F) in severe cases

with extensive rash.
PRURITIS
• The most distressing symptom, which is usually present until all lesions
are crusted.
Con’t...
CLINICAL VARIANTS

Haemorrhagic varicella
• very extensive eruption of haemorrhagic vesicles
• Accompanied by high fever and severe constitutional symptoms
• Rare in the previously healthy patient.

• More common in tropical regions where malnutrition may be a factor

• Most cases in temperate regions occur in immunocompromised
patients.
Con’t...
 congenital varicella syndrome

• Infection during pregnancy, has extra risks for both mother and baby

• Maternal infection may lead to pneumonitis in about 2.5%

• Infection in pregnancy, especially during the second trimester, caries

an approximate 2% risk of fetal damage
Con’t...
• There may be skin scarring, multiple neurological problems and limb
hypoplasia

• 30% mortality within the first year of life

• Maternal primary infection with in 4 days before & 2 days after delivery
spread infection to the immunologically unprotected neonate

• can result in very severe infection of the baby, with a mortality of

about 30%.
Complications
• In the normal child, varicella is rarely complicated.
• The most common complication is secondary bacterial infection of skin
lesions usually by Staphylococci or Streptococci
• which may produce impetigo, cellulitis, erysipelas, and, rarely, necrotizing
fasciitis.
• In adults, fever and constitutional symptoms are more prominent and
prolonged
• the rash is more profuse, and complications are more frequent
Con’t...
Pneumonitis
• characterized by cough, dyspnea, tachypnea, high fever, pleuritic chest
pain, cyanosis, and hemoptysis beginning 1 to 6 days after rash onset.

•The severity of the symptoms usually exceeds the physical findings

• imaging typically reveals diffuse, peribronchial nodular densities

throughout both lung fields in the perihilar regions and at the bases.

•mortality is estimated to be between 10% & 30%

Con’t...
CNS complication
• Formerly common, varicella-associated Reye syndrome (acute
encephalopathy with fatty degeneration of the liver)

• now very rare since the etiologic role of salicylates was recognized and
their use in children with fever contraindicated

• transverse myelitis or ophthalmoplegia

Con’t...
• Acute cerebellar ataxia & encephalitis

• other complications includes

• myocarditis, glomerulonephritis, orchitis, pancreatitis, gastritis and

ulcerative lesions of the bowel, arthritis, Henoch-Schönlein
vasculitis, optic neuritis, keratitis, and iritis.
Diagnosis
HX & P/E
• Varicella can diagnosed by the appearance and evolution of the rash

• history of exposure within the preceding 2 to 3 weeks

• The rapid evolution of lesions from macules to papules, to vesicles, to

pustules and crusts, and the simultaneous presence of lesions at all stages
Con’t...
labratory diagnosis
• Tzanck smears
• prepared at the bedside from material scraped from the base of vesicular
lesions and
• stained with hematoxylin and eosin, Giemsa, or similar stains
• When virus-containing vesicle fluid is inoculated into human fibroblast tissue
cultures,
• multinucleated giant cells containing acidophilic intranuclear inclusion bodies form by
fusion of infected cells with adjacent infected and uninfected cells
Con’t...
PCR
• The best diagnostic test for detection of VZV
• very high sensitivity and specificity, relatively quick (1 day or less)
• PCR can distinguish VZV from HSV, and wildtype VZV from Oka vaccine

Serologic tests
• permit the retrospective diagnosis of varicella and herpes zoster
• identify susceptible individuals who may be candidates for isolation &
prophylaxis
culture
• VZV is extremely labile, and only 30% to 60% of cultures from proven
cases are generally positive.

• select new vesicles containing clear fluid for aspiration, because the
probability of isolating VZV diminishes rapidly as lesions become pustular.

• VZV is almost never isolated from crusts.

Con’t...
Histopathology

•The lesions of varicella and herpes zoster are indistinguishable

•The presence of multinucleated giant cells and epithelial cells

containing acidophilic intranuclear inclusion bodies

•Punch biopsies provide more reliable material to facilitate dx in the

prevesicular stage in atypical lesions such as
•the chronic verrucous lesions produced by acyclovir-resistant VZV in
pts with AIDS
Differential diagnosis
Treatment
 In normal children, varicella is generally benign and self-limited
 Symptomatic treatment

•meticulous skin care with daily bathing and cool compresses

•keep the enviroment cool

•Calamine lotion
•Antipyretics

•Antihistamines
•Antibiotics for secondary bacterial infection
Antivirals are indicated for :
• should be considered for otherwise healthy persons at increased risk for
moderate-to severe varicella
• persons aged >12 yrs
• persons with chronic cutaneous or pulmonary disorders
• persons receiving long-term salicylate therapy

• persons receiving short, intermittent, or aerosolized courses of corticosteroids

• Immunocompromised persons
• pregnant women with varicella who have extensive rash, toxicity, any signs of
systemic infection
• Persons with complications of varicella
Con’t...
 Acyclovir
• guanosine analog that is selectively phosphorylated by VZV thymidine
kinases & is concentrated in infected cells

•Cellular enzymes then convert acyclovir monophosphate to acyclovir

triphosphate, which interferes with viral DNA synthesis by inhibiting viral
DNA polymerase

•Acyclovir should be initiated early preferably in first 24 hrs

•Reduce number of lesions,time of cessation in new lesion formation,
fastens crusting of lesions, extent of disease and severity of symptoms
Con’t...
• Two prodrugs, valacyclovir & famciclovir po, are better absorbed
than acyclovir

• they produce much higher blood levels of antiviral activity and

permit less frequent dosing than acyclovir

• are preferred to acyclovir for oral therapy of VZV infections

Prevention
 Pre-exposure vaccination
 post-exposure immunoglobulin
 Antiviral prophylaxis
Herpes zoster
Introduction
•Zoster (zoster = a girdle, a reference to its segmental distribution)
•result of reactivation of latent VZV

•occurs sporadically throughout the year without seasonal prevalence

•The occurrence of HZ is independent of the prevalence of varicella

•there is no convincing evidence that HZ can be acquired by contact with

pts with varicella or HZ
Epidemiology
• incidence of herpes zoster is determined by factors that influence the
host–virus relationship
• the presence of immune responses necessary to prevent reactivation
of latent VZV.
• The average annual incidence has been estimated at 2–4/1000
• incidence of herpes zoster in community-dwelling populations ranges
from 2 to 5 per 1000 person-years.
Con’t...
• Risk factors
• increasing age
• decreased VZV-specific cell-mediated immunity.
• bone marrow and solid organ transplants, HIV
• hematologic and solid tumor malignancies
• immune-mediated diseases
• chemotherapy or therapy with immune modulators or
corticosteroids
• female sex
• physical trauma in the affected dermatome
• IL-10 gene polymorphisms
• family history of herpes zoster and white race
Con’t...
• recurrent herpes zoster is reported to range from 1% to 6%

• Recurrent herpes zoster is more common in patients who are

immunocompromised,
• multidermatomal or bilateral disease

• immunocompetent persons almost always involve a different dermatome

than that involved in the first episode.

• Patients with herpes zoster are less contagious than patients with
varicella.
Con’t...

• Virus can be isolated from vesicles and pustules in uncomplicated herpes

zoster for up to 7 days after the appearance of the rash

• much longer periods in immunocompromised individuals.

• spread of infection by means of direct contact with their lesions, & some
airborne transmission
Pathogenesis
• During the course of varicella, VZV passes from lesions in the skin and
mucosal surfaces into the contiguous endings of sensory nerves

• transported centripetally up the sensory fibers to the sensory ganglia

• In the ganglia, the virus establishes a latent infection that persists for life

• HZ occurs most often in dermatomes in which the rash of varicella

achieves the highest density
• those innervated by the first (ophthalmic) division of the trigeminal
nerve & by spinal sensory ganglia from T1 to L2
Con’t...
• latent VZV may reactivate sporadically, producing infectious virus

• The frequency and mechanism of these reactivations are unknown

• but VZV reactivation and replication resulting in HZ has been associated

•most clearly with immunosuppression

• decline in VZV-specific cellular immunity that occurs with increasing age
Con’t...
• The small quantity of viral antigens released during such contained re-
activations
• stimulate and sustain host immunity to VZV

• When VZV-specific cellular immunity falls below some critical level, re-
activated virus can no longer be contained

• Virus multiplies and spreads within the ganglion

• causing neuronal necrosis and intense inflammation
• a process that is often accompanied by severe neuralgia
Con’t...
• Infectious VZV then spreads antidromically down the sensory nerve,
causing intense neuritis

• released from the sensory nerve endings in the skin, where it produces
the characteristic cluster of zoster vesicles

• Spread of the ganglionic infection proximally along the posterior nerve

root to the meninges and cord results in

• local leptomeningitis, cerebrospinal fluid pleocytosis, and segmental

myelitis
Con’t...
• Infection of motor neurons in the anterior horn and inflammation of the
anterior nerve root

• account for the local palsies that may accompany the cutaneous eruption

• extension of infection within the CNS may result in rare complications of

herpes zoster

• e.g. meningoencephalitis, transverse myelitis

Clinical feature
Prodrome

• Pain and paresthesia in the involved dermatome

• precede the eruption by 1 to 3 days, but occasionally by a week or longer

• Abnormal sensations vary from superficial itching, tingling, or burning to

severe, deep, boring, or lancinating pain

• The pain may be constant or intermittent, and it is often accompanied by

tenderness and hyperesthesia of the skin in the involved dermatome.
Con’t...
• Prodromal pain is uncommon in immunocompetent persons younger than
30 years

• It occurs in the majority of persons with herpes zoster over the age of 60
years.

• A few patients experience acute segmental neuralgia without ever

developing a cutaneous eruption—a condition known as zoster sine
herpete
Con’t...
Rash

• The most distinctive feature of herpes zoster is the localization and

distribution of the rash, which is unilateral and is generally limited to the
area of skin innervated by a single sensory ganglion.

• The thoracic ( T3 to L2 53%)

• cervical (usually C2,3,4, 20%)
• trigeminal, including ophthalmic (15%)
• lumbosacral (11%) dermatomes
Con’t...
• herpes zoster lesions are uncommon distal to the elbows or knees

• lesions begin as erythematous macules and papules in a dermatomal

distribution

• Vesicles form within 12 to 24 hours and evolve into pustules by the 3rd
day
• These dry and crust in 7 to 10 days.
• The crusts generally persist for 2 to 3 weeks
Con’t...
• In normal individuals, new lesions continue to appear for 1 to 4 days

• The rash is most severe and lasts longest in older people

• least severe and of shortest duration in children

• frequency of ophthalmic zoster increases in old age

• In the elderly and undernourished, the local eruption often becomes necrotic,
and healing, require many weeks, &followed by severe scarring
Con’t...
Con’t...
The Ramsay Hunt syndrome

• (facial palsy in combination with HZ

of the external ear, ear canal, or
tympanic membrane, with or without
tinnitus, vertigo, and deafness)

• results from involvement of the facial

and auditory nerves
Con’t...
pain
• pain is the cardinal symptom of herpes zoster, especially in the elderly
• >85% over age 50 have dermatomal pain or discomfort during the acute
phase ranges from mild to severe
• associated with decreased physical & social functioning, emotional distress

Pruritis
• prominent and distressing symptom throughout the acute phase of herpes
zoster.
• frequently persists until all crusts have fallen off.
Clinical variants
• Maternal zoster

• in pregnancy is not associated with intrauterine infection

• Zoster in infancy has followed maternal varicella
• baby’s primary infection having occurred in utero

• Generalized varicella (‘disseminated zoster’)

• In patients with lymphomas or who are otherwise immunocompromised

• may be haemorrhagic.
• Rarely in such cases, the zoster may successively involve further dermatomes.
• Systemic involvement may follow and can be fatal.
Con’t...
• Trigeminal nerve zoster

• In ophthalmic nerve zoster, the eye is affected in two‐thirds of cases,

• vesicles on the side of the nose indicate involvement of the nasociliary
nerve (Hutchinson sign).
• Ocular complications include
• uveitis, keratitis, conjunctivitis, conjunctival oedema (chemosis)
• ocular muscle palsies, proptosis,
• scleritis (which may be acute or delayed for 2–3 months)
• retinal vascular occlusion, and ulceration, scarring and even
necrosis of the lid.
Con’t...
• Zoster of the maxillary division of the trigeminal nerve
• produces vesicles on the uvula and tonsillar area

• Zoster of the mandibular division

• the vesicles appear on the anterior part of the tongue
• the floor of the mouth and the buccal mucous membrane.
• In oro‐facial zoster, toothache may be the presenting symptom
 Con’t...
Herpes zoster oticus
• The facial nerve, mainly a motor nerve, has vestigial sensory fibres supplying
• the external ear (including pinna and meatus)
• the tonsillar fossa and adjacent soft palate.
• Classical sensory nerve zoster in these fibres
• causes pain and vesicles in part or all of that distribution,
• though the skin involvement may be minimal and limited to the external
auditory meatus.
• Herpes zoster oticus accounts for about 10% of cases of facial palsy
• The paralysis is usually complete and full recovery occurs in only about 20% of
untreated cases.
complicat
ions
Con’t...
• In immunocompetent patients, it is not uncommon to identify a few vesicles
in areas distant from the involved and immediately adjacent dermatomes

• More extensive dissemination (with 25-50 lesions or more), disseminated

herpes zoster may occur in immunocompromised patients

• Ophthalmic zoster may be accompanied by a wide range of complications.

• Corneal sensation is generally impaired and, when that impairment is severe

• may lead to neurotrophic keratitis with chronic ulceration and bacterial

infection.
Con’t
Post herpetic neuralgia

• PHN has been variably defined as any pain after rash healing or any pain 1
month, 3 months, 4 months, or 6 months after rash onset

• Patients with PHN may suffer from constant pain (described as “burning,
aching, throbbing”),

• Intermittent pain (“stabbing, shooting”), and/or

• stimulus-evoked pain, including allodynia (“tender, burning, stabbing”)

Con’t...
• Allodynia
• pain elicited by stimuli that are normally not painful
• present in approximately 90% of patients with PHN
• Patients with allodynia may suffer severe pain after even the lightest
touch to the affected skin, such as by a breeze or by contact with
clothing.
• These subtypes of pain may produce disordered sleep, depression,
anorexia, weight loss, chronic fatigue, and social isolation

• they often interfere with dressing, bathing, general activity, traveling,

shopping, cooking, and housework
Con’t...
• Dorsal root ganglia contain visceral, as well as cutaneous, afferent
neurons, which likely explains the occurrence of visceral as well as
cutaneous lesions in patients with herpes zoster

 Risk factors for PHN

 Increasing age
 presence of prodromal pain
 severe pain during the acute phase of herpes zoster
 extensive rash
 significant sensory abnormalities in the affected dermatome.
 Con’t...
• HZ in immunocompromised

•Increased incidence and severity with cutaneous and visceral dissemination

•Lesions are more ulcerative and necrotic with scarring, protracted course

•Multidermatomal involvment
•multiple recurrences as HIV progresses

•In AIDS acyclovir-resistant VZV

•may result in chronic, verrucous, hyperkeratotic or ecthymatous cutaneous
lesions
Pathogenesis of pain in HZ &
PHN

• Injury to the peripheral nerve & neurons in the ganglion triggers afferent
pain signals

• Inflammation in the skin triggers nociceptive signals that amplify

cutaneous pain

• Damage to neurons in the spinal cord and ganglion, and to the peripheral
nerve
Con’t...
• Damaged primary afferent nerves may become spontaneously active
& hypersensitive to peripheral stimuli & sympathetic stimulation

• Excessive nociceptor activity and ectopic impulse generation

• in turn sensitize CNS neurons, augmenting and prolonging central

responses to innocuous as well as noxious stimuli
 Disease course and prognosis

• The pain and the constitutional symptoms subside gradually as the eruption
disappears.
• In uncomplicated cases recovery is complete in 2–3 weeks in children and
young adults, and 3–4 weeks in older patients.

• In immunosuppressed individuals, especially due to HIV infection, zoster may

run a protracted course, with a small number of lesions developing into
verrucous or crusted nodules.

• Recurrent shingles can occur, either affecting the same dermatome (in 45% of
cases) or at a different site
Diagnosis
• Mainly clinical diagnosis
 the character and dermatomal location of the rash, coupled with
dermatomal pain or other sensory abnormalities
• A cluster of vesicles, particularly near the mouth or genitals, may
represent herpes zoster

• but it also may be recurrent HSV infection Zosteriform herpes simplex

• is often impossible to distinguish from herpes zoster on clinical grounds.
• history of multiple recurrences in the same dermatome distinguishes
zosteriform herpes simplex from herpes zoster.
Treatment
• Topical therapy

• application of cool compresses

• calamine lotion or Caladryl Clear cornstarch, or baking soda

• Occlusive ointments and creams or lotions containing glucocorticoids should

not be used.
• Topical treatment with antiviral agents is not effective

• Bacterial superinfection of herpes zoster lesions is uncommon and should be

treated with warm soaks
• bacterial cellulitis requires systemic antibiotic therapy.
Con’t...
• Antiviral treatment
• The major goals of antiviral therapy
• limit the extent, duration, and severity of pain and rash in the primary
dermatome
• prevent disease elsewhere
• The utility of antiviral agents is unproven if treatment is initiated more than 72
hours after rash onset.
Con’t...
• Nevertheless, we believe that it is prudent to initiate antiviral
therapy even if more than 72 hours have elapsed after rash onset
in patients with

• herpes zoster involving cranial nerves (eg, ophthalmic zoster),

• in patients who continue to have new vesicle formation,
• in patients who are of advanced age
Con’t...
• Anti inflammatory therapy
• use of corticosteroid is controvertial
• glucocorticoids did reduce acute pain in most trials

• and in one trial of acyclovir and prednisone, the time to uninterrupted

sleep, return to baseline daily activity, and cessation of analgesic therapy
was reduced

• Consequently, some experts advocate oral glucocorticoids for otherwise

healthy older adults whose rash is complicated by moderate-to-severe pain
and who have no contraindications to glucocorticoids
Con’t...

• Others believe that the common adverse effects of glucocorticoids

outweigh their benefits

• Analgesics
• aggressive pain control with nonopiate or opiate analgesics
•If pain control remains inadequate, regional or local anesthetic nerve
blocks should be considered for acute pain control
Con’t...
• Treatment of PHN

•it resolves spontaneously in most patients, although this often requires

several months
•treatment options
• gabapentin
• pregabalin
• tricyclic antidepressants
• opioid analgesics, tramadol
• 5% lidocaine patch
Prevention
• Long-term suppressive acyclovir treatment is only practical in
immunocompromised patients at proven risk of developing herpes zoster
within a defined time period
• in the year following bone marrow or solid organ transplantation.

• Live attenuated Vaccine

• >60yrs
• PHN by 66.5%
• Reduced the incidence of HZ by 51.3%
• No decrease in Hospitalization &death
References
• Fitzpatricks dermatology,9th edition
• Rooks text book of dermatology, 9th edition
• Bolognia 4th edition
• Andrews’ Diseases of the Skin clinical dermatology
• Uptodate 21.6
thank you