Herpes zoster is a localised disease caused by reactivation of the varicella zoster virus that enters the cutaneous nerve endings during an earlier episode of chicken pox, travels to the dorsal root ganglia, and remains in latent form. The condition is characterised by occurrence of multiple, painful, unilateral vesicles and ulceration, and shows a typical single dermatome innervated by single dorsal root or cranial sensory ganglion.

1. HERPES ZOSTER
Presented by
Dr. Rahul Srivastava
Professor
Rama Dental College Hospital
& Research Centre Kanpur

2. HERPES ZOSTER (HZ)
HZ is also known as shingles, which is derived from
the Latin cingulum, meaning ‘girdle’. This is
because a common presentation of HZ involves a
unilateral rash that can wrap around the waist or
torso like a girdle.

3. The name zoster is derived from classical Greek,
referring to a belt-like binding (known as a zoster)
used by warriors to secure armour.
Von Bokayin, in 1988, hypothesised for the first
time that chicken pox and HZ were caused by the
same infectious agent.

4. Varicella is commonly known as chickenpox; it
occurs in children while herpes zoster occurs in
adults or the elderly.
After the primary disease is healed,VZV becomes
latent in the dorsal root ganglia of spinal nerves
or extramedullary ganglia of cranial nerves.

5. A child without prior contact with VZV can
develop chickenpox after contact with an
individual with HZ.
The incidence of HZ is up to 15 times higher in
HIV-infected patients and it is found in 25% of
patients with Hodgkin’s lymphoma.

6. Etiology
Upon reactivation, the virus replicates in
neuronal cell bodies and virions shed from the
cells which are carried down the nerve to the
area of skin innervated by that ganglion.

7. In the skin, the virus causes local inflammation
and blistering. The pain caused by zoster is due
to inflammation of affected nerves with the virus.
Triggers for herpes zoster include
 Emotional stress.
 Use of medications (immunosuppressants).
 Acute or chronic illness.
 Exposure to the virus.
 Presence of a malignancy.

8. PHASES OF INFECTION
The three phases of the infection include:
Preeruptive stage presents with abnormal skin
sensations or pain within the dermatome
affected. This phase appears at least 48 hours
prior to any obvious lesions. At the same time, the
individual may experience headaches, general
malaise, and photophobia.

9. The acute eruptive phase is marked by the vesicles
and the symptoms seen in the pre-eruptive phase.
The lesions initially start as macules and quickly
transform into painful vesicles.
The vesicles often rupture, ulcerate and eventually
crust over. Patients are most infectious in this
stage until the lesion dry out.

10. Pain is severe during this phase and often
unresponsive to traditional pain medications. The
phase may last 2-4 weeks but the pain may
continue.

11. Chronic infection is characterized by recurrent
pain that lasts more than 4 weeks. Besides the
pain, patients experience paresthesias, shock-like
sensations, and dysesthesias. The pain is
disabling and may last 12 months or longer.

12. Clinical Features
A. The infection tends to involve individuals above
45 years of age, with the highest incidence
among persons aged between 68 and 90 years.
B. Among the divisions of the trigeminal nerve, the
ophthalmic division is most commonly involved
followed by the maxillary and mandibular
divisions.

13. C. Involvement of the trigeminal nerve leads to
lesions on the upper eyelid, forehead and scalp
with V1, midface and upper lip with V2 and
lower lip with V3.
D. With the involvement of V2, patients experience
a prodrome of pain, burning and tenderness,
usually on the palate on one side.

14. E. Zoster characteristically presents with a
prodrome of fever, malaise and excruciating
burning pain followed by the outbreak of
vesicles that appear in one to three crops over
three to five days.
F. Lesions are distributed unilaterally within a
single dermatome.

15. G. Clinically, lesions start as closely grouped
erythematous papules which, rapidly become
vesicles on an erythematous and edematous
base.
H. It may occur in continuous or interrupted bands
in one, two or more contiguous dermatomes
unilaterally.

16. I. Facial and intraoral lesions occur unilaterally
and are characteristic features of HZ.
J. The lesions usually begin to dry and
crustations appear after 3–5 days.

17. K. Total duration of the disease is generally
between 7 and 10 days; however, it may take
several weeks for the hypopigmented skin to
return to normal.
Dental complications:
Osteonecrosis.
Exfoliation of teeth.
Periodontitis.
Calcified and devitalized pulps.
Periapical lesions and resorption of roots.

18. Developmental anomalies:
Irregular short roots.
Missing teeth.

19. Secondary bacterial infection is another common
complication of HZ.
Other complications such as scarring of skin,
keratitis, retinal necrosis causing blindness,
keratouveitis, cranial and peripheral nerve
palsies, cerebral ataxia and pneumonia may lead
to death.

20. Zoster sine herpete (ZSH)
Zoster sine herpete (ZSH) refers to a condition in
which dermatomal distribution pain occurs in the
absence of an antecedent rash.
First defined by Lewis, who described zoster
patients with dermatomal distribution pain in
areas outside that affected by zoster rash, ZSH
later became a distinct disease entity when PCR
provided definitive virologic confirmation.

21. James Ramsay Hunt syndrome
A special form of zoster infection of the geniculate
ganglion, with the involvement of the external ear
and oral mucosa, has been termed Hunt's
syndrome first described in 1907 by James
Ramsay−Hunt.

22. It manifests as facial paralysis as well as pain in
the external auditory meatus and pinna of the
ear. In addition, vesicular eruptions occur in the
oral cavity and oropharynx with hoarseness,
tinnitus, vertigo and occasional other
disturbances.

23. When the glossopharyngeal ganglion is damaged,
lesions are seen on the posterior one third of the
tongue, uvula and posterior mouth along with
pharyngeal pain.
It can also involve the vagus nerve, which is the
tenth cranial nerve leading to paralysis of the
pharynx, larynx and blisters on the base of the
tongue.

24. Postherpetic Neuralgia
Postherpetic neuralgia (PHN) is a frequent
complication of HZ characterized by intense pain.
While the usual HZ pain lasts 2 to 4 weeks, PHN is
defined as pain persistent after 4 or 9 weeks.
Gabapentin and lidocaine patch 5% is the first
line for PHN and opoid analgesics and tricyclic
depressants the second line of treatments.

25. Prednisolone (administered at a dosage of 60 mg
/day for first week of zoster, tapered over 21 days
and given with antiviral therapy) can accelerate
quality of life improvements, including return to
usual activity.

26. The recommended dosages of commonly used
tricyclic depressants are listed below
Amitriptyline
0–25 mg orally at bedtime; increase dosage by
25 mg every 2–4 weeks until response is adequate,
or to a maximum dosage of 150 mg/day
Nortriptyline
0–25 mg orally at bedtime; increase dosage by
25 mg every 2–4 weeks until response is adequate,
or to a maximum dosage of 125 mg/day
Imipramine
25 mg orally at bedtime; increase dosage by 25 mg
every 2–4 weeks until response is adequate, or to a
maximum dosage of 150 mg/day
Desipramine
25 mg orally at bedtime; increase dosage by 25 mg
every 2–4 weeks until response is adequate

27. Diagnosis
A. Herpes zoster is clinically diagnosed with
burning pain, characteristic morphology, and
typical distribution.
B. Herpes simplex virus can occasionally produce a
rash in a pattern called as zosteriform herpes
simplex.

28. Tests for varicella-zoster virus
A. The Tzanck smear of vesicular fluid shows
multinucleated giant cells. It has lower
sensitivity and specificity than direct fluorescent
antibody (DFA) or Polymerase chain reaction
(PCR).
B. Varicella-zoster virus-specific IgM antibody in
blood is detected during the active infection of
chickenpox or shingles but not when the virus is
dormant.

29. C. Direct fluorescent antibody testing of vesicular
fluid or corneal fluid can be done when there is
eye involvement.
D. PCR testing of vesicular fluid, a corneal lesion, or
blood in a case with eye involvement or
disseminated infection.

30. E. Molecular biology tests based on in vitro nucleic
acid amplification (PCR tests) are currently
considered the most reliable. Nested PCR test has
high sensitivity, but is susceptible to
contamination leading to false-positive results.
F. The latest real-time PCR tests are rapid, easy to
perform, as sensitive as nested PCR, have a lower
risk of contamination, and also have more
sensitivity than viral cultures.

31. TREATMENT

32. Conventional treatment options
The objective of conventional therapy in the
treatment of HZ is to accelerate healing of the
lesions, reduce the accompanying pain and prevent
complications.

33. Topical Capsaicin
Capsaicin is an alkaloid derived from cayenne
pepper (Capsicum frutescens).
A well-studied compound, capsaicin is of particular
importance in the treatment of PHN because of its
effect on C-fibre sensory neurons.

34. These neurons release inflammatory neuropeptides
such as substance P that mediate neurogenic
inflammation and chemical-initiated pain.
It should not be applied until skin lesions have
healed.
Capsaicin 0.075% cream- Apply 4 times per day.
Capsaicin 8% patch- Application time of 30–90
minutes.

35. Topical lidocaine
Lidocaine 5% patch - One patch can be applied to the
location of pain. Up to 3 patches can be used at the
same time for a maximum of 12 hours.

36. Antiviral agents
Drug Dosage Remarks
Acyclovir
Adults: 5 × 800 mg/day p.o.
Limited
bioavailability
3 × 500 mg/day i.v. In uncomplicated HZ
3–5 × 10 mg/kg/day for 10
day, usually 5–7 days
In severe HZ, in case
of
immunosuppression
Children: 3 × 10 mg/kg/day
Brivudin
Adults: 125 mg once a day
p.o.
For 5 days.
Valaciclovir Adults: 3 × 1000 mg/day p.o. For 7 days
Famciclovir Adults: 3 × 250–500 mg/day
2nd line in ACV-
resistant patients

37. Corticosteroids
Oral corticosteroids have commonly been used for
pain management in HZ, although clinical trials
have yielded inconsistent results for reducing
development of PHN.
Oral prednisone and prednisolone, starting dose
from 35 to 60 mg/day, generally tapering over 3 to
4 weeks.

38. Corticosteroids
Oral corticosteroids have commonly been used for
pain management in HZ, although clinical trials
have yielded inconsistent results for reducing
development of PHN.
Oral prednisone and prednisolone, starting dose
from 35 to 60 mg/day, generally tapering over 3 to
4 weeks.

39. Pain control
A. In patients with severe pain, use of narcotics
may be indicated.
B. Use of nerve block injections is another option in
the conventional medical model.
C. Local anaesthetic may be injected around the
affected nerves, providing pain relief typically
lasting 12–24 h.

40. Transcutaneous electrical nerve stimulation
Use of transcutaneous electrical nerve stimulation
(TENS) therapy has been beneficial in the
management of PHN.
Vaccination
Centers of Disease Control & Prevention (CDC)
recommends two doses of chickenpox vaccine for
children, adolescents, and adults who have never
had chickenpox and were never vaccinated.

41. Children are routinely recommended to receive the
first dose at 12 through 15 months of age and the
second dose at 4 through 6 years of age.
CDC recommends a single dose of Zostavax® (zoster
vaccine live) for people 60 years old or older, whether
or not the person reported a prior episode of herpes
zoster (shingles).

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