This document provides information about chickenpox and shingles. It discusses the origin of the term "chickenpox", the virus properties, epidemiology and pathogenesis of varicella zoster virus. It describes the clinical features and treatment of chickenpox and shingles. Complications like secondary bacterial infections and post-herpetic neuralgia are also summarized. The diagnosis and management of both chickenpox and shingles infections are outlined in less than 3 sentences.

1. CHICKEN POX
Presented by:
Anish Dhakal
21st November, 2018
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2. CHICKEN POX: ORIGIN
OF THE TERM?
• One is that it's from the blisters
that are seen with the illness.
These red spots — which are
about 5mm to 10mm wide —
were once thought to look like
chickpeas (Kabuli Chana).
• Another theory is that the rash
of chickenpox looks like the
peck marks caused by a
chicken.
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3. VIRUS PROPERTIES
• Belong to the alpha
herpesvirus subfamily of
herpes viruses
• Double stranded DNA
enveloped virus
• Genome size 125 kbp, long
and short fragments with a
total of 4 isometric forms.
• Single serotype only,
although there is some cross
reaction with HSV.

4. HERPES VIRUSES
1. Herpes simplex virus type 1 (HSV-1)
2. Herpes simplex virus type 2 (HSV-2)
3. Varicella-Zoster virus (VZV, HHV-3)
4. Epstein-Barr virus (EBV HHV-4)
5. Cytomegalo virus (CMV HHV-5)
6. Human herpesvirus 6 (HBLV/HHV-6)
7. Human herpesvirus 7 (HHV-7)
8. Human Herpes virus-8 (HHV-8): Kaposi's sarcoma-
associated herpesvirus (KSHV)
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Leading cause of human viral disease, second only to
influenza and cold viruses.
Contains Eight currently identified members.

5. EPIDEMIOLOGY
• Highest prevalence occurring in the 4 - 10 years old age
group.
• Varicella is highly communicable, with an attack rate of
90% in close contacts.
• Most people become infected before adulthood but 10% of
young adults remain susceptible.

6. PATHOGENESIS
• The virus is thought to gain entry via the respiratory tract and
spreads shortly after to the lymphoid system.
• VZV infects macrophages and pneumocytes in the respiratory
mucosa.
• Virus spreads to lymphocytes and monocytes and to the
reticulo-endothelial system.
• Secondary viremia occurs and virus travels to epithelial sites
• Appearance of characteristic vesicular rash containing
multinucleated giant cells with intracellular inclusions
• After an incubation period of 14 days, the virus arrives at
its main target organ, the skin.

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• Following the primary infection, the virus remains latent
in the cerebral or posterior root ganglia. In 10 - 20% of
individuals, a single recurrent infection occurs after
several decades.
• The virus reactivates in the ganglion and tracks down
the sensory nerve to the area of the skin innervated by
the nerve, producing a varicella form rash in the
distribution of a dermatome.
• Mode of transmission:
• Respiratory aerosols
• Direct contact with skin lesions

8. CHICKEN POX:
• Primary infection results in varicella (chickenpox)
• Incubation period of 14-21 days
• Presents fever, lymphadadenopathy. a widespread
vesicular rash
• Rash in face, upper body then entire body
• Person is contagious 1-2 days before the rash
appears and until all blisters have formed scabs

9. CLINICAL FEATURES
• The prodromal symptoms in children are
absent or consist of low fever, headache, and
malaise
 appear directly before or with the onset of the eruption
• Symptoms are more severe in adults
• Fever, chills, malaise, and backache occur 2 to
3 days before the eruption.

10. CLINICAL FEATURES
• Varicella is characterized by a vesicular eruption
consisting of delicate “teardrop” or “dew drop”
vesicles on an erythematous base (rose petal)
• The eruption starts with faint macules that develop rapidly into
vesicles within 24 h.
• Successive fresh crops of vesicles appear for a few days, mainly on
the trunk, face, and oral mucosa.
• The vesicles quickly become pustular and umbilicated, then crusted
• Since the lesions appear in crops, lesions of various
stages are present at the same time, a useful clue to the
diagnosis.  macules, papules, vesicles, pustules and
crust

11. DEW DROP ON ROSE PETAL

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 The vesicle becomes cloudy and
depressed in the center
(umbilicated), the border is irregular
(scalloped)B
 A crust forms in the center and
eventually replaces the remaining
portion of the vesicle at the
periphery C

13. THE RASH BEGINS ON THE TRUNK (CENTRIPETAL
DISTRIBUTION) AND SPREADS TO THE FACE AND
EXTREMITIES (CENTRIFUGAL SPREAD)
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14. • Lesions tend not to scar, but larger ones and those that
become secondarily infected may heal with a
characteristic round, depressed scar.

15. TREATMENT
• Antiviral Acyclovir  20
mg/kg (800 mg maximum) five
times daily for 7-10 days
• Analgesia: Pain (Don’t use
Aspirin  risk of Reye’s
syndrome in children)
• Antihistaminics: Pruritus
• In Acyclovir resistant: Foscarnet

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18. • Most common complication is secondary
bacterial infection of the vesicles. 18

19. PREVENTION
• Live attenuated viral vaccine
for varicella is a currently
recommended childhood
immunization.
• Two doses are now
recommended, one between
age 12 and 15 months and the
second at 4–6 years.

20. USE OF LIVE
ATTENUATED VACCINE!
• A live attenuated vaccine is available. There had been great
reluctance to use it in the past, especially in
immunocompromised individuals since the vaccine virus
can become latent and reactivate later on.
• However, recent data suggests that the vaccine is safe, even
in children with leukemia provided that they are in
remission.
• It is highly debatable whether universal vaccination should be
offered since chickenpox and shingles are normally mild
diseases.
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21. SHINGLES

22. HERPES ZOSTER
(SHINGLES)
• Herpes Zoster mainly affect a single dermatome of the
skin.
• Majority of patients are more than 50 years of age.
• The latent virus reactivates in a sensory ganglion and
tracks down the sensory nerve to the appropriate
segment.
• There is a characteristic eruption of vesicles in the
dermatome which is often accompanied by intensive pain
which may last for months (postherpetic neuralgia)

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Herpes zoster may involve one, two, or three
adjacent dermatomes

24. SHINGLES
• Skin lesions: Usually in the
thorax.
• Shingles of an intercostal
nerve produces vesicular
eruptions and burning pain in
the affected dermatome
• Maculopapular with an
erythematous base and
usually heal in about 2
weeks.
• Reactivation can affect the
eye via the trigeminal nerve
and the brain via the
cranial nerve VII and VIII.
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25. 2
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26. CLINICAL FEATURES
• The erythematous, maculopapular and vesicular lesions of
herpes zoster are clustered rather than scattered
• Most important clinical manifestation is pain
• Common complication: chronic pain or postherpetic
neuraligia
• Post-herpetic neuralgia: pain that persists for longer
than a month after the onset of herpes zoster

27. CLINICAL VARIANTS
• Zoster Sine Herpete- acute segmental neuralgia without
ever developing a cutaneous eruption
• Ramsay Hunt Syndrome- herpes zoster otticus- due to
involvement of the facial and auditory nerve, there is
facial palsy with herpes zoster of the external ear or
tympanic membrane
• Zoster Ophthalmicus- ophthalmic division of the fifth cranial
nerve is involved. If the external division of the nasociliary
branch is affected  vesicles on the side and tip of the
nose (Hutchinson’s sign)

30. CONGENITAL VARICELLA
SYNDROME
• 90% of pregnant women already immune, therefore primary
infection is rare during pregnancy.
• Primary infection during pregnancy carries a greater risk
of severe disease, in particular pneumonia.
First 20 weeks of Pregnancy
• Up to 3% chance of transmission to the fetus,
recognised congenital varicella syndrome

31. CONGENITAL VARICELLA
SYNDROME
Sign and Symptoms:
Affected newborns may have a low birth weight and
characteristic abnormalities
Intra-uterine growth retardation
Skin abnormalities (scaring, indurate, erythematic)
Cataract
Microcephaly,seizure
Developmental delay
Treatment:
Newborn children of infected mothers should be given
varicella zoster immunoglobulin as soon as possible
after birth.

32. NEONATAL VARICELLA
• VZV can cross the placenta in the late stages of pregnancy
to infect the fetus congenitally.
• If rash in mother occurs more than 1 week before
delivery, then sufficient immunity would have been
transferred to the fetus.
• Zoster immunoglobulin should be given to susceptible
pregnant women who had contact with suspected cases
of varicella.
• Zoster immunoglobulin should also be given to infants
whose mothers develop varicella during the last 7 days of
pregnancy or the first 14 days after delivery.

33. DIAGNOSIS
Usually only for atypical presentations, particularly in the
immunocompromised.
• Virus Isolation - rarely carried out as it requires 2-3
weeks for a results.
• Direct detection - electron microscopy may be used for
vesicle fluids but cannot distinguish between HSV and
VZV. Immunofluorescense on skin scrappings can
distinguish between the two.
• Serology - the presence of VZV IgG is indicative of past
infection and immunity. The presence of IgM is
indicative of recent primary infection.

34. DIAGNOSIS
• Clinical diagnosis: Characteristic appearance of lesions
• Definitive diagnosis:
• Culture of the virus from the lesions followed by detection of
specific antigens.
• Tzanck smear: Characteristic appearance of cells (Multinucleated
giant cells) in biopsy specimens of skin lesions
• Rise in antibody titre: Useful in case of varicella but less useful in
zoster.
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35. Cytopathic Effect of VZV in cell culture: (Ballooning of cells)
Cytopathic Effect of VZV

36. • Clinical Diagnosis
1. A Tzanck smear from a vesicle
will usually show characteristic
multinucleate giant cells.
2. Multinucleated giant cells contain
acidophilic intranuclear body (Cowdry
Type A inclusions)

37. MANAGEMENT
• Herpes zoster in a healthy individual is not normally a cause
for concern. The main problem is the management of the
postherpetic neuralgia.
• The International Herpes Management Forum
recommends that antiviral therapy should be offered
routinely to all patients over 50 years of age presenting
with herpes zoster.
• Three drugs can be used for the treatment of herpes zoster:
acyclovir, valicyclovir, and famciclovir. There appears to be
little difference in efficacy between them.

38. MANAGEMENT CONTD…
• Within 48-72 hour of onset of rash and over age 50:
 800mg Acyclovir five times a day for 7-10 days
 Reduction of post herpetic neuralgia incidence
• Valacyclovir :1000 mg PO three times daily for 7 days
• Famciclovir : 500 mg PO three times daily for 7 days
• Analgesia: Pain
• Antihistaminic: Pruritus
• In Acyclovir resistant: Foscarnet
• If post herpetic neuralgia  gabapentine (600 mg BD/TDS)
& amitryptilline

39. PREVENTION: ZOSTER
• Preventive measures should be considered for individuals at
risk of contracting severe varicella infection e.g. leukaemic
children, neonates, and pregnant women
• Where urgent protection is needed, passive immunization
should be given. Zoster immunoglobulin (ZIG) is the
preparation of choice but it is very expensive. Where ZIG is
not available, HNIG should be given instead.
• Antiviral agents in acute phase and oral steroids may
help prevent postherpetic neuralgia

40. REFERENCES
• Illustrated Synopsis of Dermatology and Sexually Transmitted
diseases, Neena Khanna, 5th Edition
• John Hunter, John Savin and Mark Dahl, Clinical Dermatology,
3rd edition
• Illustrated Textbook of Dermatology, JS Pasricha et al.
• Uptodate.com

41. ONE DAY DURING A VIVA
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