Chickenpox is caused by the varicella-zoster virus and causes a characteristic itchy vesicular rash. It is highly contagious and spreads through respiratory droplets. The rash progresses rapidly from macules to papules to vesicles and crusts over within 4-7 days. Complications can occur in immunosuppressed individuals and include pneumonia and encephalitis. Vaccination with the live attenuated varicella vaccine provides effective protection.

1. Chickenpox
(varicella)
Dr. Rajalekshmy.P.R
Dept of Swasthavritta
Amrita School of Ayurveda 1

2. INTRODUCTION
• Acute highly infectious disease caused
by varicella-zoster virus.
• World wide in distribution and occurs
in both epidemic and endemic forms.
• Chickenpox and herpes zoster are
regarded as different host responses to
same etiological agent.
• Characterized by vesicular rash that
may be accompanied by fever and
malaise. 2

3. HISTORY
• Primary varicella infection was not
reliably distinguished from smallpox until
19th century.
• 1875-Steiner demonstrated that varicella
was caused by an infectious agent by
inoculating volunteers with vesicular fluid
from a patient with acute varicella.
• Clinical observations of relationship
between varicella and herpes zoster were
made in 1888 by Von Bokay, when
children without the evidence of varicella
immunity acquired varicella after contact
with herpes zoster. 3

4. • 1954-VZV was isolated from
vesicular fluid of both chickenpox
and zoster lesions in cell culture by
Thomas weller.
• 1970- live attenuated vaccine was
developed in Japan.
• March 1995- Vaccine licensed for use
in US.
• May 2006- the first vaccine to reduce
the risk of herpes zoster was licensed.
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9. Some facts…
• How it got its name?
• It has been said to be
derived from chickpeas,
based on resemblance of
the vesicles to
chickpeas or to come
from the rash resembling
chicken pecks.
Some parents believe that
it is better for children to
contract chickenpox than
to get the vaccine, and
they deliberately expose
their children to the virus,
sometimes by taking them
to chickenpox parties.
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10. AGENT
• Varicella –Zoster virus(Human
(alpha)herpes virus 3).
• DNA virus; member of herpes
group.
• VZV only affects humans, and
commonly causes chickenpox in
children, teens and young adults
and herpes zoster (shingles) in
adults and rarely in children.
• Varicella-zoster virus (VZV)
causes primary, latent, and
recurrent infections.
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11. • The primary infection is manifested as
varicella (chickenpox) and results in
establishment of a lifelong latent
infection in cranial nerves sensory
ganglia and spinal dorsal root ganglia.
• When cellmediated immunity wanes
with age or following immune
suppressive therapy, virus may
reactivate resulting in herpes zoster in
about 10-30% persons.
• Latent infection causes painful,
vesicular ,pustular eruption in the
distribution of one or more sensory
nerve roots.
• Virus can be grown in tissue culture.
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12. SOURCE OF INFECTION
• A case of chickenpox
• Virus occurs in the
oropharyngeal secretions and
lesions of skin and mucosa.
• Rarely, the source of infection
may be a herpes zoster patient.
• Virus can be isolated from the
vesicular fluid during the first 3
days of illness.
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13. INFECTIVITY
• Period of communicability 1 to 2days before and 4 to 5 days
after appearance of rash.
• Infectivity ceases once the lesions are crusted.
• Virus tend to die out before pustular stage.
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14. SECONDARY ATTACK RATE
• Chickenpox is highly communicable.
• Secondary attack rate in household contact is up to 90%.
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15. HOST FACTORS
AGE
Among children below 10 yrs of age
Can occur in adults also(severe)
IMMUNITY
One attack confers lifelong immunity.
Secondary attacks are rare.
Cell mediated immunity prevents recurrence
and reactivation of latent infection.
IgG antibodies persist for life time and
prevents from varicella.
SEX
Both sex equally affected
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16. CONGENITAL VARICELLA SYNDROME
Infection during first trimester
• Foetus gets intra uterine infection.
• Resulting in severe damage
• Characterized by LBW, micro opthalmia,
choroido retinitis, cataract, hypotrophic
limbs with hypotonicity and zoster like
lesions/scars.
Infection during last trimester
• No developmental defects
• Mild attack with rashes(maternal
antibodies)
Infection during last few days
before delivery
• Newborn will develop
chickenpox during neonatal
period and it will be severe.
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17. ENVIRONMENTAL FACTORS
• Chickenpox shows a seasonal trend in India, mostly occur during first
six months of the year.
• In temperate climates there is little evidence of seasonal trends.
• Overcrowding favours transmission.
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18. TRANSMISSION
• Transmitted from person to person by droplet
infection and droplet nuclei.
• Portal of entry - respiratory tract.
• Fomites doesn’t play a significant role in
transmission.
• Virus can cross the placenta and cause congenital
varicella.
• Chickenpox can also spread from people
with shingles.
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19. PATHOGENESIS
Inhalation of respiratory droplets
Virus infects upper respiratory tract
Viral proliferation in regional lymph
nodes of the URT( 2-4 days after
initial infection)
Stage of primary viremia
Viral replication in other organs
(liver & spleen)
VZV infection of cells of the malphigian
layer produces both intercellular oedema
and intracellular oedema, resulting in the
characteristic vesicle.
diffuse viral invasion of capillary
endothelial cells and the epidermis.
Stage of secondary viremia
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20. INCUBATION PERIOD
• Usually 14 to 16 days
• 10 to 21 days have also been reported.
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21. CLINICAL FEATURES
• Wide clinical spectrum.
• May vary from a mild illness with only a few scattered lesions to
severe febrile illness with widespread rash.
• Divided into 2 stages
a) Pre-eruptive stage
b) Eruptive stage
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22. PRE-ERUPTIVE STAGE
• Onset is sudden with mild or moderate
fever, pain in back, shivering and malaise.
• Very brief stage lasting for 24 hr.
• In adults-more severe and last for 2-3 days
before rash comes out.
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23. ERUPTIVE STAGE
• In children the rash is often the first sign.
• It comes on the day the fever starts.
Characteristics
• Distribution
• Rapid evolution
• Pleomorphism
• Fever
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24. DISTRIBUTION
• Symmetric rashes.
• Centripetal in distribution.
a.First appears on the trunk (abundant)
b.Then to face, arms and legs (less abundant)
• Mucosal surface are generally involved.
• Axilla may be affected.
• Palms and soles not usually affected.
• Density of eruptions diminishes centrifugally.
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25. RAPID EVOLUTION
Macule Papule Vesicle Pustule
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26. • Rash advances quickly through the
stage of the macule, papule, vesicles
and scab.
• Vesicles are dew – drops like in
appearance, present on the skin,
containing the clean fluid superficial in
site, with the easily ruptured wall and
surrounded by an area of inflammation
and are not umblicated.
• The vesicles may form the crusts
without going through the pustular
stage.
• Scabbing begin 4 – 7 days after the rash
appearance.
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27. PLEOMORPHISM
• All stages of the rash (Papule,
vesicles & crusts) may be seen
simultaneously at one time in
same area.
• This due to the rash appearing in
the successive crops for the 4 – 5
days in same area.
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28. FEVER
• The fever does not run high.
• Temperature rises with each fresh crop of rash.
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29. smallpox chickenpox
1.Incubation period 12days(7-17days) 15days(7-21days)
2.Prodromal symptoms Severe Usually mild
3.Distribution of rash • Centrifugal
• Palms and soles involved.
• Axilla usually free.
• Predominant on extensor & bony
prominence.
• Centripetal
• Rarely affected.
• Axilla affected.
• Mostly on flexor surface.
4.Characteristics of rash • Deep-seated.
• Vesicles multilocular & umbilicated.
• Only one stage of rash seen.
• No area of inflammation around vesicle
• Superficial.
• Unilocular & unumbilicated.
• Pleomorphic.
• Area of inflammation around rash
seen.
5.Evolution of rash • Slow deliberate and majestic passing
through definite stage.
• Scab formed in 10-14 days after rash
appears.
• Evolution of rashes very rapid.
• Forms in 4-7days after the rash
appears.
6.fever • Subsides with the appearance of rash, but
may rise again in the pustular stage.
• Temperature rises with each fresh
crop of rash.
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30. VARITIES OF CHECKEN POX
• Varicella bulla: characterized by formation of bullous
eruptions.
• Varicella ganrenosa: It is seen in ill-nourished children
and there are dark crusts are formed in the eruptions
which on separation leave behind ulcers.
• Varicella haemorrhagica: Uncommon virulent form of
varicella . Hemorrhages occur into the vesicles and
bleeding may take place from the mucous membrane.
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31. COMPLICATIONS
• Chickenpox is mild and self limiting disease.
• In uncomplicated cases mortality less than 1%.
• Severe complication occur in immunosuppressed patients and may
also occur in normal children and adults.
• Varicella pneumonia is rare in healthy children but is the most
common complication in neonates, adults and immuno-compromised
patients.
• Other complications-haemorrhages, pneumonia, encephalitis, acute
cerebellar ataxia and Reye’s syndrome.
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32. • Maternal varicella during pregnancy causes foetal wastage
and birth defects – cutaneous scars, atrophied limbs,
microcephaly, LBW, cataract, micropthalmia, chorio-
retinitis, deafness, cerebro-cortical atrophy.
• If varicella develops within 5 days afer delivery, newborn is
at risk of disseminated disease and should receive varicella
zoster immunoglobulin.
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33. • Associated with acute retinal necrosis and progressive outer
retinal necrosis, both of which occur with increased frequency
among AIDS patients.
• Cellulitis, erysipelas, osteomyelitis, scarlet fever and rarely
meningitis are observed.
• Immuno compromised patients are at increased risk of
complications of varicella, including those with malignancies,
organ transplants or HIV infection and those receiving high doses
of corticosteroids.
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34. PROGNOSIS
• Chickenpox that affects a healthy child is usually a self-limiting
disease.
• Increased morbidity occurs in adult and immune compromised
populations.
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35. LABORATORY DIAGNOSIS
• Rarely required as clinical signs are clear-cut.
• Examination of the vesicle fluid in electronic
microscope shows round particles(brick shaped in
smallpox).
• Scrapings of vesicle floors shows multinucleated
giant cells coloured by Geimsa stain(not in
smallpox).
• Serology is used for epidemiological surveys.
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36. CONTROL
Notification
Isolation of cases for 6
days after onset of rash
Disinfection of articles
soiled by nose and
throat discharge
• Anti viral therapy against varicella –
Acyclovir, Valacylovir, Famiciclovir
and foscarnet.
• Acyclovir can prevent development
of systemic disease in varicella
infected immune suppressed patients
and halt progress of zoster in adults.
• Acyclovir does not prevent post
herpetic neuralgia.
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37. PREVENTION
•Passive- Varicella zoster immunoglobulin
•Active- Vaccine
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38. VARICELLA ZOSTER IG
• Given within 72 hrs of exposure particularly in immune suppressed
person.
includes:
•Susceptible person receiving immunosuppressive therapy
•Congenital cellular immunodeficiency.
•Acquired immunodeficiency.
•Susceptible and exposed persons eg. In pregnant women
•New-borns, premature infant with low birth weight.
• VZIG has no therapeutic effect.
•IM injection; Dose: 12.5unit/kg body weight, maximum of 625 units.38

39. VACCINATION
• Live attenuated freeze dried varicella vaccine(varivax)
• Developed by using Oka strain of virus in Japan, grown on human
diploid cells.
• Recommended for children between 12 months and 12 years.
• Dose-0.5ml subcutaneously
• 90% efficacy
• Immunity lasts for 10 to 15 yrs.
• For primary immunization in adults, 2 doses are recommended with 4
to 8 weeks interval.
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40. CONTRAINDICATIONS
• Should not be given to
immune compromised
individuals including HIV +ve
children and adults or
pregnant women.
ADVERSE REACTIONS
• Occurs 4-6 weeks after
vaccination.
• 25%-tenderness and erythema
• 10-15%- fever
• 5%- localized maculopapular or
vesicular rash
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