1

Chickenpox(varicella)

Dr. Rajalekshmy.P.RDept of Swasthavritta

Amrita School of Ayurveda

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.

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.

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.

5

6

7

8

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.

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.

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.

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.

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.

14

SECONDARY ATTACK RATE• Chickenpox is highly communicable.

• Secondary attack rate in household contact is up to 90%.

15

HOST FACTORSAGE

Among children below 10 yrs of ageCan 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

16

CONGENITAL VARICELLA SYNDROMEInfection 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.

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.

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.

19

PATHOGENESISInhalation 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

20

INCUBATION PERIOD

• Usually 14 to 16 days• 10 to 21 days have also been reported.

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

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.

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

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.

25

RAPID EVOLUTION

Macule Papule Vesicle Pustule

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.

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.

28

FEVER• The fever does not run high. • Temperature rises with each fresh crop of rash.

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.

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.

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.

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.

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.

34

PROGNOSIS• Chickenpox that affects a healthy child is usually a self-limiting

disease.• Increased morbidity occurs in adult and immune compromised

populations.

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.

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.

37

PREVENTION

•Passive- Varicella zoster immunoglobulin•Active- Vaccine

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.

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.

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

41