chickenpox, based on park's social and preventive medicine

1. CHICKENPOX
(Varicella)
Dr.K.R.Rahul
Dept. of Swasthavritta.
Amrita School of Ayurveda.

2. CHICKENPOX
 How it got its name?
 Also known as Varicella
 The first documented use of the term chicken pox was in 1684
 Chicken pox is an acute highly infectious disease.
 Caused by the varicella – Zoster virus (VZV).
 Primary infection results in Varicella.
 Characterized by the vascular rash, that may be accompanied by the fever and
malaise.
 World wide in distribution occurs both as endemic and epidemic form.

3. AGENT FACTORS
Agent
 Varicella – Zoster Virus
 Human α Herpes virus type III
 VZV is a DNA virus
 A member of Herpes virus group.
 Primary infection causes chickenpox followed by
Latent infection in cranial nerves sensory ganglia
and spinal dorsal root ganglia.
 Latent infection causes painful, vesicular ,pustular
eruption in the distribution of one or more sensory nerve roots.

4. AGENT FACTORS
Source of infection
 Oropharyngeal secretion
 Lesion of the skin and mucosa
 Rarely patients with Herpes Zoster .
 Virus can be isolated from the vesicular fluid during the first 3days of illness
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.
Secondary attack rate
 Chickenpox is highly communicable
 Secondary attack rate in household contact is up to 90%

5. HOST FACTORS
Age
 Occurs primarily in children under 10yrs.
 Disease can be severe in adults.
Immunity
 One attack gives durable immunity.
 Maternal antibodies protects infant during first few months.
 Cell mediated immunity helps in the recovery from VZV.
 IgG antibodies persist for life time and prevents from varicella.

6. HOST FACTORS
Pregnancy
 The dangers to the foetus associated with a primary VZV infection are greater in the
first six months.
 In 3rd trimester mother is more likely to have severe symptoms.
 Maternal infection is associated with premature delivery.
 Infection leads to congenital varicella syndrome.
 Effects on the foetus can range in severity from underdeveloped toes and fingers to
severe anal and bladder malformation.

7. ENVIRONMENTAL FACTORS
 Chickenpox shows a seasonal trend in India, mostly occur in first 6months of the
year.
 In temperate climates there is little evidence of seasonal trends.

8. TRANSMISSION
 Transmitted from person to person by droplet infection via droplet nuclei.
 Portal of entry is through respiratory tract.
 Fomites doesn’t play a significant role in transmission.
 Virus can cross the placenta and cause congenital varicella.
 Chickenpox can also be spread from people with shingles.

9. INCUBATION PERIOD
 Usually 14 to 16 days, 10 to 21 days are also reported

10. CLINICAL FEATURES
 Vary from mild illness to severe febrile illness with wide spread rashes.
 Mild prodromal (fever, malaise) for 1-2 days
 Successive crops (2-4 days) of pruritic vesicles
 Generally appear first on head; most concentrated on trunk
 Can spread over the entire body causing between 250 to 500 itchy blisters
 Generally mild in healthy children
Divided into 2 stages
a) PRE-ERUPTIVE STAGE
b) ERUPTIVE STAGE

11. PRE-ERUPTIVE STAGE
 Sudden onset with mild or moderate fever.
 Headache, backache and sore throat.
 In children this stage is very brief (about 24hrs).
 In adults the illness is more severe and last for2 to 3 days.

12. ERUPTIVE STAGE
 In children the rash is often first sign coming on the day
the fever starts.
The distinctive features of rash are:
 Centripetal Distribution
 Rapid Evaluation
 Pleomorphism
 Fever

13. ERUPTIVE STAGE
Distribution
 Rash is symmetric.
 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. But palms and soles are not affected.
 Density diminishes centrifugally.

14. ERUPTIVE STAGE
Rapid evolution
 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
the area of the 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

15. ERUPTIVE STAGE
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.
Fever
 The fever does not run high.
 Temperature rises with each fresh crop of rash.

16. 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.

17. COMPLICATION
 Chickenpox is mild and self limiting disease.
 In uncomplicated cases mortality less than 1%.
 Severe complication occur in immunosuppressed patients and may occur in normal
children and adults.
Hemorrhage (varicella haemorrhagica)
Pneumonia.
Encephalitis.
Acute cerebellar Ataxia.
Reye’s Syndrome
Fetal death and birth defects in case of the maternal varicella during the
pregnancy.
Acute retinal necrosis and progressive outer retinal necrosis in AIDS patients.

18. COMPLICATION
The most common complications are:
 Bacterial infections of the skin and soft tissues in children
 Septicaemia
 Toxic Shock Syndrome
 Necrotizing Fasciitis
 Osteomyelitis
 Bacterial pneumonia
 Septic arthritis.

19. LABORATORY DIAGNOSIS
 Rarely required as clinical signs are clear-cut.
 Examination of the vesicle fluid in electronic microscope shows round particles.
 Used for culturing virus.
 Serology is used for epidemiological surveys.

20. CONTROL
 Usual control methods are –Notification, isolation and disinfection.
 Isolation of cases for about 6 days after onset of rash.
 Disinfection of articles soiled with nose and throat discharge.
 Anti viral therapy against varicella – Acyclovir, Valacylovir, Famiciclovir and
foscarnet.
 Acyclovir- can prevent the development of systemic disease in immunocompromised
patients, but it doesn’t prevent the post-herpetic neuralgia.

21. PREVENTION
1. VERICELLA ZOSTER IMMUNOGLOBULIN (VZIG)
Given with in 72 hrs of exposure particularly in immune suppressed person.
includes:
Susceptible person receiving immunosuppressive therapy
Congenital cellular immunodeficiency.
Acquired immunodeficiency.
Pregnant women
New-borns, premature infant with low birth weight.
VZIG has no therapeutic effect.
Dose: 12.5unit/kg body weight, maximum of 625 units, repeat dose in 3 week.
Not given along with varicella vaccine.

22. PREVENTION
2. Vaccine
 Live attenuated varicella vaccine is used
 Recommended for children between 12-18 months, who have not
had chickenpox.
 90% efficiency is suggested.
 Should not be given to immunocompromised person, HIV positive
person, pregnant women.

23. Thank you