• Chickenpox or varicella is an acute, highly infectious
disease caused by Varicella-zoster (V –Z) virus.
• The disease was named after chick peas, ; it reflects a
corruption of the Old English word giccin, which meant
itching.
• Characterized by vesicular rash that may be
accompanied by fever and malaise.
• World-wide in distribution and occurs in endemic and
epidemic forms.
• Chickenpox and Herpes zoster are now regarded as
different host responses to the same etiological agent.
EPIDEMIOLOGICAL DETERMINANTS
AGENT FACTORS
• AGENT: causative agent - Human (alpha) herpes virus.
• Primary infection causes chicken pox.
• Recovery followed by latent infection.
- Reactivation results in zoster- a painful, vesicular,
pustular eruption in distribution of one or more
sensory nerve roots.
• Can be grown in tissue culture.
INCUBATION PERIOD: Usually 14-16 days,
although extremes as wide as 7-21 days have
been reported.
AGENT FACTORS
• SOURCE OF INFECTION:
―Usually a case of chicken pox.
―It appears in the oropharyngeal secretions and lesions of
skin and mucosa.
―Rarely may be a patient with herpes zoster.
―It can be isolated from the vesicular fluid during the first 3
days of illness.
• INFECTIVITY:
−Period of communicability: 1-2 days before the
appearance of rash, and 4-5 days thereafter.
−It tends to die out before the pustular stage.
−Patient ceases to be infectious once the lesion have
crusted.
• SECONDARY ATTACK RATE: About 90% in household
contacts.
HOST FACTORS
• AGE: Children under 10 years of age. Few escape until adulthood but
can be severe in adults.
• IMMUNITY:
−One attack give durable immunity. Secondary Attacks are rare.
−The acquisition of maternal antibody protects the infant during the
1st few months of life.
−No age is exempt in the absence of immunity.
−IgG antibodies persist for life and their presence is correlated with
protection against varicella.
−Cell mediated immunity is important in recovery and in protection
against reactivation.
• PREGNANCY: Infection during pregnancy presents a
risk for the fetus and the neonate.
ENVIRONMENTAL FACTORS
• It shows a seasonal trend, occurring mostly during the first six months
of the year.
• Overcrowding.
• In temperate climates, there is little evidence of seasonal trend.
TRANSMISSION
• Droplet infection and droplet nuclei.
• “Face to face” (personal) contact.
• PORTAL OF ENTRY: Respiratory tract.
• Virus is extremely labile, so fomites unlikely to transmit.
• Contact infection plays a significant role when an individual with
herpes is an index case.
• CONGENITAL VARICELLA- it crosses the placental barrier and infects
the foetus.
CLINICAL FEATURES
• Clinical spectrum: Mild illness with few scattered lesions severe
febrile illness with widespread rash.
PRE-ERUPTIVE STAGE:
−Sudden onset with mild to moderate fever.
−Pain in the back, shivering and malaise.
−DURATION: about 24 hours.
−In adults, prodromal illness is usually more severe and may last for 2-3
days before the rash comes out.
ERUPTIVE STAGE:
−In children the rash comes on day the fever starts and is the first sign.
−The distinctive features of rash are:-
o Distribution:
Rash is symmetrical.
Appears on the trunk and then comes to face, arms ,legs.
Mucosal surfaces (buccal, pharyngeal) are generally involved.
Axilla may be affected. Palms and soles usually not involved.
The density of eruption diminishes centrifugally.
o Pleomorphism:
All stages of rash (papules, vesicles and crusts) may be seen
simultaneously in the same area.
This is due appearance of rash in successive crops for 4-5 days in the
same area.
o Rapid evolution:
The rash advances quickly through the stages of-
macule papule vesicle scab.
Vesicles filled with clear fluid resembling “dew-drops” on the skin.
Superficial in site, with easily ruptured walls and surrounded by an
area of inflammation.
Vesicles may form crusts without going through the pustular stage.
Many of the lesions may abort.
Scabbing begins 4-7 days after the rash appears.
o Fever:
The fever does not run high but shows exacerbations with each fresh
crop.
COMPLICATIONS
• It’s a mild, self-limiting disease.
• Severe complications may be seen in immunosuppressive patients and normal
children and adults.
Haemorrhages ( varicella haemorrhagica)
Pneumonia
Encephalitis
Acute cerebellar ataxia
Reye’s syndrome
Maternal varicella may cause foetal wastage and birth
defects.
Intrauterine infection occurring near term may cause typical varicella in
the new born with varying degrees of severity.
Virus has a potential of oncogenicity.
Congenital defects in
babies
• Damage to brain: encephalitis, microcephaly, hydrocephaly,
aplasia of brain
• Damage to the eye: microphthalmia, cataracts, chorioretinitis,
optic atrophy.
• Other neurological disorder: damage to cervical and lumbosacral
spinal cord, motor/sensory deficits, absent deep tendon reflexes,
anisocoria/Horner's syndrome.
• Damage to body: hypoplasia of upper/lower extremities, anal and
bladder sphincter dysfunction.
• Skin disorders: (cicatricial) skin lesions, hypo pigmentation.
LABORATORY DIAGNOSIS
• Most rapid and sensitive
−Examination of vesicle fluid
under electron microscope.
−Round particles which may be
used for cultivation are seen.
• Scrapings of floor of vesicles show
multinucleated giant cells coloured
by Giemsa stain.
• Serology is mainly for
epidemiological surveys.
No specific treatment for
chicken pox.
Notification.
Isolation of cases for
about 6 days after onset
of rash.
Disinfection of articles
soiled by nose and throat
discharges.
PREVENTION
• VARICELLA ZOSTER IMMUNOGLOBULIN(VZIG):
• VZIG given within 72 hours of exposure has been
recommended for prevention.
• DOSAGE:1.25-5ml intramuscularly.
• The current recommendation is that it should be
preserved for immunosuppressed contacts of acute
cases or newborn contacts.
• It has also been shown to provide improvement in high
risk children with varicella.
VACCINE:
A live attenuated vaccine developed by
Takahasi in Japan has been extensively studied
in field trials.
The frequency of mild local reaction at
inoculation site is 1%.
A general reaction mainly rash or mild
varicella may occur.
Seroconversion in healthy seronegative
children is over 90%.
The potential to establish a latent infection,
which may produce zoster in later years or
more severe form, than natural disease is a
major objection for the live vaccine.
