Chicken pox

(varicella)
Introduction

 Chickenpox is a viral infection caused by the varicella

zoster virus (VZV).
 While the origin of the term chickenpox is unknown,
some believe that it was derived from chickpeas due to
the blisters’ resemblance to chickpeas.
 Others think the term is based on child pox or itching
pox..
 Most typically, the illness appears in children, and a rash appears
anywhere between 10 – 21 days after becoming infected with the
virus.
 On average, a child may develop from 250 – 500 blisters, which
are itchy and filled with fluid.
 The blisters first appear on the face, scalp or torso.
 After several days, the first blisters will form scabs; however, more
blisters may develop later.
 Often, they affect the inside of the mouth and the
eyelids.
 The rash usually heals completely without scarring.
 Chickenpox has also been observed in other primates
like chimpanzees and gorillas.
Varicella Zoster virus(VZV)
 VZV is a DNA virus and is a member of the herpesvirus
group.
 Like other herpesviruses, VZV has the capacity to persist
in the body after the primary (first) infection as a latent
infection.
 As neurotropic and neuroinvasive viruses, HSV-1 and -2
persist in the body by hiding from the immune system in
the cell bodies of neurons.
Structure of VZV

• Viral tegument
A viral
tegument or tegument, more
commonly known as a viral
matrix, is a cluster of proteins
that lines the space between
the envelope
and nucleocapsid of
all herpesviruses.
• Viral genome
dsDNA
Primary and secondary infection

 VZV persists in sensory nerve ganglia. Primary infection

with VZV results in chickenpox. Herpes zoster (shingles) is
the result of reactivation of latent VZV infection.
 The virus is believed to have a short survival time in the
environment.
Difference between smallpox and
chickenpox
Difference between chickenpox
and measles
Transmission of VZV

 Chickenpox is transmitted from person to person by

droplet infection and droplet nuclei.
 Most person are infected by “face-to-face” (personal)
contact.
 The portal of entry of virus is respiratory tract.
 Since virus is extremely labile, it is unlikely that fomites
play significant role in its transmission.
Cont.…

 Overcrowding favours its transmission.

 Infection during pregnancy presents a risk for fetus and
neonates.
 Virus can cross the placenta and infect the fetus, a
condition known as congenital varicella.
 During pregnancy, period of risk may extend through first
20 weeks.
 Risk is small (less than 2%).
Congenital varicella syndrome
features
 Damage to optic stalk and lens vesicles.
1. Microphthalmia
2. Cataracts.
3. Chorioretinitis.
4. Optic atrophy
 Damage to brain
 Hypoplasia of extremity.
 Anal/urinary sphincter dysfunction.
Pathogenesis

 VZV is transmitted in respiratory secretions and in the fluid

of skin lesions either by airborne droplets or through
contact.
 Primary infection: (varicella) results from inoculation of
the virus on the mucosa of upper respiratory tract &
tonsillar lymphoid tissues.
 Glycoprotein E present on VZV is essential for its
attachment with cell surface and infectivity.
 virus replicate in the local lymphoid tissue then by
viremia spread to the reticuloendothelial system.
Cont.…

 During viremia, the mononuclear cells carry the virus to

form new crops of vesicles.
 Also goes back to upper respiratory tract during late
incubation period.
 It become infectious 2 days before rash.
 Host immune system limit viral replication.
 In immunocompromised individuals, the continuous viral
replication affect the liver, lungs, brain and other organs.
Cont.…

 Virus is transported through the sensory axons through

the dorsal root ganglion throughout spinal cord, causing
late infection in the neuron.
 Subsequent reactivation of virus causes herpes zoster.
 The skin lesion in both varicella and herpes zoster contain
VZV and lesions have identical histopathology.
 Varicella causes both humoral and CMI that is very
protective.
 Suppression of CMI to VZV correlate with increased risk of
VZV as herpes zoster.
INCUBATION PERIOD

• Usually 14 to 16 days, 10 to 21 days are also reported

• During these period the patient is asymptomatic
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
PRE-ERUPTIVE STAGE(prodromal
period)
 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 for 2 to 3 days.
ERUPTIVE STAGE(Exanthem period)

 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
ERUPTIVE STAGE

 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.
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.
Conti….

 The vesicles may form the crusts without going through

the pustular stage
 Scabbing begin 4 – 7 days after the rash appearance
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.
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 hemorrhagic)
 Pneumonia.
Conti……….

 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
COMPLICATION

 The most common complications are:

 Bacterial infections of the skin and soft tissues in children
Septicemia
 Toxic Shock Syndrome
 Necrotizing Fasciitis
 Osteomyelitis
 Bacterial pneumonia
 Septic arthritis.
 Epidemiology of chicken pox
CHICKEN POX OCCURS IN ALL COUNTRIES OF THE
WORLD.
IT IS RESPONSIBLE FOR 7000 DEATHS ANNUALLY.
IN US, IT CAUSES >9000 HOSPITALIZATION.
ITS HIGHEST PREVALENCE IN 4 TO 10 YEAR OLD
AGE.
Epidemiology of chicken pox in Pakistan
Laboratory diagnosis

 Lab diagnosis is usually not required.

 But it required some test
 Most frequently source of isolation is vesicular fluid
 Stained smears from vesicular scrapping
 Serology test varicella IgM antibodies
 ELISA test is also useful
 Electron microscopy show round particles
Prevention

 Chicken pox or varicella vaccine protect 70% to 90% of

those people who are vaccinated
 Varicella vaccine contain live virus so is not
recommended to children having compromised
immune or severe illness
 Also not given to children who are allergic to Neomycin
and gelatin
Treatment

 Drug used in the treatment of chickenpox are antiviral

drugs
 Antihistamine
 Antipyretics
 Calamine lotion
 Commonly used drugs are
 Acyclovir available as ZOVIRAX and FOSCARNET
 Famiclovir available as FOSCOVIR
Route of administration

 Antiviral medicine can be taken orally.

 Intravenously can applied on the skin.
 Local antiseptics e.g. chlorohexidine should be
applied to the skin if there is secondary infection
 Vaccine should not be given to
 Immunocompromised patients
 Pregnant women
Chickenpox vaccine dose Chickenpox vaccine age

 First dose  12- 15 months

 Second dose  4-6 years of age
 May be given
earlier with a gap of
3 months after the
first dose
 People not been  People 13 years of
vaccinated age and older
earlier pox vaccine should get two dose
for adults atleast 28 days
Treating chickenpox with Folk
medicine
Treating chickenpox with scientific
medicine