Varicella-zoster virus is responsible for causing a primary varicella infection (chickenpox) and a secondary herpes zoster infection (shingles). Although varicella typically manifests as a mild disease in otherwise healthy children, it can also manifest as a moderate-to-severe disease, most notably in immunocompromised and adult hosts. Acyclovir is the antiviral agent of choice for the management of varicella infections. Routine vaccination with Varivax has been very effective in reducing chickenpox incidence

1. Medical Microbiology & Infectious Disease Assignment
TOPIC- CHICKENPOX
Submitted by
NIMRA NEYAZ
B.Sc(H)Medical Biotechnology
BSM/14/116
VIIth Semester
Amity Institute of Biotechnology

2. CHICKENPOX
ETIOLOGY
 Causative Organism- Varicella Zoster Virus, which belongs to Alpha sub-family of Herpes
virus family.
 VZV is also known as Human Herpes 3 virus
 Host- man; Reservoir- infected individuals
 VZV is an enveloped, double-stranded DNA virus.
 Chickenpox is the manifestation of primary infection
 Shingles(zoster) is the manifestation of the reactivated latent infection of endogenous VZV.

3. Structure of VZV
• Lipid envelope studded with spiky
glycoproteins which help in attachment with
host cell receptors.
• Tegument made of viral proteins, containing
DNA polymerases.
• Icosahedral nucleocapsid
• Core contains linear double stranded DNA

4.  Mode Of Transmission
• Direct contact with the lesions.
• Droplet infection
• Air-borne
 Brief Epidemiology
• Occurs as both Epidemic and Endemic forms in India.
• In temperate climates, it exhibits an annual epidemic trend, peaking in late winter to
spring
• Historically, children between the ages of 1 and 4 years accounted for 39% of cases,
while children aged 5 to 9 years and adults ≥20 years accounted for 38% and 7%,
respectively (National Health Interview Survey data, 1990-1994).
• Newborns, pregnant women more susceptible, immune-compromised patients are also
at greater risk.
• The virus can cross placental barrier leading to Congenital Varicella Syndrome

5. SYMPTOMS & CLINICAL FEATURES
 Incubation period= 10-21 days
 Takes usually 1-3 weeks for symptoms to appear
Pre-Eruptive Stage
backache
malaise
Eruptive stage
Papule,vesicles,scabs
crusts
Mild fever Rashes on trunk, face, arms and legs

6. Chickenpox rash develops in 3 stages
Spots-small,raised red bumps on
face and trunk
Blisters-fluid-filled itchy
papules.
SCABS & CRUSTS-vesicles
turn cloudy and turn patchy

7. Life Cycle of Varicella zoster virus
• Enveloped VZV particles attach to cell membranes with
Mannose-6-phosphate receptor
• fuse and release of tegument proteins.(Receptor-
Mediated Endocytosis)
• genomic DNA is injected into the nucleus and
circularizes.
• immediate-early genes expressed, followed by early and
late genes.
• Nucleocapsids are assembled and package newly
synthesized genomic DNA, move to the inner nuclear
membrane and
• budding across nuclear membrane.
• Capsids enter the cytoplasm, and virion glycoproteins
mature in the trans-Golgi region and tegument proteins
assemble in vesicles; capsids undergo secondary
envelopment and are transported to cell surfaces
• newly assembled virus particles released.

8. PATHOPHYSIOLOGY
 Route of infection-Mucosa of upper respiratory
tract or conjunctiva
 Local replication followed by spread to tonsils and
other regional lymphoid tissues, where VZV gains
access to T cells(CD4+ & CD8+)
 Infected T cells then deliver the virus to cutaneous
sites of replication. Vesicular rashes develop by
the end of 10th day.
 VZV establishes latency in sensory ganglia after
transport to neuronal nuclei along neuronal axons
or by viraemia.
 Reactivation from latency enables a second phase
of replication to occur in skin, which typically
causes lesions in the dermatome that is innervated
by the affected sensory ganglion.

10. Recent study

11. DIAGNOSIS
 Enzyme immunoassay-detects rise in Varicella Immunoglobin G
 Fluorescent Antibody testing
 ELISA
 Tzanck smear
 Detection of viral DNA by PCR
 Culture of lesion samples

12. COMPLICATIONS
 Pneumonia
 Encephalitis
 Reye Syndrome (acute encephalopathy along with fatty degeneration of liver)
 Hemorrhage
 Septicemia

13. PROPHYLAXIS
 Two doses of live-attenuated vaccines(VARIVAX)-1st dose at 12-15 months of
age & 2nd dose around 4-6 years of age. It is a single-agent vaccine containing a
live, attenuated (Oka strain) virus
 Varicella Zoster Immunoglobin(VariZIG) is effective in preventing the disease if
given within 96 hours of exposure. provides passive immunity to persons at high risk of
severe chickenpox

14. TREATMENT
Some Symptomatic measures include:
 Good hygiene (e.g., daily baths, preferably with antibacterial soap) and thorough skin care are important
for the prevention of secondary bacterial infections
 Further measures of supportive therapy include OTC medications such as acetaminophen for fever, topical
agents that include calamine, daily lukewarm soaks with colloidal oatmeal, and oral or topical
antihistamines; the latter three will provide management and a soothing relief of the pruritus
 The child’s fingernails should also be cut short in an effort to prevent secondary bacterial skin infections
 Antiviral medication only when the case is severe(It is advisable to let the disease complete its course)
 Acyclovir is given which is a viral DNA polymerase inhibitor.
 Immunoglobin intravenous(Privigen) can also be given to lessen the severity of the disease.
.

15. Antiviral therapy
Fig: Mechanism of action of Acyclovir in cells infected with Varicella Zoster
Virus

16.  Acyclovir, an antiviral agent used in the management of varicella, is available in both oral
and IV formulations.
 It is an acyclic analogue of guanosine that must be phosphorylated by viral thymidine
kinase and subsequently by host cell enzymes into its active triphosphate form for its
antiviral activity through inhibition of viral DNA polymerase (
 Acyclovir is the antiviral agent of choice in the treatment of varicella and should be initiated
within 24 hours of the onset of rash.
 It has been proven to shorten both the duration and severity of chickenpox by decreasing
viral shedding and the formation of new lesions, as well as by accelerating lesion healing in
both healthy and immunologically compromised children

17. References
 World Health Organization – position paper, Chickenpox vaccine; Weekly epidemiological record.
1998, 73 :241-248.
 Heymann L D 2004, Chickenpox control of communicable diseases manual, 18th edition
 Freer G, Pistello M. Varicella-zoster virus infection: natural history, clinical manifestations, immunity
and current and future vaccination strategies. New Microbiol. 2018 Apr;41(2):95-105.
 Dayan RR, Peleg R. Herpes zoster - typical and atypical presentations. Postgrad Med. 2017
Aug;129(6):567-571.
 Heininger U., Seward J.F. Varicella. Lancet. 2006;368:1365–1376.
 Cohen JI, Brunell PA, Straus SE, Krause PR. Recent advances in varicella-zoster virus infection. Ann
Intern Med. 1999;130:922-932.
 American Academy of Pediatrics. Committee on Infectious Diseases. Varicella vaccine update.
Pediatrics. 2000;105:136-141.

18. THANK YOU!