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• Chickenpox - also known as varicella, is a highly
contagious viral infection caused by the varicella-
zoster virus (VZV).
• VZV is a DNA virus that is a member of the
herpesvirus group.
• After the primary infection, VZV stays in the body
(in the sensory nerve ganglia) as a latent
infection.
Pathophysiology
• After initial inhalation of contaminated
respiratory droplets, the virus infects
the conjunctivae or the mucosae of the
upper respiratory tract.
• Viral proliferation occurs in
regional lymph nodes of the upper
respiratory tract 2-4 days after initial
infection; this is followed by primary
viremia on postinfection days 4-6.
Pathophysiology Cont …d
• A second round of viral replication occurs in
the body’s internal organs,
• most notably the liver and the spleen, followed
by a secondary viremia 14-16 days post-
infection.
• This secondary viremia is characterized by
diffuse viral invasion of capillary endothelial
cells and the epidermis.
Pathophysiology Cont …d
• VZV infection of cells of the malpighian
layer produces both
intercellular edema and intracellular
edema, resulting in the characteristic
vesicle.
• Exposure to VZV in a healthy child
initiates the production of host
immunoglobulin G (IgG), immunoglobulin
M (IgM), and immunoglobulin A (IgA)
antibodies; IgG antibodies persist for life
and confer immunity.
Pathophysiology Cont …d
• After primary infection, VZV is
hypothesized to spread from mucosal
and epidermal lesions to local
sensory nerves.
• VZV then remains latent in the dorsal
ganglion cells of the sensory nerves.
• Reactivation of VZV results in the
clinically distinct syndrome of herpes
zoster (shingles).
CHICKEN POX.pptx

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CHICKEN POX.pptx

  • 1.
  • 2. • Chickenpox - also known as varicella, is a highly contagious viral infection caused by the varicella- zoster virus (VZV). • VZV is a DNA virus that is a member of the herpesvirus group. • After the primary infection, VZV stays in the body (in the sensory nerve ganglia) as a latent infection.
  • 3. Pathophysiology • After initial inhalation of contaminated respiratory droplets, the virus infects the conjunctivae or the mucosae of the upper respiratory tract. • Viral proliferation occurs in regional lymph nodes of the upper respiratory tract 2-4 days after initial infection; this is followed by primary viremia on postinfection days 4-6.
  • 4. Pathophysiology Cont …d • A second round of viral replication occurs in the body’s internal organs, • most notably the liver and the spleen, followed by a secondary viremia 14-16 days post- infection. • This secondary viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis.
  • 5. Pathophysiology Cont …d • VZV infection of cells of the malpighian layer produces both intercellular edema and intracellular edema, resulting in the characteristic vesicle. • Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity.
  • 6. Pathophysiology Cont …d • After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. • VZV then remains latent in the dorsal ganglion cells of the sensory nerves. • Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).