Chickenpox pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Overview[edit | edit source]

Chickenpox is a highly contagious disease contracted by the inhalation of aerosolized nasopharyngeal secretions or through direct contact with the vesicles from an infected host. Chicken pox has an incubation period of 10-21 days. Viral proliferation occurs in regional lymph nodes of the upper respiratory tract leading to viremia. Viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis. VZV infection of cells of the malpighian layer produces both intercellular and intracellular edema, resulting in the characteristic vesicles.

Pathophysiology[edit | edit source]

Chickenpox is contracted by the inhalation of aerosolized nasopharyngeal secretions from an infected host. The highly contagious nature of VZV explains the epidemics of chickenpox that spread through schools, as one child who is infected quickly spreads the virus to many classmates.

Transmission[edit | edit source]

• The mode of transmission is by inhalation of aerosolized nasopharyngeal secretions from an infected host.^[1]
• Chickenpox can also be spread from people with shingles by direct contact.
• Viral shedding occurs 1-2 days prior to development of the rash and continues until all their chickenpox blisters have formed scabs.
• Nosocomial transmission of Varicella-zoster virus (VZV) has also been reported.^[2]

Incubation Period[edit | edit source]

• The incubation period of chickenpox is typically from 14 to 16 days. However, the interval may vary from 10 to 21 days.^[3]

• The infectivity period begins 48 hours prior to the appearance of the rash and lasts till crusts appear.

Dissemination[edit | edit source]

• After initial inhalation of contaminated aerosolized droplets, the virus infects the conjunctivae and 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, and is followed by primary viremia.

Pathogenesis[edit | edit source]

• Viral replication occurs in the liver, spleen, followed by a secondary viremia 14-16 days post infection. Secondary viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis.
• VZV infection of cells of the malpighian layer produces both intercellular and intracellular edema, resulting in the characteristic vesicles.
• Exposure to VZV initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity.
• After primary infection, 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).

Genetics[edit | edit source]

There is no genetic predisposition associated with chickenpox. Similarities in sibling response to varicella vaccine are supportive of the hypothesis that genetic factors play a role in the antibody response to the varicella vaccine.^[4]

Associated Conditions[edit | edit source]

• Thrombocytopenia^[5]

• Pancytopenia^[5]

• Red eye in chickenpox: varicella-related acute anterior uveitis^[6]

Gross Pathology[edit | edit source]

Rash findings[edit | edit source]

The typical rash in chickenpox may show the following findings:

• Superficial
• Unilocular
• Umblicated
• Area of inflammation around rash

• Pleomorphism (papules, vesicles and crusts may be seen simultaneously at the same area)

Microscopic Pathology[edit | edit source]

Rash findings[edit | edit source]

Skin lesions in chickenpox may show the following findings:

• Multi-nucleated giant cells
• Steel-gray nuclei with accentuation of nucleoplasm at their periphery
• Necrosis
• Acantholysis
• Vascular dilation

• 

  Transmission electron micrograph (TEM) of a Varicella (Chickenpox) Virus. From Public Health Image Library (PHIL). ^[7]

• 

  Various viruses from the Herpesviridae family seen using an electron micrograph. From Public Health Image Library (PHIL). ^[7]

• 

  photomicrograph reveals some of the cytoarchitectural histopathologic changes which you’d find in a human skin tissue specimen that included a chickenpox, or varicella zoster virus lesion (500x mag). From Public Health Image Library (PHIL). ^[7]

• 

  Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (50x mag). From Public Health Image Library (PHIL). ^[7]

• 

  Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (50x mag). From Public Health Image Library (PHIL). ^[7]

• 

  Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (500x mag). From Public Health Image Library (PHIL). ^[7]

• 

  Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (1200x mag). From Public Health Image Library (PHIL). ^[7]

References[edit | edit source]