Chickenpox pathophysiology

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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

Chickenpox is a highly contagious disease contracted by the inhalation of aerosolized nasopharyngeal secretions droplets or through direct contact with the vesicles from an infected host. It takes from 10 to 21 days after exposure to a person with chickenpox or shingles for someone to develop chickenpox. 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 vesicle.

Pathophysiology

Chickenpox is contracted by the inhalation of aerosolized nasopharyngeal secretions droplets 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. High viral titers are found in the vesicles of chickenpox; hence, the viral transmission may also occur through direct contact with these vesicles and the risk is lower comparatively.

Transmission

The mode of transmission is via respiratory droplets^[1]
Chickenpox can also be spread from people with shingles by direct contact.
Transmission of the disease occurs 1-2 days prior to the development of the rash and continues until all their chickenpox blisters have formed scabs.
Nosocomial transmission of Varicella-zoster virus (VZV) is also reported.^[2]

Incubation Period

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 is regarded to last from 48 hours before the appearance of the rash till the crusts appear.

Dissemination

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

Viral replication occurs in the liver, spleen, followed by a secondary viremia 14-16 days postinfection. 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 vesicle.
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

There is no genetic predisposition associated with the disease chickenpox. However, regarding varicella vaccination, similarities in siblings' 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

There are no associated conditions with chickenpox.

Gross Pathology

There area no gross pathological findings findings observed in chickenpox. ^[5]

Microscopic Pathology

Varicella virus grown in a tissue culture; magnified 500X.
Transmission electron micrograph (TEM) of a Varicella (Chickenpox) Virus. From Public Health Image Library (PHIL). ^[6]
Various viruses from the Herpesviridae family seen using an electron micrograph. From Public Health Image Library (PHIL). ^[6]
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). ^[6]
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). ^[6]
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). ^[6]
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). ^[6]
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). ^[6]