Chickenpox 

The varicella-zoster virus (VZV) is the etiologic agent of the clinical syndrome of chickenpox (varicella). Zoster, a different clinical entity, is caused by reactivation of VZV after primary infection. VZV is a double-stranded deoxyribonucleic acid virus included in the Alphaherpesvirinae subfamily. (See Etiology.)

Chickenpox is usually acquired through inhalation of airborne respiratory droplets from an infected host. High viral titers are found in the characteristic vesicles of chickenpox; viral transmission may also occur through direct contact with these vesicles, though the risk of transmission is lower. (See Etiology.)

Chickenpox is largely a childhood disease, with more than 90% of cases occurring in children younger than 10 years. The disease is benign in the healthy child, and increased morbidity occurs in adults and immunocompromised patients. (See Epidemiology and Prognosis.)

Since the introduction of widespread pediatric immunization in the United States in 1995, the incidence of varicella has declined significantly, approaching up to a 90% decline. (See Epidemiology.)

Chickenpox is usually diagnosed clinically on the basis of the characteristic rash and successive crops of lesions. These may be found in various developmental and healing stages in affected sites. Patient exposure to an infected contact within the incubation period of 10-21 days is an important diagnostic clue. The more complicated course in adults with chickenpox can be associated with a more widespread rash; prolonged fever; and an increased likelihood of complications, the most common being varicella pneumonia. (See Clinical Presentation.)

VZV can be isolated on vesicular fluid cultures, which provides a definitive diagnosis. Direct immunofluorescence has excellent sensitivity. (See Workup.)

Oral acyclovir should be considered for healthy persons at increased risk of severe varicella infections. Valacyclovir and famciclovir are other agents used in treatment. Intravenous acyclovir therapy is recommended for patients who are immune-suppressed or immune-compromised. Varicella-zoster immune globulin (VZIG) is indicated for use in highly susceptible, VZV-exposed immunocompromised or immunosuppressed populations. A live attenuated varicella vaccine (Oka strain) was approved by the US Food and Drug Administration in 1995 for prophylactic use in healthy children and adults. (See Treatment and Management and Medication.)

Go to Pediatric Chickenpox for more complete information on this topic.

Chickenpox is usually acquired by the inhalation of airborne respiratory droplets from an infected host. The highly contagious nature of varicella-zoster virus (VZV) underlies the epidemics that spread quickly through schools. High viral titers are found in the characteristic vesicles of chickenpox; thus, despite the lower associated risk, viral transmission may also occur through direct contact with these vesicles.

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.

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. 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. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. 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).

Chickenpox is usually acquired by the inhalation of airborne respiratory droplets from a VZV-infected host. High viral titers are found in the characteristic vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles.

Chickenpox is a common disease, with most cases occurring in the pediatric population. Varicella has neither a racial nor a sexual predilection.^[1]

United States statistics

Since the introduction of widespread pediatric immunization in the United States in 1995, the incidence of varicella has declined significantly, approaching a decline of up to 90%. Mortality from varicella has also declined since the initiation of the US vaccination program, with mortality decreasing by approximately 66%.^[2]

International statistics

Countries with tropical and semitropical climates have a higher incidence of adult chickenpox than do countries with a temperate climate (eg, United States, Europe).

Chickenpox that affects a healthy child is usually a self-limited disease. Increased morbidity occurs in adult and immunocompromised populations.

Parents of infected children should be instructed to trim their children’s fingernails to minimize skin damage from scratching and the associated complications of bacterial superinfection. Also, it is important to advise parents not to use aspirin for fever control, because the development of Reye syndrome is associated with salicylate administration in children with chickenpox.

For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education articles Chickenpox and Skin Rashes in Children.