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Chickenpox is an acute, systemic viral illness caused by infection with VZV (human herpesvirus type 3). [1] It afflicts approximately 84 million cases annually and is predominantly seen in pediatric populations. [2]
The varicella-zoster virus (see the image below) is the etiologic agent of the clinical syndrome of chickenpox (varicella). [1,3] Herpes zoster (shingles), a different clinical entity, is caused by reactivation of VZV after primary infection. Varicella-zoster virus is a double-stranded deoxyribonucleic acid virus included in the Alphaherpesvirinae subfamily. (SeeEtiology.)
Vesicular eruption on the trunk demonstrating papules, vesicles, and crusts. Reprinted with permission from Cutis 65: 355, 2000.Chickenpox primarily spreads through airborne respiratory droplets and can also transmit via direct contact with the vesicles, although this method poses a lower risk. (SeeEtiology) It predominantly affects children under 10 years, where it usually presents benignly, but it can lead to increased morbidity in adults and immunocompromised individuals. (SeeEpidemiology andPrognosis)
Since the introduction of the varicella vaccine in the United States in 1995, the incidence of chickenpox has decreased by nearly 90%. (SeeEpidemiology) Diagnosis is typically clinical, based on the characteristic rash and patient history of exposure within the 10-21 day incubation period. Adults may experience a more severe course with widespread rash and complications such as varicella pneumonia. (SeeClinical Presentation)
Definitive diagnosis can be achieved through vesicular fluid cultures or direct immunofluorescence (SeeWorkup). Treatment options include oral acyclovir for those at risk for severe infections, with valacyclovir and famciclovir as alternatives. Intravenous acyclovir is advised for immune-compromised patients, and varicella-zoster immune globulin (VZIG) is recommended for highly susceptible, exposed immunocompromised individuals. The live attenuated varicella vaccine (Oka strain) has been available since 1995 for prophylactic use in healthy children and adults.
SeePediatric Vaccinations: Do You Know the Recommended Schedules?, a Critical Images slideshow, to help stay current with the latest routine and catch-up immunization schedules for 16 vaccine-preventable diseases.
Also, see the15 Rashes You Need to Know: Common Dermatologic Diagnoses slideshow for help identifying and treating various rashes.
Go toPediatric Chickenpox for more complete information on this topic.
Varicella-zoster virus is transmitted person to person primarily through the respiratory route by inhalation of aerosols from vesicular fluid of skin lesions of varicella or herpes zoster. It can also spread by direct contact with the vesicular fluid of skin lesions and possibly infected respiratory tract secretions. [4,5] Varicella-zoster virus enters the host through the upper respiratory tract or the conjunctiva. After initial inhalation of contaminated respiratory droplets, the virus infects the conjunctivae or the mucosae of the upper respiratory tract, [6] with viral proliferation occurring in regional lymph nodes 2-4 days after infection. This is followed by primary viremia on days 4-6 post-infection, and a secondary round of viral replication in internal organs, notably the liver and spleen, leading to a secondary viremia 14-16 days post-infection, characterized by diffuse viral invasion of capillary endothelial cells and the epidermis. [6]
Varicella is highly contagious with secondary attack ratios of approximately 85% (range 61%–100%) in susceptible household contacts, though it is less contagious after community exposure. [4] Herpes zoster is about 20% as infectious as varicella, and contact with herpes zoster rash in susceptible individuals results in varicella, not herpes zoster. [4] The communicability of varicella begins about 1-2 days before the onset of rash and ends when all lesions have crusted, typically 4-7 days after the onset of the rash in immunocompetent individuals; this period may be extended in immunocompromised individuals. [4] Vaccinated individuals who contract chickenpox may develop lesions that do not crust, and they are considered contagious until no new lesions have appeared for 24 hours. Patients with herpes zoster are contagious while they have active, vesicular lesions, usually for 7-10 days. In utero infection also can occur through transplacental passage of the virus during maternal varicella infection. [4]
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] Cell-mediated immune responses are also crucial in limiting the scope and duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves, remaining latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles). [6]
Chickenpox usually is 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 also may occur through direct contact with these vesicles.
Coronavirus disease 2019 (COVID-19) may rarely occur simultaneously with chickenpox, producing serious pulmonary disease even in a healthy immunocompetent individual. [7] Reactivation may occur with immunosuppression and during coronavirus disease 2019 (COVID-19) infection. Some varicelliform eruptions during COVID-19 are actually varicella. [8,9,10]
Varicella, commonly known as chickenpox, is endemic globally. In temperate climates, it predominantly affects children, with the highest incidence observed among preschool and elementary school-aged populations; less than 5% of adults are susceptible. [4] Seasonally, the disease typically manifests in late winter and early spring. In contrast, in tropical climates, varicella infection generally occurs later in childhood and is more prevalent among adults, particularly in sparsely populated areas. The disease incidence in these regions peaks during the driest and coolest months. Its incidence was reduced during the COVID pandemic. In Poland, the incidence of chickenpox by 2022 was found to be back at pre-COVID pandemic levels. [11]
The implementation of the childhood varicella vaccination program in the United States in 1996 has led to substantial reductions in the incidence of this disease. [4] Although varicella remains endemic, the risk for VZV exposure in the United States now is comparatively lower than in most other regions globally. As of 2019, 18% of countries had integrated routine varicella vaccination into their national immunization schedules, and an additional 6% target vaccinations to specific high-risk groups.
Due to the worldwide prevalence of varicella, all travelers susceptible to the virus are at risk for infection during international travel. [4] Additionally, exposure to herpes zoster can result in varicella among susceptible individuals, although it is significantly less transmissible than primary varicella infection. Infants, adults, and immunocompromised individuals lacking immunity are at the highest risk for severe varicella.
In the early 1990s, before the introduction of the chickenpox vaccination program, chickenpox was extremely prevalent in the United States. [12] Annually during this period, over 4 million cases of chickenpox were reported, leading to between 10,500 and 13,500 hospitalizations, and resulting in 100 to 150 deaths. Notably, a significant portion of these cases and hospitalizations, as well as half of the deaths, occurred among children. This underscores the substantial impact of chickenpox on pediatric populations prior to widespread immunization efforts.
Countries with tropical and semitropical climates have a higher incidence of adult chickenpox than do countries with a temperate climate (eg, United States, Europe).
In the United States, high vaccination rates are achieved across many states and jurisdictions, with mandates requiring children to be vaccinated against vaccine-preventable diseases before starting school. [13] Conversely, in Japan, whereas the varicella vaccine was incorporated into routine immunization programs in 2014, it is not mandatory for school entry, resulting in lower vaccination rates compared to the United States. The basic reproduction number for varicella, estimated to be between 8 and 10, suggests that the current vaccination coverage in Japan is inadequate to control the spread of the disease, highlighting the need for increased vaccination efforts.
Additionally, although herpes zoster predominantly affects individuals older than 50 years, a decrease in varicella incidence could lead to an increase in herpes zoster cases among younger populations. [13] This shift underscores the importance of herpes zoster vaccination, particularly for those with diminished cell-mediated immunity (CMI) against VZV. Developing methods to assess CMI activity is crucial for identifying individuals at risk and effectively targeting vaccination efforts.
Chickenpox typically presents as a mild illness in children. However, severe or life-threatening cases are more likely to occur in the following groups [1]:
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.
Please seePediatric Chickenpox.
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Anthony J Papadopoulos, MD Private Practice
Anthony J Papadopoulos, MD is a member of the following medical societies:American Academy of Dermatology,American College of Mohs Surgery,Medical Society of New Jersey,Sigma Xi, The Scientific Research Honor Society
Disclosure: Nothing to disclose.
Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School
Camila K Janniger, MD is a member of the following medical societies:American Academy of Dermatology
Disclosure: Nothing to disclose.
Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies:Alpha Omega Alpha,American Academy of Dermatology,New York Academy of Medicine, Royal College of Physicians of Edinburgh,Sigma Xi, The Scientific Research Honor Society
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies:American Academy of Dermatology
Disclosure: Nothing to disclose.
Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio
Van Perry, MD is a member of the following medical societies:American Academy of Dermatology andAmerican Society for Laser Medicine and Surgery
Disclosure: Nothing to disclose.
Susan M Swetter, MD Director, Pigmented Lesion and Melanoma Program, Professor, Department of Dermatology, Stanford University Medical Center and Cancer Institute, Veterans Affairs Palo Alto Health Care System
Susan M Swetter, MD is a member of the following medical societies:American Academy of Dermatology,American Medical Association,American Society of Clinical Oncology,Eastern Cooperative Oncology Group,Pacific Dermatologic Association,Society for Investigative Dermatology,Society for Melanoma Research, andWomen's Dermatologic Society
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies:American Academy of Dermatology,Association of Military Dermatologists,Texas Dermatological Society, andTexas Medical Association
Disclosure: Nothing to disclose.
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