Chickenpox, also known as varicella, is a highly contagious disease caused by the varicella-zoster virus (VZV). The condition manifests as a skin rash with small, itchy blisters that eventually scab over. While primarily affecting children, varicella poses greater risks to adolescents, adults, pregnant women, immunocompromised individuals, and neonates, often necessitating antiviral therapy or supportive treatments like varicella zoster immune globulin.
Typical chickenpox rash on a child's back.
Diagnosis is typically clinical, though laboratory tests may confirm cases or identify complications. Vaccination, through 1- or 2-dose regimens, effectively prevents varicella, with some countries adopting universal pediatric immunization programs. The disease spreads easily, making timely intervention and prevention critical, particularly for vulnerable populations.
Introduction to Chickenpox
Chickenpox, or varicella, is a contagious disease caused by the varicella-zoster virus (VZV). The virus causes chickenpox, typically a primary infection in nonimmune hosts, and herpes zoster, or shingles, which results from the reactivation of a latent infection.
Chickenpox is an airborne disease spread worldwide by coughing, sneezing, and contact with skin lesions. Symptoms begin 10 to 21 days after exposure; the average incubation period is about 2 weeks. Chickenpox results in a skin rash forming small, itchy blisters that scab over. The rash typically starts on the chest, back, and face and then spreads, accompanied by fever, fatigue, pharyngitis, and headaches, usually lasting 5 to 7 days. The virus may spread 1 to 2 days before the rash appears until all lesions are crusted over.
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Complications include pneumonia, brain inflammation, and bacterial skin infections. The disease is more severe in adults than in children. Chickenpox is diagnosed based on the presenting symptoms and confirmed by polymerase chain reaction testing of the blister fluid or scabs. Tests for antibodies may be performed to determine if immunity is present. Although reinfections by varicella may occur, these reinfections are usually asymptomatic and much milder than the primary infection.
Since its introduction in 1995, the varicella vaccine has significantly reduced the number of cases and complications, preventing about 70% to 90% of infections and 95% of severe disease. Routine immunization for children is recommended. Immunization within 3 days of exposure may still improve outcomes in children.
Etiology of Chickenpox
Chickenpox, or varicella, is caused by VZV, a herpes virus with worldwide distribution. The virus establishes latency after primary infection, a feature unique to most herpes viruses. Chickenpox is acquired by inhalation of infected aerosolized droplets. This virus is highly contagious and can spread rapidly. The initial infection is in the mucosa of the upper airways. The virus enters the circulation after 2 to 6 days, and another bout of viremia occurs in 10 to 12 days. At this time, the characteristic vesicles appear.
Immunoglobulin (Ig)A, IgM, and IgG antibodies are produced, but the IgG antibodies confer lifelong immunity. After the primary infection, varicella localizes to sensory nerves and may reactivate later as shingles.
Risk Factors for Severe Varicella
Risk factors for severe varicella in adolescents and adults are as follows:
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- Steroid therapy: doses equivalent to 1 to 2 mg/kg/d of prednisolone administered for 2 weeks or longer are significant risk factors for severe illness. Even brief medication at these dosages shortly before or during the incubation period of varicella can result in severe or fatal varicella.
- Immunocompromised conditions: (eg, cancer, antineoplastic agents, human immunodeficiency virus, other congenital or acquired immunodeficiency disorders). Cellular immunodeficiency, as compared to humoral immunodeficiency, is thought to predispose individuals to severe varicella.
- Pregnant women are at an elevated risk of developing severe varicella, particularly pneumonia. Moreover, maternal varicella accompanied by viremia can be transmitted transplacentally to the fetus. This results in newborn varicella. Infants born between 5 days before and 2 days after the onset of the varicella rash in the mother are at the highest risk for serious illness.
The first month of a neonate's life is a vulnerable phase for severe varicella, particularly if the mother is seronegative. Delivery before 28 weeks of gestation predisposes a neonate to risk, as transplacental transfer of IgG antibodies occurs following this period.
Epidemiology of Varicella
VZV has a global distribution, with 98% of the adult population being seropositive. Varicella occurs in all countries and is responsible for about 7000 deaths annually. Most cases occur in winter and spring. In the United States, VZV accounts for more than 9000 hospitalizations annually; its highest prevalence is in the 4- to 10-year-old age group.
Following the implementation of the varicella vaccine in 1995, the overall incidence of varicella has diminished by approximately 85%, demonstrating evidence of herd immunity. The age of peak incidence transitioned from 5 to 9 years to 10 to 14 years of age, and an increased occurrence of breakthrough varicella among vaccinated children in the later age group prompted the inclusion of a second varicella vaccine dose in the standard childhood immunization schedule in 2006.
Varicella is typically symptomatic, and before the introduction of the varicella vaccine, this condition affected 90% of children in the United States by the age of 10. Herpes zoster signifies the reactivation of latent VZV infection, occurring in around 20% of healthy adults and 50% of immunocompromised individuals, with considerable morbidity and mortality in the latter group. Secondary cases in household contacts tend to have more severe disease than primary cases.
In the tropics, varicella tends to occur in older people and may cause more serious disease.
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Pathophysiology of Chickenpox
The causative agent, VZV, belongs to the human herpesvirus subfamily Alphaherpesvirinae and is a deoxyribonucleic acid virus similar to all herpesviruses. The virus invades via the respiratory system (conjunctival or upper respiratory mucosa) and establishes itself in the upper respiratory tract. Viral replication occurs in regional lymph nodes within 2 to 4 days; then, 4 to 6 days later, primary viremia disseminates the virus to reticuloendothelial cells in the spleen, liver, and other locations.
After a week, a secondary viremia propagates the virus to the internal organs and skin, resulting in the characteristic skin lesions. This viremia disseminates the virus to the respiratory regions and facilitates the transmission of varicella before the onset of the rash. During this period, infections of the central nervous system or liver may arise, including encephalitis, hepatitis, or pneumonia.
Varicella can contribute to humoral and cell-mediated immune responses. These responses elicit enduring immunity. Individuals may experience recurrent subclinical infections; however, secondary episodes of chickenpox are exceedingly uncommon in immunocompetent individuals. Reexposure and subclinical infections may enhance the immunity developed following a chickenpox episode.
Exposure causes the production of host IgG, IgM, and IgA. IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are important in limiting the duration of primary varicella infection. After primary infection, varicella is theorized to spread from mucosal and epidermal lesions to local sensory nerves; it then remains latent in the dorsal ganglion cells of the sensory nerves. The immune system keeps the virus in check. However, reactivation can still occur later in life, resulting in the clinically distinct syndrome of herpes zoster (shingles).
Histopathology
Herpes simplex, varicella, and herpes zoster infections exhibit indistinguishable histological features. Intraepidermal vesicles often exhibit ballooning degeneration of keratinocytes together with the presence of multinucleated giant cells, which result from the fusion of infected keratinocytes. A hallmark is acantholysis, where individual keratinocytes separate and float freely within the blister space. These detached cells often display distinctive viral changes, including chromatin clumping at the nuclear edges, the presence of multiple nuclei, and inclusion bodies within the nuclei. Clinical correlation, immunohistochemistry, and viral culture or polymerase chain reaction are necessary to distinguish these viral infections.
History and Physical Examination
The prodromal symptoms in adolescents and adults are aching muscles, nausea, decreased appetite, and headache, followed by a rash, oral sores, malaise, and a low-grade fever. Oral manifestations may precede the skin rash. In children, the illness may not be preceded by prodromal symptoms, and the initial sign could be a rash or oral cavity lesions. An eruption of pruritic, erythematous macules and papules ensues on the head and face before disseminating to the trunk and limbs. Lesions swiftly develop within approximately 12 hours into 1 to 3 mm clear vesicles encircled by narrow red halos (âdew drops on a rose petalâ).
The quantity of vesicles ranges from a few to several hundred, frequently including the oral mucosa. Sparing of the distal and lower extremities is common. Older vesicles develop into pustules and crusts, with each lesion healing within 7 to 10 days. The existence of lesions at all developmental stages is characteristic of varicella. At the blister stage, intense pruritus is present.
Blisters may occur on the palms, soles, and genital area. Commonly, visible evidence develops in the oral cavity and tonsil areas through small ulcers, which can be painful and itchy; this enanthem may precede the external exanthem by 1 to 3 days. These symptoms appear 10 to 21 days after exposure. Adults may have a widespread rash and more prolonged fever, and they are more likely to develop pneumonia, the most critical complication in adults. Because watery nasal discharge containing live virus precedes exanthems by 1 to 2 days, the infected person is contagious 1 to 2 days before recognizing the disease. In most cases, the infection resolves itself within 2 to 4 weeks.
Evaluation and Diagnosis
The diagnosis of varicella infection is primarily based on the signs and symptoms. Confirmation is made by examination of the fluid within the vesicles, scraping of lesions that have not crusted, or by blood for evidence of an acute immunologic response. Polymerase chain reaction (PCR) has the highest yield and can be used for nonskin samples such as bronchoalveolar lavage and cerebrospinal fluid. Direct fluorescent antibody testing has largely replaced the Tzanck test. The vesicular fluid can also be cultured, but the yield is low compared to PCR.
Blood tests identify a response to acute infection (IgM), previous infection, and subsequent immunity (IgG). Prenatal diagnosis of fetal varicella can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (deoxyribonucleic acid) test of the amniotic fluid can be performed. However, the risk of spontaneous abortion due to amniocentesis is higher than the risk of the baby developing fetal varicella.
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Chickenpox on Black Skin
The initial presentation of chickenpox on black skin are small bumps in the affected area. These may appear raised or slightly swollen. The skin on and around these bumps is typically discoloured compared to the surrounding skin. Depending on the individual's skin tone, they may appear purple, dark pink or dark brown.
As the chickenpox infection progresses, the rash or bumps progress to vesicles, which are fluid-filled sacs that form under the skin. These resemble blisters. Some people only have these vesicles scattered throughout the affected area, however, in some cases, the vesicles can merge and form an area that looks like a burn or a plaque. This can appear white or grey in colour. Meanwhile, the surrounding skin remains discoloured, appearing purple, pink or dark brown.
In rare cases, chickenpox in black patients presented with complications including varicella gangrenosa, which presents as painful necrotic (with dead tissue) lesions. Another potential complication in black people is development of keloids after chickenpox. Keloids are a type of scar which assume the shape of a growth or a tumour.
Challenges in Diagnosing Skin Conditions on Dark Skin
Diagnosing skin conditions in patients with dark skin can present unique challenges to healthcare professionals due to the complexities of pigmentation and the way the pigment interacts with the clinical presentation of skin conditions. This is particularly true in diseases where visual identification of symptoms on the skin is key to conclusively making a diagnosis.
Chickenpox rash on the stomach of a child.
For chickenpox, the rash described above may not be easily visible, potentially leading to misdiagnosis or late diagnosis. In these cases, a potential improvement of the diagnostic pathway is to utilise a PCR test to detect the presence of the varicella-zoster virus.
Treatment / Management
As a protective measure, those infected are usually required to stay home while infectious. Keeping nails short and wearing gloves may prevent scratching and reduce the risk of secondary infections. Topical calamine lotion may relieve pruritus. Daily cleansing with warm water helps avoid secondary bacterial infection. Acetaminophen may reduce fever; however, aspirin should be avoided as it may cause Reye syndrome.
Children: Treatment is symptomatic relief. If taken within 24 hours of the start of the rash, acyclovir decreases symptoms by 1 day. Still, acyclovir does not affect complication rates and is not recommended for individuals with normal immune function.
Adults: Infection tends to be more severe, and treatment with antiviral drugs (acyclovir or valacyclovir) is advised if they can be started within 24 to 48 hours of rash onset. Acyclovir, when initiated within 24 to 72 hours following the appearance of the cutaneous eruption, has demonstrated efficacy in reducing both the length and severity of varicella. Antivirals are typically indicated in adults, including pregnant women, because this group is more prone to complications.
The preferred treatment is usually oral therapy, but intravenous antivirals are indicated for immunocompromised patients, especially those undergoing chronic systemic corticosteroid therapy, due to their heightened risk of severe illness and sequelae. Supportive care, such as increasing water intake and using antipyretics and antihistamines, is essential to management.
Administration of varicella zoster immune globulin (125 U/10 kg, maximum 625 U) intramuscularly within 96 hours after varicella exposure is advised to offer passive prophylaxis to nonimmune immunocompromised adults, pregnant women, and high-risk neonates. Protection endures for around 3 weeks. An alternative for postexposure varicella prophylaxis in these patient populations is the administration of intravenous immunoglobulin.
| Treatment | Dosage/Application | Purpose |
|---|---|---|
| Calamine Lotion | Topical | Relieves itching |
| Acetaminophen | Oral | Reduces fever |
| Acyclovir/Valacyclovir | Oral/IV | Antiviral medication to combat the virus |
| Varicella Zoster Immune Globulin | Intramuscular | Passive prophylaxis post-exposure |
Prevention
The most important and common way to prevent varicella infection is through vaccination. Vaccination against varicella is not part of the Expanded Programme of Immunisation in most African Countries, but is indicated for children and adults in high risk categories. The ideal age of vaccination is between 12-15 months.
There is a two-dose chickenpox vaccine (Varivax) thatâs about 94 percent effective at preventing the disease for your lifetime. Adults who havenât had chickenpox will get two doses about one month apart.
Your doctor may advise against receiving this vaccine if:
- you have a moderate or severe illness
- you plan to become pregnant in the next 30 days
- you have an allergy to any ingredient in the vaccine, such as gelatin or neomycin, or if you had a serious allergic reaction to a previous dose of the chickenpox vaccine
- you have undergone chemotherapy or radiation for cancer
- you have been taking steroid drugs
- you have a disease that compromises your immune system, such as HIV
- you recently received a blood transfusion
