Chickenpox (varicella) is a highly contagious viral disease in children caused by the varicella-zoster virus (VZV). Its clinical features include the sequential and simultaneous appearance of various types of rashes on the skin and mucosa, such as macules, papules, vesicles, and crusts. Both chickenpox and shingles (herpes zoster) are caused by the same virus but represent two distinct clinical manifestations. Chickenpox occurs as a primary infection, while shingles results from a reactivated infection.
Pathogen
Varicella-zoster virus (VZV) belongs to the Herpesviridae family, Alpha subfamily, and is a double-stranded DNA virus. It exists as a single serotype but shares partial cross-immunity with herpes simplex virus (HSV). The virus is poorly resistant in vitro and is sensitive to heat, acids, and various organic solvents.
Epidemiology
Children infected with chickenpox serve as the primary source of transmission. The virus spreads via respiratory droplets or direct contact with skin lesions of infected individuals. The infectious period lasts from 1–2 days before the rash appears up until the lesions crust over, generally spanning about 7–8 days. The disease shows universal susceptibility, predominantly affecting children, with peak incidence between ages 2 and 6. Pregnant women who contract chickenpox within one week before delivery may transmit the virus to the fetus, leading to symptoms within 10 days of birth.
Pathogenesis
The virus enters the body through respiratory mucosa, replicates in the nasopharyngeal mucosa and lymphatic tissues, and subsequently invades the bloodstream, causing viremia. If the immune system fails to clear the virus, it proliferates again in the mononuclear phagocyte system before reentering the bloodstream and causing damage to various organs. Lesions primarily affect the skin and mucosa, though occasionally internal organs may be involved. After 1–4 days of rash eruption, specific cell-mediated immunity and antibodies develop, viremia resolves, and symptoms gradually subside.
Pathology
Chickenpox lesions predominantly occur in the skin and mucosa, characterized by multinucleated giant cells and intranuclear inclusion bodies. In the dermis, swelling of vascular endothelial cells and degeneration of epithelial cells in the spinous layer of the epidermis eventually lead to vesicle formation filled with virus-rich fluid. The fluid is later absorbed, leading to crust formation. Occasionally, ruptured vesicles leave shallow ulcers, which heal quickly. In children with compromised immunity, disseminated disease may occur, affecting the lungs, liver, spleen, pancreas, kidneys, intestines, and other organs, with focal necrosis, edema, congestion, and hemorrhage observed in afflicted tissues. Encephalitis cases may reveal cerebral edema, congestion, and punctate hemorrhages.
Clinical Manifestations
Typical Chickenpox
Prodromal symptoms such as fever, malaise, and anorexia may occur before the rash appears. Within 24–48 hours, the rash develops, characterized by:
- Initially appearing on the head, face, and trunk, later extending to the limbs; sparse lesions occur on distal areas, showing a centripetal distribution.
- Rashes beginning as red macules and papules, transforming into clear, tense vesicles that become turbid and exhibit central depressions within 24 hours. Vesicles rupture easily, rapidly forming crusts within 2–3 days.
- Rashes appearing in waves, accompanied by noticeable itching, with macules, papules, vesicles, and crusts coexisting during the peak of the disease.
- Mucosal lesions affecting areas such as the oral cavity, conjunctiva, and genitalia occasionally rupture to form shallow ulcers.
Chickenpox progresses as a self-limiting disease, with mild systemic symptoms and rash, resolving within approximately 10 days. Crusted lesions typically heal without leaving scars.
Severe Chickenpox
This is more common in immunocompromised children, presenting with persistent high fever, severe systemic symptoms, numerous rashes that may merge into large blisters or exhibit hemorrhagic features. Complications such as secondary infection or thrombocytopenia-associated fulminant purpura may occur.
Congenital Chickenpox
Maternal infection during early pregnancy may result in fetal congenital malformations. If maternal chickenpox develops shortly before delivery, neonatal chickenpox may occur, with a mortality rate of 25%–30%.
Complications
The most common complication involves secondary skin infections, including impetigo, cellulitis, and sepsis. Chickenpox pneumonia primarily affects immunocompromised children and neonates. Neurological complications may include post-varicella encephalitis, transverse myelitis, facial nerve paralysis, and Reye’s syndrome. Among other rare cases, myocarditis, hepatitis, nephritis, and arthritis may develop.
Laboratory Tests
Blood Routine
The total white blood cell count is typically normal or slightly reduced.
Herpes Scraping
Fresh basal tissue and vesicle fluid can be scraped and smeared for analysis. Multinucleated giant cells may be observed through Giemsa staining, while hematoxylin-eosin staining may reveal intranuclear inclusion bodies. Viral antigen detection using direct fluorescent antibody staining of vesicle fluid is straightforward and effective.
Serological Tests
Detection of varicella virus-specific IgM antibodies in serum can assist in early diagnosis. A fourfold or greater increase in the titer of specific IgG antibodies in paired serum samples also aids in diagnosis.
Virus Isolation
Vesicle fluid, throat secretions, or blood can be collected for viral culture and isolation.
Antigen and Nucleic Acids
Direct immunofluorescence can detect VZV antigens in vesicle fluid or lesion specimens within 15–20 minutes. RT-PCR can identify viral genes in samples within several hours, offering greater sensitivity and speed compared to viral isolation.
Diagnosis and Differential Diagnosis
Clinical diagnosis of typical varicella is straightforward. Laboratory tests may be used to confirm atypical cases. Differential diagnoses for varicella include papular urticaria and other diseases causing vesicular skin lesions, such as infections by enteroviruses or Staphylococcus aureus, as well as reactions to medications or contact dermatitis.
Treatment
Varicella is a self-limiting disease, and in cases without complications, general care and symptomatic management are prioritized. Isolation is recommended for patients, and supportive care includes regular changing of undergarments, trimming the nails, or wearing gloves to prevent scratching and minimize secondary infections. Rooms should be well ventilated, and patients should be provided with adequate fluids and easily digestible foods. Calamine lotion can be applied locally to relieve itching, and sedatives may be prescribed if necessary.
The antiviral drug acyclovir is preferred and should be administered as early as possible, typically within 48 hours of rash onset. Oral dosage is 20 mg/kg per dose (up to 800 mg), taken four times daily for 5 days. Severe cases require intravenous administration, 10–20 mg/kg per dose every 8 hours, for 7–10 days. Valacyclovir, initiated within 48 hours of rash appearance, is effective and recommended by the FDA for children aged 2 years and older at 20 mg/kg per dose every 8 hours. Secondary bacterial infections should be treated with antibiotics.
Prevention
The varicella live attenuated vaccine can be administered either as a monovalent vaccine or in combination with measles, mumps, and rubella vaccines. Children with varicella should be isolated until all lesions have crusted over. Susceptible children with an exposure history should be quarantined for 3 weeks. Passive immunization is recommended for individuals at high risk of severe disease, including patients on high-dose steroids, those with impaired immunity, malignancies, pregnant women exposed to the virus, and newborns of mothers with active varicella. Intramuscular injection of varicella-zoster immune globulin (125–625 U) within 72 hours of exposure may provide passive immunity.
Prognosis
Varicella is generally a benign and self-limiting disease with favorable outcomes. Crusted lesions typically heal without scarring. In newborns and immunocompromised individuals, severe forms of the disease may develop, such as encephalitis or other serious complications, potentially leading to death.