Varicella

Robin English
Pediatrics in Review 2003;24;372
DOI: 10.1542/pir.24-11-372

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
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Article

infectious diseases

Varicella
Robin English, MD*

Objectives

After completing this article, readers should be able to:

1. Discuss the consequences of primary infection with varicella-zoster virus and

reactivation.
2. Describe the ramifications of group A Streptococcus infection.
3. Identify those in whom varicella infection is most severe.
4. Explain the treatment options for varicella.
5. Recognize how to prevent varicella.

Introduction
Varicella is a common exanthematous disease that primarily affects children. In general,
clinicians are very familiar with the clinical presentation of this disease, but in the last several
years, fewer and fewer cases have been seen and diagnosed. This is due primarily to the
development of a safe and effective vaccine, which has been studied extensively. In the
future, primary care clinicians will see less of this disease, although the potential severity of
disease and associated risk of morbidity and mortality necessitate a continued awareness of
the clinical features and risk of complications. The American Academy of Pediatrics (AAP)
and the Advisory Committee on Immunization Practices (ACIP) of the Centers for
Disease Control and Prevention (CDC) have set a goal for more than 90% of American
children to be immunized against varicella by the year 2010.

Definitions
Chickenpox is the clinical syndrome that results from primary infection with varicellazoster virus (VZV), which is a herpesvirus. Herpes zoster (also called shingles or
zoster) appears after reactivation of latent VZV, which can occur at any time after a
primary infection. Disseminated zoster can occur after reactivation in immunocompromised patients and consists of severe rash with systemic findings. Congenital varicella
syndrome, or varicella embryopathy, is the result of varicella infection in a woman during
the first or second trimester of pregnancy.

Epidemiology
Varicella infection is more common during the late winter and early spring. The disease
also is more prevalent in temperate areas than in tropical climates. Prior to the development
of the vaccine, an estimated 4 million cases, with 10,000 hospitalizations and 100 deaths,
occurred in the United States each year, most frequently involving children younger than
the age of 10 years. Since then, reports of varicella infection have declined. The CDC has
encouraged states to improve surveillance for varicella, but only 14 states maintained a
continuous level of reporting from 1987 to 1997.
Varicella infection is found only in humans. The mode of transmission is person-toperson via direct contact with infected mucosa or airborne particles from respiratory
secretions. Transplacental passage of the virus also can occur. Transmission to susceptible
household contacts is expected (approximately 90%), and secondary cases often are more
severe than index cases. Nosocomial transmission has been reported. Subclinical varicella
can occur, as indicated by many adults who have no history of the disease demonstrating
detectable antibodies to the virus. Immunity after natural varicella infection is considered
lifelong.
*Assistant Professor of Clinical Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA.
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infectious diseases varicella

Figure 1. Typical varicella vesicles.

The incubation period for chickenpox is 10 to

21 days, with most people being infected within 14 to
16 days of exposure. Communicability is highest in the
period from 1 to 2 days prior to the appearance of the
rash to 1 to 2 days after its onset. Healthy children may
be considered noncontagious after all lesions have
crusted over, although communicability may be prolonged in immunocompromised patients who have severe infection. Susceptible children may become infected
with varicella after direct contact with active zoster lesions because these lesions contain infectious virus, but
not after exposure to respiratory secretions from individuals who have zoster. Exposure to children who have
chickenpox is not believed to reactivate zoster.

Pathogenesis
After a person is exposed to VZV, the virus undergoes
two phases of replication during the incubation period.
Primary replication, which begins 3 to 4 days after exposure, occurs in the oropharynx and regional lymph nodes
and is followed by a period of primary viremia. A secondary viremia, with intracellular replication within the reticuloendothelial system, occurs 10 to 21 days after
exposure. Late in the secondary viremic phase, the virus is
delivered to the skin, at which time the typical cutaneous
lesions become evident. These lesions may continue to
develop for the next 3 to 7 days as a result of infected
mononuclear cells. The virus also is carried to the respiratory mucosa toward the end of the incubation period,

which is the reason for communicability before the onset of rash. Following viremia, the virus becomes
latent in dorsal root ganglia cells. It
remains there until reactivation, at
which time the virus travels back to
the skin along the sensory nerve.
Reactivation likely is due to declining cell-mediated immunity, which
explains the increased incidence in
the elderly and in immunocompromised patients.
The viremic phase of varicella
infection may be prolonged in individuals who are immunocompromised. Because cell-mediated
immunity plays a role in the termination of viremia, patients who
have this type of immunodeficiency
are more at risk than those who
have primary humoral immunodeficiency. Prolonged viremia is the
reason for prolonged communicability and dissemination of the virus to organs such as the heart, brain, lungs,
and liver. Accordingly, immunocompromised children
are at greater risk for developing complications such as
pneumonia, meningoencephalitis, and hepatitis.

Clinical Aspects
Clinical Presentation
The rash of varicella often is preceded by a 24- to
48-hour period of fever, malaise, and other systemic
symptoms. The typical exanthem begins as erythematous, pruritic macules that develop into papules and
fluid-filled vesicles. The crusting of the vesicles is the final
stage of the lesions before resolution, and scarring occurs
rarely. One of the most characteristic features of the
exanthem is the presence of all stages of lesions simultaneously (Fig. 1). The average number of lesions is approximately 300 to 400, but the number can vary from
fewer than 50 in healthy children to more than 1,000 in
immunocompromised children or in severe infection.
The average length of time from the development of the
initial lesion to the crusting of all lesions is approximately
4 to 5 days.
Neonates born to women who develop primary varicella infection 5 days before to 2 days after delivery are at
increased risk of severe varicella infection, which may be
fatal. Clinical features of perinatally acquired varicella
include severe rash, pneumonia, hepatitis, and death in
20% to 30% of cases. Infants born to mothers who are
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infectious diseases varicella

infected before 5 days prior to delivery have less severe disease because of the transplacental transfer
of VZV-specific maternal immunoglobulin G.
Congenital varicella syndrome
results when a mother is infected
within the first 20 weeks of gestation. Zigzag skin scarring and
limb atrophy are characteristic findings of this embryopathy. Brain abnormalities, including hydrocephalus and microcephaly, and eye
abnormalities, such as cataracts and
chorioretinitis, also may occur.

Complications
The most common complication of
varicella is secondary bacterial infection, usually with Streptococcus Figure 2. Secondary infection in patient who has varicella. Photo courtesy of Joseph
pyogenes or S aureus (Fig 2). S pyo- Zenel, MD.
genes, or group A Streptococcus
(GAS), is emerging as an increasmost common causes of postviral cerebellar ataxia and
ingly common pathogen in patients who have varicella,
postviral transverse myelitis.
and it may cause severe invasive disease. A multicenter
study published in 2001 found that the risk of invasive
GAS infection was somewhat increased in nonwhite chilHerpes Zoster
dren in low-income households, in persons exposed at
Zoster, or shingles, is characterized by vesicles clushome, and in persons who had a long duration of fever.
tered in a dermatomal distribution. The initial presenting
Several case reports and studies have suggested a causal
symptom frequently is pain at the future site of the
relationship between the use of nonsteroidal antilesions, which usually arise within a few days. Pruritus
inflammatory drugs (NSAIDs) and the development of
also may occur. The most common sites for the developnecrotizing GAS infections, but the previously noted
ment of zoster lesions are those supplied by the trigemmulticenter study found no clear causal association. Parinal nerve and the thoracic ganglia. New lesions occur
ents were more likely to administer anti-inflammatory
over 2 to 3 days, then begin to crust over the next week.
and antipyretic medications to children who had more
Most lesions resolve within 2 weeks. Immunocomprosevere varicella disease, and it is known that severe varimised persons may experience a prolonged course or
cella disease can predispose a patient to invasive GAS
develop disseminated zoster, which is characterized by a
disease. Thus, the association between NSAID use and
severe, varicelliform rash with systemic findings such as
GAS infection may be due to these confounding varipneumonitis, hepatitis, and disseminated intravascular
ables.
coagulation. The development of herpes zoster in chilOther invasive complications of varicella infection
dren does not necessarily imply an occult malignancy or
include pneumonitis, meningoencephalitis, hepatitis,
other immunodeficiency.
arthritis, and glomerulonephritis. These complications
The most common complication of herpes zoster is
are more common in children who are immunocompropostherpetic neuralgia, which is defined as pain that lasts
mised, especially those who have T-cell defects, leukelonger than 1 month. This is uncommon in children and
mia, or lymphoma. Hemorrhagic varicella is a severe
occurs most often in persons older than 50 years of age.
form of the disease that also is found more commonly in
Immunocompromised patients also have an increased
immunocompromised patients. Hemorrhagic varicella
risk of this complication.
carries a 70% mortality risk. Varicella also is one of the
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infectious diseases varicella

Acyclovir Dosing for Varicella and Zoster

Infections

acyclovir is not routinely recommended for healthy children

younger than 12 years of age because the disease generally has a
Infection
Dosing
benign, self-limited course. HowVaricellaimmunocompetent
80 mg/kg per day PO divided qid for 5 d
ever, studies have shown a moderpatient
Maximum dose, 3,200 mg/d
ate decrease in the severity of sympVaricellaimmunocompromised
30 mg/kg per day IV divided tid for 7 to 10 d
toms if acyclovir is used within
patient
(<1 y of age)
2
24 hours of the onset of the rash.
1,500 mg/M per day IV divided tid for 7 to
Oral acyclovir may be consid10 d (>1 y of age)
Zosterimmunocompetent and
30 mg/kg per day IV divided tid for 7 to 10 d
ered
for those at risk for more seimmunocompromised
(<1 y of age)/1,500 mg/M2 per day
vere infection, including children
patients
divided tid for 10 d (>1 y of age)
older than age 12 years, persons
OR
who have chronic disease, and per4 g/d PO in 5 divided doses for 5 to 7 d
sons who are taking chronic aspirin
(>12 y of age)
or corticosteroid therapy. If oral
acyclovir is used, it should be initiDiagnosis
ated early in the course of the exanthem (see Table 1 for
The clinical appearances of primary varicella and herpes
recommended doses).
zoster infections are so characteristic that laboratory testIntravenous acyclovir should be used for immunoing often is not necessary. However, several diagnostic
compromised patients who have varicella-zoster infectests are available if the diagnosis is in question. A Tzanck
tion and should be initiated within 24 hours of the onset
smear performed on a vesicle scraping shows multinucleof the rash (Table 1). In general, acyclovir is a safe
ated giant cells, but it does not distinguish between
medication, although adverse effects such as nausea,
varicella zoster and herpes simplex. Viral culture and
diarrhea, and renal toxicity have been reported. Patients
direct fluorescent antigen (DFA) performed on a vesicle
who have renal dysfunction should receive reduced
scraping can differentiate between the two; the DFA is
doses. Intravenous foscarnet is available for the treatment
more rapid and sensitive than the culture. The virus is
of acyclovir-resistant infections. Because renal toxicity
isolated best from vesicle scrapings during the first 3 to
and electrolyte abnormalities are the most important
4 days of the rash. A polymerase chain reaction percomplications of foscarnet therapy, serum creatinine and
formed on vesicle fluid often can identify and help to
electrolyte levels should be monitored closely.
differentiate wild type varicella from vaccine-induced
Currently, acyclovir is the treatment of choice for
varicella.
herpes zoster infections in both immunocompromised
Immunity to varicella zoster may be determined in
and immunocompetent children (see Table 1 for dosimmunocompetent persons by a significant increase in
ing). Famcicyclovir and valacyclovir are effective treatserum antibody (immunoglobulin G) to varicella. Latex
ments for zoster infections in adults, although these
agglutination is more sensitive than enzyme immunoasmedications have not been studied adequately for use in
say in determining immunity, including vaccine-induced
the pediatric population.
immunity. These tests are less reliable in immunocomPostexposure Prophylaxis
promised individuals.
Varicella vaccine and varicella-zoster immune globulin
Management
(VZIG) are both available for the prevention of disease in
Treatment
susceptible persons exposed to VZV. Significant expoThe treatment of primary varicella-zoster infection is
sure includes household contacts, close play or hospital
supportive, including antipyretics and antihistamines or
contacts, newborns born to mothers who develop varioatmeal baths to control fever and itching. Because of the
cella 5 days prior to or 2 days after delivery, and those
risk of Reye syndrome, aspirin should be avoided. As
who have direct contact with active zoster lesions. Susmentioned previously, case reports have supported the
ceptibility should be determined by the history of previavoidance of NSAIDs as well, although the association
ous disease, keeping in mind that 70% to 90% of adults
between the use of these agents and the development of
who do not have a reliable history of varicella are iminvasive GAS infection has not been proven. The use of
mune. For immunocompetent persons, serologic testing
Table 1.

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infectious diseases varicella

is reliable but not necessary. Immunocompromised persons demonstrate unreliable results.

Varicella vaccine has been shown to prevent or modify
the disease course if administered to healthy susceptible
children within 3 days (and possibly 5 days) of exposure.
If the susceptible child is in the prodromal phase of
varicella disease, vaccine administration does not increase
the risk of developing more severe disease or vaccineassociated adverse effects. The vaccine also is safe for
persons who have immunity from a previous subclinical
infection.
VZIG is effective in preventing disease if administered
within 4 days of exposure to varicella; maximum effectiveness is achieved if it is administered as soon as possible
after exposure is recognized. VZIG is administered intramuscularly, and the most common adverse effect is pain
at the injection site. Patients who receive monthly intravenous immune globulin (IVIG) do not require VZIG if
the last IVIG infusion was administered up to 3 weeks
before exposure. In the case of significant exposure,
VZIG should be given to susceptible immunocompromised children and adolescents, susceptible
healthy adults, susceptible pregnant women, and newborns
whose mothers developed varicella 5 days before to 2 days after
delivery. Hospitalized preterm infants who are younger than
28 weeks gestation should receive VZIG after exposure, regardless of maternal immune status; those older than 28 weeks
gestation should receive it if the mother lacks a reliable
history or serologic evidence of immunity. Bone marrow
transplant recipients should be given VZIG after exposure, regardless of prior history of varicella. The duration
of protection from varicella after VZIG administration is
unknown.

Immunocompromised patients who have zoster and

immunocompetent patients who have disseminated zoster should be placed on airborne and contact precautions
for the entire duration of the illness. Contact precautions
are recommended for immunocompetent persons who
have localized zoster until all lesions are crusted over.
Immunocompetent children who have uncomplicated varicella infection may return to school when all
lesions are crusted over. Immunocompromised children
and other children who have prolonged or complicated
courses should not return to school until the rash has
resolved. Children and adult child care workers who have
zoster may return to school or work if all lesions can be
covered.
Susceptible exposed hospital and child care staff
should be excused from patient or child contact from 8 to
21 days after exposure to an infected person. If exposure
to an infected person does not result in disease in susceptible personnel, immunization with the vaccine is recommended.

Intravenous
acyclovir should
be used for immunocompromised patients
who have varicella-zoster infection and
should be initiated within 24 hours of the
onset of the rash.

Isolation
Airborne and contact precautions should be initiated for
hospitalized patients who have varicella for at least 5 days
after the onset of the rash and maintained until all vesicles
are crusted. Exposed susceptible patients should be kept
on airborne and contact precautions from 8 to 21 days
after onset of the rash in the index case. These precautions also should be practiced for neonates born to
mothers who had varicella until the infants are 21 days of
age. Patients who receive VZIG should be isolated for a
total of 28 days.

Prevention
The varicella vaccine, which was licensed for use in March
1995, is a live-attenuated preparation of the wild Oka
strain of varicella. The AAP and ACIP recommended its
routine use in susceptible children older than 12 months
of age shortly after its licensure. After evaluation of the
safety and efficacy of the vaccine, these groups continue
to support this recommendation.
Despite these recommendations, many children remain unimmunized against varicella. The AAP Committee on Infectious Diseases has identified possible barriers
to universal immunization, including the misconception
that varicella is always a mild disease, concern over vaccine safety, and concern about waning immunity. Many
pediatricians are not recommending the varicella vaccine
routinely, and only a few states require proof of disease or
vaccination before the child enters school or child care.
One study conducted in an urban environment showed

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infectious diseases varicella

that parents are significantly influenced by their pediatricians views on vaccination against varicella. This suggests that improved efforts to educate community pediatricians on the safety and efficacy of the vaccine are
necessary to achieve universal vaccination.
A safety surveillance of the varicella vaccine evaluated
adverse events reported to the United States Vaccine
Adverse Event Reporting System (VAERS) from March
1995 to July 1998. More than 6,500 cases of adverse
events were reported during this time, which is a rate of
67.5 per 100,000 doses sold. Of these, the most common were rash, possible vaccine failure, and injection site
reactions. Rashes, most often vesicular, accounted for
more than 50% of the reports. Of the specimens tested,
wild-type varicella was found in 61% (with symptoms
occurring approximately 1 week after immunization),
and the Oka strain was identified in 31% (with symptoms
occurring an average of 4 weeks after immunization).
Possible vaccine failure was reported in approximately
20%, and many of these were reported following subsequent negative serologic tests. Injection site reactions
occurred in 8.7% of patients and usually occurred within
1 week of vaccination.
More serious but rare adverse events have been reported, including pneumonia, hepatitis, erythema multiforme and Stevens-Johnson syndrome, thrombocytopenia, anaphylaxis, and neurologic events, such as seizures
and neuropathies. In most of these events, no evidence
linked administration of the vaccine to the development
of symptoms. In addition, evidence of wild-type virus was
found in many patients who had both mild and serious
adverse events, highlighting the importance of the continued presence of wild-type virus in the community.
Herpes zoster has been reported after vaccine administration, but it is much less frequent than zoster occurring after natural varicella and often is associated with the
isolation of wild-type virus, suggesting infection prior to
vaccination. Transmission of vaccine-associated virus is
extremely rare and occurs only if a rash develops in the
vaccinee. The risk of developing disease after this type of
exposure is so rare that the routine use of VZIG or
acyclovir as prophylaxis is not recommended, even in
immunocompromised patients.
In addition to being safe, the varicella vaccine has
been found to be efficacious. Numerous studies have
been performed since its licensure, and the evidence
suggests that the vaccine is approximately 85% to 90%
effective in preventing all forms of the disease and 95% to
100% effective in preventing moderate-to-severe disease.
Recently, a study of more than 1,100 healthy children
evaluated the persistence of antibody 6 years after vacci-

Table 2.

Dosing for Varicella Vaccine

Age

Dosing

12 to 18 mo
19 mo to 13 y

0.5 mL SC/IMsingle dose

0.5 mL SC/IMsingle dose (at any
time)
0.5 mL SC/IM2 doses, 4 to
8 weeks apart

13 y to adulthood

nation. This study determined that the antibody persistence rate over the 6 years was 99%, with breakthrough
events occurring in 0.2% to 2.3% of children per year.
Breakthrough cases were generally mild. Children who
have high levels of varicella antibody after vaccination
appear to be at decreased risk for developing breakthrough infection. Studies performed to date have supported the evidence that most vaccinees have long-term
persistence of antibodies to VZV. Further studies are
necessary to determine the role, if any, of booster doses
of the varicella vaccine in providing lifelong immunity.
The varicella vaccine should be administered to all
healthy susceptible children older than 1 year of age. The
AAP and ACIP also recommend its use up to 3 days after
exposure to varicella (see Table 2 for dosing and administration). Contraindications to vaccination include concurrent moderate-to-severe febrile illness, chronic highdose steroid use (2 mg/kg per day for 14 d), pregnancy, and a history of anaphylaxis with any component
of the vaccine, including gelatin and neomycin. In addition, the vaccine should not be administered routinely to
children who have cell-mediated immunodeficiencies, leukemia, lymphoma, or other bone marrow malignancies.
One exception to the contraindications is the child
who has acute lymphoblastic leukemia, has been in remission for at least 1 year, and has reasonable lymphocyte
and platelet counts. In these patients, immunization has
been shown to be safe and effective, although approval
by institutional review boards currently is required for its
use. Another exception is the child who has human
immunodeficiency virus (HIV) infection and is asymptomatic or mildly symptomatic. A recently published
study demonstrated that such HIV-infected children
who received two doses of vaccine had seroconversion
rates of 60%, with adverse effects similar to those seen in
immunocompetent children.
Household contacts of immunocompromised individuals may receive the vaccine, but they should avoid
direct contact with the immunocompromised person if a
rash develops after vaccination. Immunodeficiency
should be excluded before vaccination in a person whose
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infectious diseases varicella

family history includes hereditary immunodeficiency.

Administration of the vaccine should be postponed until
3 to 11 months after the administration of IVIG, depending on the dose of IVIG used. IVIG should be
withheld until 2 weeks after the varicella vaccine is given.

Summary
Varicella infection is generally a benign, self-limited disease, but serious complications can occur, especially in
immunocompromised children, neonates, and adults.
Ongoing education on the risks of infection and the
benefits of vaccination is necessary to minimize the incidence as well as the morbidity and mortality of this
disease.

Suggested Reading
American Academy of Pediatrics. Varicella-zoster virus. In: Pickering LK, ed. 2000 Red Book: Report of the Committee on Infectious

Diseases. 25th ed. Elk Grove Village, Ill: American Academy of

Pediatrics; 2000:624 628
Committee on Infectious Diseases. Varicella vaccine update. Pediatrics. 2000;105:136 141
Lesko SM, OBrien KL, Schwartz B, Vezina R, Mitchell A. Invasive
group A streptococcal infection and nonsteroidal antiinflammatory drug use among children with primary varicella. Pediatrics.
2001;107:1108 1115
Levin MJ, Gershon AA, Weinberg A, et al. Immunization of HIVinfected children with varicella vaccine. J Pediatr. 2001;139:
305310
Skull SA, Wang EEL. Varicella vaccination a critical review of the
evidence. Arch Dis Child. 2001;85:8390
Taylor JA, Newman RD. Parental attitudes toward varicella vaccination. Arch Pediatr Adolesc Med. 2000;154:302306
Vessey SJR, Chan CY, Kuter BJ, et al. Childhood vaccination
against varicella: persistence of antibody, duration of protection,
and vaccine efficacy. J Pediatr. 2001;139:297304
Wise RP, Salive ME, Braun MM, et al. Postlicensure safety
surveillance for varicella vaccine. JAMA. 2000;284:1271
1279

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infectious diseases varicella

PIR Quiz
Quiz also available online at www.pedsinreview.org.
6. A previously well 13-year-old boy develops fever and a papulovesicular and pustular rash over his trunk.
Assuming that this represents acute varicella-zoster infection, you would expect:
A.
B.
C.
D.
E.

Acetylsalicylic acid to be a reasonable choice for fever management.

Appreciable benefit from varicella-zoster immune globulin.
Low risk of severe disease.
Occasional animal-to-human transmission.
Persistent infection of primary sensory neurons.

7. A healthy 12-year-old girl who had chickenpox 6 years ago develops a linear, pruritic, and vesicular
eruption on her left chest. You diagnose herpes zoster. In this situation, the most appropriate next step is
to:
A.
B.
C.
D.
E.

Initiate a thorough evaluation for occult malignancy.

Institute airborne and contact isolation until all lesions are crusted over.
Prescribe a course of oral acyclovir.
Recommend a prophylactic topical antibiotic.
Recommend home schooling until all lesions are crusted over.

8. A previously well 6-year-old girl develops chickenpox. The complication for which she is most at risk is:
A.
B.
C.
D.
E.

Glomerulonephritis.
Hemorrhagic varicella.
Invasive group A streptococcal disease.
Pneumococcal meningitis.
Varicella pneumonia.

9. A woman develops chickenpox 3 days before delivery. The labor and delivery prove uneventful. The baby
girl is term, appropriate for gestational age, and appears healthy. In this situation, benefit/risk analysis
mandates the administration of:
A.
B.
C.
D.
E.

Intramuscular varicella-zoster immune globulin.

Intravenous foscarnet.
Only observation.
Oral acyclovir.
Subcutaneous varicella vaccine.

10. You are asked to discuss the varicella vaccine with a group of residents. Of the following, the most
appropriate statement to include in your discussion is that:
A.
B.
C.
D.
E.

Postexposure varicella vaccine does not prevent or modify disease.

Pre-exposure varicella vaccine reliably prevents severe disease.
Transmission of varicella vaccine virus is a common event.
Vaccine-induced antibody falls to nonprotective levels in most children within 6 years.
Varicella vaccine causes severe reactions in individuals who have developed immunity after exposure to
the wild virus.

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Varicella
Robin English
Pediatrics in Review 2003;24;372
DOI: 10.1542/pir.24-11-372

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