AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Varicella, commonly known in the United States as chickenpox, is caused by the varicella-zoster virus. The disease is generally regarded as a mild, self-limiting viral illness with occasional complications. Before vaccination for varicella became widespread in the United States, this disease caused as many as 100 deaths annually. Since the varicella vaccine was introduced in the United States in 1995, disease incidence has substantially decreased.

Even today, varicella is not totally benign. One study suggested that nearly 1:50 varicella cases are associated with complications. Among the most serious complications are varicella pneumonia and encephalitis; both are associated with a high mortality rate. In addition, significant concerns have been raised about the association of varicella with severe invasive group A streptococcal disease.¹

The United States adopted universal vaccination against varicella in 1995, which reduced the morbidity and mortality rates of this disease. For obvious reasons, children who are not vaccinated remain susceptible. Children with varicella expose adult contacts in households, schools, and daycare centers to the risk of severe, even fatal, disease. Varicella is common and highly contagious and affects nearly all susceptible children before adolescence.

Household transmission rates are 80-90%. Second cases within the household are often more severe. School or daycare center contact is associated with lower but still significant transmission rates. Children who are susceptible rarely acquire the disease by contact with adults with zoster. Maximum transmission occurs during late winter and spring.

Varicella is associated with humoral and cell-mediated immune responses. These responses induce long-lasting immunity. Repeat subclinical infection can occur in these persons, but second attacks of chickenpox are extremely rare in immunocompetent persons.

Pathophysiology

The varicella-zoster virus enters through the respiratory system and colonizes the upper respiratory tract. The virus initially replicates in the regional lymph nodes; 4-6 days later, a primary viremia spreads the virus to reticuloendothelial cells in the spleen, liver, and elsewhere.

After a week, a secondary viremia disseminates the virus to the viscera and skin, eliciting the typical skin lesions. This viremia also spreads the virus to respiratory sites and is responsible for the contagion of varicella before the appearance of the rash. Infection of the CNS or liver also occurs at this time.

Frequency

United States

Before varicella vaccine use became widespread, 4 million cases of chickenpox were reported annually. The disease was responsible for 11,000 hospitalizations each year and approximately 50-100 deaths. Currently, less than 10 deaths occur per year, most of them in unimmunized people.

International

Varicella affects nearly all children who do not have immunity. Annual incidence is estimated at 80-90 million cases. Most developing countries have low immunization rates because of the cost involved, and varicella disease is a risk for travelers to such countries.

Mortality/Morbidity

In otherwise healthy children aged 1-14 years, the mortality rate is estimated at 2 deaths per 100,000 cases.

• Most deaths in the United States before universal vaccination were from associated encephalitis, pneumonia, secondary bacterial infection, and Reye syndrome.
• The mortality rate in children who are immunocompromised is much higher.
• The disease can be serious in neonates, depending on the timing of infection in the mother.

Race

Varicella has no racial predilection.

Sex

Varicella has no sex predilection.

Age

The maximum incidence of varicella is in children aged 1-6 years. Persons older than 14 years account for 10% of varicella cases. This rate might change because younger children are being vaccinated.

CLINICAL

Section 3 of 11  

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History

• Exposure
• • Varicella spreads primarily by airborne respiratory droplets.
  • Most patients have a history of exposure in the home, daycare center, or school.
• Incubation: The incubation period is typically 10-14 days, although it may extend to 21 days.
• Prodrome
• • Low-grade fever preceding skin manifestations by 1-2 days
  • Complaints of abdominal pain by some children
  • Rash, usually starting on the head and trunk and spreading to the rest of the body
  • Typically, complaints of intense pruritus
  • Headache
  • Malaise
  • Anorexia 
  • Cough and coryza 
  • Sore throat

Physical

• Rash
• • The characteristic rash appears in crops.
  • An otherwise healthy child usually has 250-500 lesions but may have as few as 10 or as many as 1500.
  • Each lesion starts as a red macule and passes through stages of papule, vesicle, pustule, and crust.
  • Redness or swelling around a lesion should lead to suspicion of bacterial superinfection.
  • The vesicle on a lesion's erythematous base leads to its description as a pearl or dewdrop on a rose petal.
  • The hallmark is the simultaneous presence of different stages of the rash.
  • Some lesions may appear in the oropharynx.
  • Eye lesions are rare.
  • New lesions continue to erupt for 3-5 days.
  • Lesions usually crust by 6 days (range 2-12 d), and heal completely by 16 days (range 7-34 d).
  • Prolonged eruption of new lesions or delayed crusting and healing can occur with impaired cellular immunity.
• Fever
• • Fever usually is low grade (100-102°F) but may be as high as 106°F.
  • In otherwise healthy children, fever typically subsides within 4 days.
  • Prolonged fever should prompt suspicion of complication or immunodeficiency.
• In utero infection: Outcomes of in utero varicella infections vary based on the timing of the infection.
• • Congenital varicella syndrome
  • • Congenital varicella syndrome occurs in 2% of children born to women who develop varicella during the first or second trimester of pregnancy.
    • This syndrome manifests as intrauterine growth retardation, microcephaly, cortical atrophy, limb hypoplasia, microphthalmia, cataracts, chorioretinitis, and cutaneous scarring.
    • Fetal injury risk is unrelated to the severity of disease in the mother.
    • Zoster exposure during pregnancy has not been associated with fetal injury.
  • Infantile zoster
  • • Infantile zoster usually manifests within the first year of life.
    • The cause is maternal varicella infection after the 20 weeks’ gestation.
    • Infantile zoster commonly involves the thoracic dermatomes.
  • Neonatal varicella
  • • Neonatal varicella can be a serious illness, depending on the timing of maternal varicella and delivery. After the initial viremia, the mother develops antibodies against the varicella virus. The severity of the disease in the newborn depends on whether transplacental passage includes only the virus or includes both the virus and the antibodies.
    • If the mother develops varicella within 5 days before or 2 days after delivery, the baby is exposed to the secondary viremia of the mother. The baby transplacentally acquires the virus but acquires no protective antibodies because of insufficient time for antibodies to develop in the mother. In these babies, neonatal varicella is likely to be severe and disseminated. Prophylaxis or treatment is required with varicella-zoster immune globulin (VZIG) and acyclovir. Without these drugs, mortality rates may be as high as 30%. The primary causes of death are severe pneumonia and fulminant hepatitis.
    • Onset of maternal varicella more than 5 days antepartum provides the mother sufficient time to manufacture and pass on antibodies along with the virus. Full-term neonates of these women usually have mild varicella because of the attenuating effect of the transplacentally acquired antibodies. Treatment with VZIG is not recommended in such cases, but acyclovir may be used, depending on individual circumstances.

Causes

• The varicella-zoster virus is a member of the human herpesvirus subfamily Alphaherpesvirinae and, as is true of all herpes viruses, is a DNA virus.
• Varicella is highly contagious; secondary attack rates range from 80-90% for household contacts.
• Transmission involves the following:
• • Transmission occurs mainly through respiratory droplets that contain the virus, making the disease highly contagious even before the rash appears.
  • Papules and vesicles, but not the crusts, have high populations of the virus.
  • The infectious period begins 2 days before skin lesions appear and ends when the lesions crust, usually 5 days later.
  • Direct person-to-person contact with lesions also spreads the virus.
  • Maternal varicella with viremia can transplacentally spread to the fetus. This leads to neonatal varicella.
• Risk factors for severe varicella include the following:
• • Neonatal period
  • • A neonate's first month of life is a susceptible period for severe varicella, especially if the mother is seronegative.
    • Delivery before 28 weeks’ gestation also renders a baby susceptible because transplacental transfer of immunoglobulin G (IgG) antibodies occurs after this time.
  • Adolescence and adulthood
  • • Steroid therapy: High doses (ie, doses equivalent to 1-2 mg/kg/d of prednisolone) for 2 weeks or more are definite risk factors for severe disease. Even short-term therapy at these doses immediately preceding or during the incubation period of varicella can cause severe or fatal varicella.
    • Malignancy: All children with cancer have an increased risk for severe varicella. The risk is highest for children with leukemia. Almost 30% of patients who are immunocompromised and who have leukemia have visceral dissemination of varicella; 7% may die. 
    • Immunocompromised state (eg, malignancy, antimalignancy drugs, human immunodeficiency virus [HIV], other congenital or acquired immunodeficient conditions): Defects of cellular but not humoral immunodeficiency are believed to render a person susceptible to severe varicella.
    • Pregnancy: Pregnant women have high risk of severe varicella, especially pneumonia.

DIFFERENTIALS

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Other Problems to be Considered

Drug reactions
Insect bites
Smallpox

WORKUP

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Lab Studies

• Laboratory studies are unnecessary for diagnosis because varicella is clinically obvious.
• Most children with varicella have leukopenia in the first 3 days, followed by leukocytosis.
• Marked leukocytosis may indicate a secondary bacterial infection but is not a dependable sign. Most children with significant secondary bacterial infections do not have leucocytosis.
• Immunohistochemical staining of skin lesion scrapings can confirm varicella.
• • The procedure is useful for high-risk patients who require rapid confirmation.
  • A Tzanck smear involves scraping the base of the lesions and then staining the scrapings to demonstrate multinucleated giant cells. However, this finding is not sufficiently sensitive or specific for varicella and should be replaced by the more specific immunohistochemical staining of such scrapings, if available.
• Serologic studies include the following:
• • Serology is mainly used to confirm past infection to assess a patient's susceptibility status. This helps determine preventive treatment requirements for an adolescent or adult who has been exposed to varicella.
  • Among the many serologic studies, the most sensitive are the indirect fluorescent antibody (IFA), fluorescent antibody to membrane antigen (FAMA), neutralization test (NT), and radioimmunoassay (RIA). These time-consuming tests require specialized equipment that renders them unsuitable for routine use.
  • Commercially available latex agglutination (LA) and enzyme-linked immunosorbent assay (ELISA) tests are sensitive and rapid. Although the complement fixation test is often used, its sensitivity is low.

Imaging Studies

• Chest radiography
• • Children with high temperatures and respiratory signs should have chest radiography to confirm or exclude pneumonia.
  • Chest radiographic findings may be normal or may show diffuse bilateral nodular infiltrates in primary varicella pneumonia.
  • Radiography may also detect focal infiltrates suggestive of secondary bacterial pneumonia.

Other Tests

• Lumbar puncture
• • Children with neurological signs should have their cerebrospinal fluid (CSF) examined.
  • The CSF of patients with varicella encephalitis may have few or as many as 100 cells that are polymorphonuclear or mononuclear, depending on the timing of the lumbar puncture.
• Glucose levels are within the reference range.
• Protein levels are within the reference range or are slightly elevated.

TREATMENT

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Medical Care

• Manage pruritus with cool compresses and regular bathing.
• Discourage scratching to avoid scarring. Trimming the child's fingernails and having the child wear mittens while sleeping may reduce scratching.

Consultations

• Consult with an infectious disease specialist in the following situations:
• • Progressive or severe varicella
  • Life-threatening complications (eg, encephalitis, pneumonia)
  • Serious secondary bacterial infections, especially group A streptococcal superinfections, which may evolve rapidly into necrotizing fasciitis and toxic shock syndrome
• Children who develop severe and life-threatening varicella complications may require hospitalization in an ICU.

Diet

• Advise parents to provide a full and unrestricted diet to the child.
• Some children with varicella have reduced appetite and should be encouraged to take sufficient fluids to maintain hydration. Adequate hydration is especially important if the child is receiving acyclovir because the drug can crystallize in the renal tubules if administered to dehydrated individuals.

Activity

No activity restrictions are needed for young children with uncomplicated varicella.

MEDICATION

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Drug Category: Antivirals

Chickenpox is not always benign. In certain well-defined groups, varicella can be severe and even fatal. Antiviral drugs are recommended for adolescents, adults, and children on steroid or salicylate therapy and for children who are otherwise immunocompromised. Acyclovir is the only adequately studied drug of this class.

Drug Category: Antipyretics

These agents inhibit central synthesis and release of prostaglandins that mediate the effect of endogenous pyrogens in the hypothalamus; thus, they promote the return of the set-point temperature to normal.

Fever is usually low grade but may be elevated. Acetaminophen is probably the safest drug to use for this purpose. Salicylate usage for varicella is associated with Reye syndrome; therefore, never prescribe these agents. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been suspected of suppressing immune function and promoting infection progress in patients infected with invasive group A streptococci.

Drug Category: Antihistamines

These agents may control pruritus by blocking effects of endogenous release of histamine. Pruritus can be severe in varicella, preventing sleep and possibly leading to scarring or secondary infection. Nonsedating antihistaminics lack sufficient antipruritic action. The value of local preparations (eg, calamine, antihistamines) is unproved. Topical antihistamines can cause significant sedation from absorption through injured skin.

FOLLOW-UP

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Further Inpatient Care

• Indications for admission to ICU include the following:
• • Altered consciousness
  • Seizures
  • Difficulty walking 
  • Respiratory distress
  • Cyanosis
  • Low oxygen saturation
• Hospitalize and treat all newborns whose mothers developed varicella less than 5 days before or within 2 days after delivery.

Deterrence/Prevention

The AAP recommends excluding affected children from school until the sixth day of rash. This may not prevent spread of varicella because the child is infective before rash appears.

• Vaccination
• • Varicella vaccine consists of live attenuated Oka strain varicella virus. The vaccine is safe and highly immunogenic. It was approved for use in the United States in 1995 and has greatly reduced the incidence and mortality due to varicella.
  • The vaccine has been found to have protective efficacy of 71-100% against varicella. However, protection against moderate and severe varicella is much higher (95-100%).
  • The varicella vaccine is effective after age 1 year. A single dose provides protection to approximately 85% of recipients. Vaccine-conferred immunity to varicella wanes over time, making more vaccine recipients susceptible to the disease. The Advisory Committee on Immunization Practices (ACIP) and the American Academy of Pediatrics (AAP) now recommend 2 doses of this vaccine for all children.² After the first dose at age 12-15 months, the second dose should be administered at age 4-6 years. All persons who have received one dose of the vaccine at any time in the past should be offered a second dose.
  • Breakthrough disease involves varicella that occurs after 42 days of immunization. When it occurs, it is usually mild disease but can spread to other susceptible people. Breakthrough disease is more common if the vaccine was given before age 14 months, within 28 days after the measles-mumps-rubella (MMR) vaccine, and if the child was on oral steroid therapy.
  • Research study protocols allow varicella vaccine administration to patients with leukemia while they are in remission.
  • Postexposure prophylaxis, if provided within 72 hours of contact, can prevent or attenuate disease in the exposed individual.
• Varicella-zoster immune globulin
• • VZIG is used as postexposure prophylaxis in high-risk individuals. Administration as soon as possible after exposure is best, but VZIG can prevent or attenuate varicella if administered within 96 hours of contact.
  • The dose is 125 U/10 kg body weight; 125 U is the minimum dose. Maximum dose is 625 IU.
  • VZIG is intramuscularly administered and is never intravenously (IV) administered. The expected duration of protection is approximately 3 weeks. Patients on replacement IV immunoglobulin (IVIG) do not need VZIG if their most recent IVIG infusion was within 3 weeks.
  • VZIG reduces complications and the mortality rate of varicella, not its incidence. Postexposure prophylaxis using varicella vaccine is preferred for immunologically normal patients. VZIG is indicated for the following persons with significant exposure:
  • • Newborns of mothers who acquired varicella 5 days before to 2 days after delivery
    • Children with leukemia or lymphoma who have not been vaccinated and have not had varicella previously
    • Persons with HIV, acquired immunodeficiency syndrome (AIDS), or other immunodeficiency disorders
    • Persons receiving drugs that suppress immune function (eg, systemic steroids)
    • Pregnant women
    • Immunocompromised individuals who have no reliable history of chickenpox

Complications

• Secondary bacterial infections
• • Varicella may predispose patients to bacterial infections. Skin lesion infections are common and occur in 5-10% of children. Skin lesions provide a portal of entry for virulent organisms; rapidly spreading cellulitis, septicemia, and other serious infections may occur.
  • The most common infectious organisms are group A streptococci and Staphylococcus aureus. Varicella places the patient at high risk for acquiring invasive group A streptococcal disease. In addition to toxic shock syndrome, group A streptococci may cause necrotizing fasciitis, bacteremia, osteomyelitis, pyomyositis, gangrene, subgaleal abscess, arthritis, and meningitis in patients with varicella.
  • Staphylococcal species also cause severe infections in children with varicella. Staphylococcal infections in these patients reportedly cause cellulitis, impetiginous pox infections, staphylococcal scalded skin syndrome, toxic shock syndrome, pericarditis, and osteomyelitis.
  • Signs and symptoms of secondary bacterial infection can be indistinguishable from uncomplicated varicella during the first 3-4 days.
  • A high level of suspicion is necessary for early recognition and timely appropriate treatment of secondary infections.
  • Suspect secondary infection if systemic manifestations do not improve in 3-4 days, the fever returns or worsens, or the child's condition deteriorates after initial improvement.
  • Suspicion of secondary bacterial infection should prompt early institution of empirical antibiotic therapy until the results of culture studies become available.
  • Neutrophilic leukocytosis and neutrophilia occur in only a few cases involving serious bacterial infections.
  • Investigations cannot be relied on to diagnose or exclude bacterial infection.
• CNS complications
• • Acute postinfectious cerebellar ataxia is the most common CNS complication, with an incidence of 1 case per 4000 patients with varicella.
  • • Ataxia has sudden onset that usually occurs 2-3 weeks after the onset of varicella. The condition may persist for 2 months.
    • Manifestations may range from mild unsteadiness to complete inability to stand and walk, with accompanying incoordination and dysarthria. Manifestations are maximal at onset; a waxing and waning course suggests another diagnosis.
    • The sensorium is clear, even when the ataxia is profound.
    • The prognosis for patients with ataxia is good, but a few children may have residual ataxia, incoordination, or dysarthria.
  • Encephalitis occurs in 1.7 patients per 100,000 cases of varicella among otherwise healthy children aged 1-14 years.
  • • The disease manifests during acute varicella a few days after rash onset. Lethargy, drowsiness, and confusion are the usual presenting symptoms.
    • Some children may have seizures, and encephalitis can rapidly progress to deep coma.
    • This serious complication of varicella has a 5-20% mortality rate.
  • Reye syndrome was associated with varicella when aspirin use was common. Identification of this association now has made acetaminophen the preferred drug, and Reye syndrome has become rare.
  • Other neurological complications include aseptic meningitis, Guillain-Barré syndrome, and polyradiculitis.
• Pneumonia
• • Pneumonia primarily occurs in older children and adults and can have a fatal outcome.
  • Respiratory symptoms usually appear 3-4 days after the rash.
• Herpes zoster
• • A delayed complication of varicella, herpes zoster infection, occurs months to years after the primary infection in about 15% of patients.
  • The complication is caused by virus that persists in the sensory ganglions.
  • Herpes zoster consists of a unilateral vesicular rash, limited to 1-3 dermatomes. The rash is often painful in older children and adults. Among the health benefits of routine varicella immunization in childhood may be a lifelong decreased risk for reactivation of the virus as shingles.
• Otitis media: About 5% of children with varicella develop otitis media, caused by the usual pathogens.
• Thrombocytopenia
• Hepatitis: Hepatitis is a self-limited accompaniment of varicella.
• • Severe hepatitis with clinical manifestations is infrequent in otherwise healthy children with varicella.
  • Significant elevations of alanine aminotransferase (ALT) occur in 20-50% of children and adolescents, but elevations return to normal within one month in almost all cases.
  • Liver involvement is independent of the severity of skin and systemic manifestations.
• Glomerulonephritis
• Hemorrhagic varicella

Prognosis

• Otherwise healthy children with varicella have excellent prognoses.
• Children with immunocompromised states are at risk for severe disease and death (eg, the mortality rate among children with leukemia is 7%).
• Neonatal varicella mortality rates can reach 30%.
• An episode of varicella confers immunity. Second episodes are exceedingly rare.

Patient Education

• Bathe the child regularly to reduce itching and prevent secondary infection.
• Scratching can lead to secondary infection and scarring.
• • Keep the fingernails short.
  • Wearing mittens or socks on the hands at night can help prevent scratching.
• Do not use medications that contain aspirin.
• Advise parents to take children to the hospital if the following symptoms occur:
• • Unusual redness, swelling, or pain over an area of the rash
  • Refusal to drink fluids 
  • Signs of dehydration, such as scanty and yellow-colored urine, increasing drowsiness, dry mouth and lips, excessive thirst, or lethargy
  • Confusion, irritability, drowsiness, or difficulty waking
  • Inability to walk or unusual weakness
  • Complaints of severe headache, stiff neck, and/or back pain
  • Frequent vomiting
  • Difficulty breathing, chest pain, wheezing, fast breathing, or severe cough
  • Fever persisting more than 4 days or fever returns after defervescence
  • A more sickly appearance than when last seen by the doctor
• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education article Chickenpox.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Early recognition of secondary bacterial infection and appropriate follow-up are major issues. Failure to recognize occult infection may result in serious illness and even death.
• Isolate patients with varicella because the disease is highly contagious and airborne spread can occur. Isolation is especially important if the hospital also admits patients who are immunocompromised because their exposure to the disease can be serious and even fatal.

Special Concerns

• Pregnancy is a particularly susceptible time. Varicella can cause various adverse outcomes for mother and infant, depending on the stage of pregnancy.
• Immunocompromised children often have severe and complicated varicella, and their mortality rate is higher than that in immunocompetent children. Consider the following categories of patients immunocompromised:
• • Children with any malignancy
  • Children on cancer chemotherapy
  • Children undergoing high-dose corticosteroid therapy
  • Children with congenital cellular immunodeficiencies
  • Children on immunosuppressive therapy
  • Children with HIV infection
• Children with eczema or dermatitis may have severe skin manifestations during varicella.

MULTIMEDIA

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Media file 1:  The pleomorphic rash characteristic of varicella. Papules, vesicles, and pustules are concurrently present.
	View Full Size Image
Media type:  Photo

REFERENCES

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1. Kouwabunpat D, Hoffman J, Adler R. Varicella complicated by group A streptococcal sepsis and osteonecrosis. Pediatrics. Oct 1999;104(4 Pt 1):967-9. [Medline]. [Full Text].
2. Advisory Committee on Infectious Diseases, American Academy of Pediatrics. Prevention of Varicella: Recommendations for Use of Varicella Vaccines in Children, Including a Recommendation for a Routine Two-Dose Varicella Immunization Schedule. American Academy of Pediatrics, Childhood Immunization Support Program. Available at http://www.cispimmunize.org/pro/pdf/Varicella-040907.pdf. Accessed 21 Jun 2007.
3. Arbeter AM, Granowetter L, Starr SE, et al. Immunization of children with acute lymphoblastic leukemia with live attenuated varicella vaccine without complete suspension of chemotherapy. Pediatrics. Mar 1990;85(3):338-44. [Medline].
4. Buchholz U, Moolenaar R, Peterson C, Mascola L. Varicella outbreaks after vaccine licensure: should they make you chicken?. Pediatrics. Sep 1999;104(3 Pt 1):561-3. [Medline]. [Full Text].
5. CDC. National, state, and urban area vaccination coverage among children aged 19-35 months--United States, 2004. MMWR Morb Mortal Wkly Rep. Jul 29 2005;54(29):717-21. [Medline]. [Full Text].
6. Chaves SS, Gargiullo P, Zhang JX, et al. Loss of vaccine-induced immunity to varicella over time. N Engl J Med. Mar 15 2007;356(11):1121-9. [Medline].
7. Derrick CW Jr, Lord L. In utero varicella-zoster infections. South Med J. Nov 1998;91(11):1064-6. [Medline].
8. Dowell SF, Bresee JS. Severe varicella associated with steroid use. Pediatrics. Aug 1993;92(2):223-8. [Medline].
9. Galil K, Lee B, Strine T, et al. Outbreak of varicella at a day-care center despite vaccination. N Engl J Med. Dec 12 2002;347(24):1909-15. [Medline]. [Full Text].
10. Jaamaa S, Salonen M, Seppala I, et al. Varicella zoster and Borrelia burgdorferi are the main agents associated with facial paresis, especially in children. J Clin Virol. Jul 2003;27(2):146-51. [Medline].
11. Pastuszak AL, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med. Mar 31 1994;330(13):901-5. [Medline]. [Full Text].
12. Verstraeten T, Jumaan AO, Mullooly JP, et al. A retrospective cohort study of the association of varicella vaccine failure with asthma, steroid use, age at vaccination, and measles-mumps-rubella vaccination. Pediatrics. Aug 2003;112(2):e98-103. [Medline]. [Full Text].
13. Zhou F, Harpaz R, Jumaan AO, et al. Impact of varicella vaccination on health care utilization. JAMA. Aug 17 2005;294(7):797-802. [Medline]. [Full Text].

Article Last Updated: Sep 17, 2007