CRISBERT I. CUALTEROS, M.D. - Varicella-zoster virus (VZV)
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CRISBERT I. CUALTEROS, M.D. Family and Medicine

Varicella-zoster virus (VZV) causes primary, latent, and recurrent infections. The primary infection is manifested as varicella (chickenpox) and results in establishment of a lifelong latent infection of sensory ganglion neurons. Reactivation of the latent infection causes herpes zoster (shingles). Although often a mild illness of childhood, chickenpox can cause substantial morbidity and mortality in otherwise healthy children; it causes increased morbidity and mortality in adolescents, adults and immunocompromised persons and predisposes to severe group A streptococcus and Staphylococcus aureus infections. Chickenpox and zoster can be treated with antiviral drugs. Infection can be prevented by immunization with live-attenuated VZV vaccine. Gestational chickenpox can be severe in the mother and can cause a rare but distinct intrauterine syndrome. Chickenpox in the newborn can be severe and life threatening.
VZV is a neurotropic human herpesvirus with similarities to herpes simplex virus, which is also an a-herpesvirus. These viruses are enveloped with double-stranded DNA genomes that encode more than 70 proteins, including proteins that are targets of cellular and humoral immunity.
Prior to the introduction of vaccine in 1995, varicella was an almost universal communicable infection of childhood in the United States. Most children were infected by 15 yr of age, with fewer than 5% of adults remaining susceptible. Annual varicella epidemics occurred in winter and spring, accounting for about 4 million cases, 11,000 hospitalizations, and 100 deaths every year. Varicella is a more serious disease with higher rates of complications and deaths among infants, adults, and immunocompromised persons. Within households, transmission of VZV to susceptible individuals occurs at a rate of 65–86%; more casual contact, such as occurs in a school classroom, is associated with lower attack rates among susceptible children. Patients with varicella are contagious from 24–48?hr before the rash appears and until vesicles are crusted, usually 3–7 days after onset of rash. Susceptible children may also acquire varicella after close, direct contact with adults or children who have herpes zoster. Varicella has declined substantially in areas with moderate to high levels of vaccine coverage; varicella that occurs among immunized children (so-called breakthrough varicella) is usually very mild.
Herpes zoster, because it is due to the reactivation of latent VZV, is uncommon in childhood and shows no seasonal variation in incidence. The lifetime risk for herpes zoster for individuals with a history of varicella is 10–15%, with 75% of cases occurring after 45 yr of age. Herpes zoster is very rare in healthy children younger than 10 years of age except for those infected in utero or in the first year of life; herpes zoster in children tends to be milder than disease in adults and is less frequently associated with postherpetic neuralgia. However, herpes zoster occurs more frequently, occasionally multiple times, and may be severe in children receiving immunosuppressive therapy for malignancy or other diseases and in those who have HIV infection.
VZV is transmitted in respiratory secretions and in the fluid of skin lesions either by airborne spread or through direct contact. Primary infection (varicella) results from the respiratory inoculation of virus. During the early part of the 10–21-day incubation period, virus replicates in the respiratory tract followed by a brief subclinical viremia. Widespread cutaneous lesions occur during a second viremic phase. Peripheral blood mononuclear cells carry infectious virus, generating new crops of vesicles for 3–7 days. VZV is also transported back to respiratory mucosal sites during the late incubation period, permitting spread to susceptible contacts before the appearance of rash. Host immune responses limit viral replication and facilitate recovery from infection. In the immunocompromised child, the failure of immune responses, especially cell-mediated immune responses, results in continued viral replication with resultant injury to lungs, liver, brain, and other organs.
VZV establishes latent infection in sensory ganglia cells in all individuals who experience primary infection. Subsequent reactivation of latent virus causes herpes zoster, a vesicular rash that usually is dermatomal in distribution. During herpes zoster, necrotic changes may be produced in the associated ganglia. The skin lesions of varicella and herpes zoster have identical histopathology, and infectious VZV is present in both. Varicella elicits humoral and cell-mediated immunity that is highly protective against symptomatic re-infection. Suppression of cell-mediated

immunity to VZV correlates with an increased risk of VZV reactivation as herpes zoster.
Clinical Manifestations.
Varicella is an acute febrile rash illness, common in children who have not been immunized. It has variable severity but is usually self-limited. It may be associated with severe complications, including bacterial super-infection, pneumonia, encephalitis, bleeding disorders, congenital infection, and life-threatening perinatal infection. Herpes zoster, uncommon in children, causes localized cutaneous symptoms, but may disseminate in immunocompromised patients.
The illness usually begins 14–16 days after exposure, although the incubation period can range from 10–21 days. Subclinical varicella is rare; almost all exposed, susceptible children experience a rash, but illness may be limited to only a few lesions. Prodromal symptoms may be present, particularly in older children. Fever, malaise, anorexia, headache, and occasionally mild abdominal pain may occur 24–48?hr before the rash appears. Temperature elevation is usually moderate, usually from 100–102°F but may be as high as 106°F; fever and other systemic symptoms persist during the first 2–4 days after the onset of the rash.
Varicella lesions often appear first on the scalp, face, or trunk. The initial exanthem consists of intensely pruritic erythematous macules that evolve through the papular stage to form clear, fluid-filled vesicles. Clouding and umbilication of the lesions begin in 24–48?hr. While the initial lesions are crusting, new crops form on the trunk and then the extremities; the simultaneous presence of lesions in various stages of evolution is characteristic of varicella ( Fig. 232–1 ). The distribution of the rash is predominantly central or centripetal in contrast to smallpox, where the rash is more prominent on the face and distal extremities. Ulcerative lesions involving the oropharynx and vagina are also common; many children have vesicular lesions on the eyelids and conjunctivae, but corneal involvement and serious ocular disease is rare. The average number of varicella lesions is about 300, but healthy children may have fewer than 10 to more than 1,500 lesions. In cases resulting from secondary household spread and in older children, more lesions usually occur, and new crops of lesions may continue to develop for a longer period of time. The exanthem may be much more extensive in children with skin disorders, such as eczema or recent sunburn. Hypopigmentation or hyperpigmentation of lesion sites persists for days to weeks in some children, but severe scarring is unusual unless the lesions were secondarily infected.
The differential diagnosis of varicella includes vesicular rashes caused by other infectious agents, such as herpes simplex virus, enterovirus, or Staphylococcus aureus; drug reactions; contact dermatitis; and insect bites. Severe varicella was the most common illness confused with smallpox before the eradication of this disease.
Vaccine is more than 95% effective in preventing typical varicella and is 70–90% effective

 Figure 232-1 Skin lesions of chickenpox. Note the varying stages of development (macules, papules, and vesicles) present at the same time. (Courtesy of PF Lucchesi.)
at preventing all disease. Asymptomatic infection with wild-type virus may occur frequently in the previously immunized child. Breakthrough disease is varicella in a child vaccinated more than 42 days before rash onset and is due to wild-type VZV. Rash occurring within the first 2 weeks of vaccination is most commonly wild-type VZV, rash occurring 2–6 weeks after vaccination could be due to either the wild or vaccine strains. The rash in breakthrough disease is frequently atypical, predominantly maculopapular, vesicles are uncommon, being seen in only about 6% of cases, and the illness is most commonly mild with fewer than 50 lesions and little or no fever. Children with breakthrough disease should be considered potentially infectious and excluded from school until lesions have crusted or, if there are no vesicles present, until no new lesions are occurring. Transmission has been documented to occur from breakthrough cases in household, childcare, and school settings.
Progressive varicella, with visceral organ involvement, coagulopathy, severe hemorrhage, and continued lesion development is a dreaded complication of primary VZV infection. Severe abdominal pain and the appearance of hemorrhagic vesicles in otherwise healthy adolescents and adults, immunocompromised children, pregnant women, and newborns may herald this. The risk of progressive varicella is highest in children with congenital cellular immune deficiency disorders and those with malignancy, particularly if chemotherapy was given during the incubation period and the absolute lymphocyte count is <500 cells/mm3 . In one large series, the mortality rate for children who acquired varicella while undergoing treatment for malignancy and who were not treated with antiviral therapy was 7%. In this series all varicella-related deaths occurred within 3 days after the diagnosis of varicella pneumonia. Children who acquire varicella after organ transplantation are also at risk for progressive VZV infection. Children on long-term, low-dose systemic corticosteroid therapy are not considered to be at higher risk of severe varicella, but progressive varicella does occur in patients receiving high-dose corticosteroids and has been reported in patients receiving inhaled corticosteroids. Unusual clinical findings of varicella, including lesions that develop a unique hyperkeratotic appearance and the continued new lesion formation for weeks or months, have been described in children with HIV infection.
Newborns have particularly high mortality in the circumstances of a susceptible mother contracting varicella around the time of delivery. Birth within 1 wk before or after the onset of maternal varicella frequently results in the newborn developing varicella, which may be severe. The initial infection is intrauterine, although the newborn often develops clinical chickenpox postpartum. The risk to the newborn is dependent on the amount of maternal anti-VZV antibody that the fetus acquired transplacentally before birth. If there was 1 wk or greater interval between maternal chickenpox and parturition, it is likely that the newborn received sufficient transplacental antibody to VZV to ameliorate neonatal infection. Alternatively, if the interval was less than 1 wk, the newborn will be unlikely to have protective VZV antibody and neonatal chickenpox may be exceptionally severe.
The recommendations for varicella-zoster immune globulin (VZIG) reflect the differing risks to the exposed infant. Newborns whose mothers develop varicella 5 days before to 2 days after delivery should receive one vial. Although neonatal varicella may occur in about half of these infants despite administration of VZIG, it is usually mild. Every premature infant born to a mother with active chickenpox at delivery (even if present > 1 wk) should receive VZIG. Because perinatally acquired varicella may be life threatening, it should be treated with acyclovir (10?mg/kg q 8?hr IV). Neonatal chickenpox can also follow a postpartum exposure of an infant delivered to a mother who was susceptible to VZV, although the frequency of complications declines rapidly in the weeks after birth. Infants with

community-acquired chickenpox who develop severe varicella, especially those who develop a complication such as pneumonia, hepatitis, or encephalitis, should also receive treatment with intravenous acyclovir (10?mg/kg q 8?hr IV).
When pregnant women contract chickenpox, about 25% of the fetuses may become infected although not every infected fetus is clinically affected. However, up to 2% of fetuses whose mothers had varicella in the first 20 weeks of pregnancy may demonstrate VZV embryopathy. The period of greatest risk to the fetus correlates with the gestational period when there is major development and innervation of the limb buds and maturation of the eyes. Fetuses infected at 6–12 wk of gestation appear to have maximal interruption with limb development; fetuses infected at 16–20 wk may have eye and brain involvement. In addition, viral damage to the sympathetic fibers in the cervical and lumbosacral cord may lead to divergent effects such as Horner syndrome and dysfunction of the urethral or anal sphincters. Most of the stigmata can be attributed to virus-induced injury to the nervous system, although there is no obvious explanation why certain regions of the body are preferentially infected during fetal VZV infection. The stigmata involve mainly the skin, extremities, eyes, and brain ( Box 232–1 ). The characteristic cutaneous lesion has been called a cicatrix, a zigzag scarring, often in a dermatomal distribution. The characteristic cicatricial scarring may represent the cutaneous residua of VZV infection of the sensory nerves, analogous to herpes zoster. The virus may select tissues that are in a rapid developmental stage, such as the limb buds. This may result in one or more shortened and malformed extremities ( Fig. 232–2 ). Frequently, the atrophic extremity is covered with a cicatrix. The remainder of the torso may be entirely normal in appearance. Alternatively, there may be neither skin nor limb abnormalities but the infant may show cataracts or even extensive aplasia of the entire brain. Occasionally, calcifications are evident within a microcephalic head ( Fig. 232–3 ). Histologic examination of the brain demonstrates necrotizing cerebral lesions involving the leptomeninges, the cortex, and the adjacent white matter.
Many infants with severe manifestations of congenital varicella syndrome have significant neurologic deficiencies, whereas those with only isolated stigmata, amenable to treatment, develop normally throughout childhood. Infants with neonatal chickenpox who receive prompt antiviral therapy have an excellent prognosis.
The diagnosis of VZV fetopathy is based mainly on the history of gestational chickenpox combined with the stigmata seen in the fetus. Virus cannot be cultured from the affected newborn, but viral DNA can be detected in tissue samples by PCR. Some

Box 232-1. Stigmata of Varicella-Zoster Virus Fetopathy
Damage to Sensory Nerves

Cicatricial skin lesions


Damage to Optic Stalk and Lens Vesicle




Optic atrophy

Damage to Brain/Encephalitis




Aplasia of brain

Damage to Cervical or Lumbosacral Cord

Hypoplasia of an extremity

Motor and sensory deficits

Absent deep tendon reflexes


Horner syndrome

Anal/urinary sphincter dysfunction



 Figure 232-2 Newborn with congenital varicella syndrome. The infant had severe malformations of both lower extremities and cicatricial scarring over his left abdomen.
infants have VZV-specific IgM antibody detectable in the cord blood sample, although the IgM titer drops quickly postpartum. Chorionic villus sampling and fetal blood collection for the detection of viral DNA, virus, or antibody have been used in an attempt to diagnose fetal infection and embryopathy. The usefulness of these tests for patient management and counseling has not been defined. Because these tests may not distinguish between infection and disease, their utility may primarily be that of reassurance when the test is negative.
Although VZIG is often administered to the susceptible mother exposed to chickenpox, it is uncertain as to whether this modifies infection in the fetus. Similarly, acyclovir treatment may be given to the mother with severe varicella; however, neither its safety nor its efficacy for the fetus is known. The damage caused by fetal VZV infection does not progress postpartum, an indication that there is no persistent viral replication. Thus, antiviral treatment of infants with congenital VZV syndrome is not indicated.
Herpes zoster is manifested as vesicular lesions clustered within one or less commonly two adjacent dermatomes ( Fig. 232–4 ). Unlike zoster in adults, zoster in children is infrequently associated with localized pain, hyperesthesias, pruritus, and low-grade fever. In children, the rash is mild, with new lesions appearing for a few days; symptoms of acute neuritis are minimal; and complete resolution usually occurs within 1–2 wk. In contrast to adults, postherpetic neuralgia is very unusual in children. Approximately 4% of patients suffer a second episode of herpes zoster; 3 or more episodes are rare. Transverse myelitis with transient paralysis is a rare complication of herpes zoster. An increased risk of herpes zoster early in childhood has been described in children who acquire varicella in the first year of life as well as in those whose mothers have a varicella infection in the third trimester of pregnancy.
Immunocompromised children may have more severe herpes zoster, which is similar to that in adults, including postherpetic neuralgia. Immunocompromised patients may also experience disseminated cutaneous disease that mimics varicella, as well as


 Figure 232-3 Magnetic resonance image of newborn with encephalitis secondary to congenital varicella syndrome. The intrauterine infection occurred about 3 mo antepartum, at which time there was extensive necrosis of the cerebral hemispheres. The image of the newborn head was taken with the patient supine; therefore, there is a fluid/fluid interface in the dependent occiput (A). The hydrocephalus (C) and calcifications in the basal ganglia (D) are visible; a cranial artifact (B) is seen secondary to a scalp vein needle.
visceral dissemination with pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy. Severely immunocompromised children, particularly those with HIV infection, may have unusual, chronic, or relapsing cutaneous disease, retinitis, or central nervous system disease without rash. A lower risk of herpes zoster in vaccinated children with leukemia compared with those who have had varicella disease suggests that varicella vaccine virus reactivates less commonly than wild-type VZV.
Laboratory evaluation has not been considered necessary for the diagnosis or management of healthy children with

 Figure 232-4 Herpes zoster.
varicella or herpes zoster. However, as disease declines to low levels, laboratory confirmation of all varicella cases will become necessary. Leukopenia is typical during the first 72 hours; it is followed by a relative and absolute lymphocytosis. Results of liver function tests are also usually (75%) mildly elevated. Patients with neurologic complications of varicella or uncomplicated herpes zoster have a mild lymphocytic pleocytosis and a slight to moderate increase in protein in the cerebrospinal fluid; the glucose concentration is usually normal.
Unusual or very severe varicella in otherwise immunocompetent individuals must be distinguished from smallpox, which may occur following deliberate release of smallpox virus ( Chapter 706 ). A suspected case of smallpox should be reported immediately to the local and state health departments. A protocol for evaluating patients with acute vesicular-pustular rash illness for the possibility of smallpox is available on the CDC website at
Rapid laboratory diagnosis of VZV is often important in high-risk patients and is sometimes important for infection control. Confirmation of varicella (or herpes simplex virus) can be accomplished by most referral hospital laboratories. VZV can be identified quickly by direct fluorescence assay (DFA) of cells from cutaneous lesions, which is widely available, and by polymerase chain reaction (PCR) amplification testing. Although multinucleated giant cells can be detected with nonspecific stains (Tzanck smear), they have poor sensitivity and do not differentiate VZV and herpes simplex virus infections. Infectious virus may be recovered using tissue culture methods; newer methods have decreased time needed for culture from 7–10 days to 3–4 days. VZV immunoglobulin G (IgG) antibodies can be detected by several methods and a 4-fold rise in IgG antibodies is also confirmatory of acute infection. VZV IgG antibody tests can also be valuable to determine the immune status of individuals whose clinical history of varicella is unknown or equivocal. Testing for VZV IgM antibodies is not useful for clinical diagnosis because commercially available methods are unreliable. A capture IgM assay is available at the national VZV laboratory at CDC
Antiviral treatment modifies the course of both varicella and herpes zoster. Antiviral drug resistance is rare but has occurred in children with HIV infection who have been treated. Foscarnet is the only drug now available for the treatment of acyclovir-resistant VZV infections.
The only antiviral drug available in liquid formulation and that is licensed for pediatric use is acyclovir. Given the safety profile of acyclovir and its demonstrated efficacy in the treatment of varicella, treatment of all children, adolescents, and adults with varicella is acceptable. However, acyclovir therapy is not recommended routinely by the American Academy of Pediatrics for treatment of uncomplicated varicella in the otherwise healthy child because of the marginal benefit, the cost of the drug, and the low risk of complications. Oral therapy with acyclovir (20?mg/kg/dose; maximum: 800?mg/dose) given as 4 doses per day for 5 days should be used to treat uncomplicated varicella in nonpregnant individuals 13 yr of age or older and children 12 mo of age or older with chronic cutaneous or pulmonary disorders; receiving short-term, intermittent, or aerosolized corticosteroids; receiving long-term salicylate therapy; and possibly second cases in household contacts. To be most effective, treatment should be initiated as early as possible, preferably within 24?hr of the onset of the exanthem. There is dubious clinical benefit if initiation of treatment is delayed more than 72?hr after onset of the exanthem. Acyclovir therapy does not interfere with the induction of VZV immunity. Intravenous therapy is indicated for severe disease and for varicella in immunocompromised patients. Acyclovir has been used to treat varicella in pregnant women; however, its safety for the fetus has not been established. Any patient who has signs of

disseminated VZV including pneumonia, severe hepatitis, thrombocytopenia, or encephalitis should receive immediate treatment. Intravenous acyclovir (500?mg/m2 q 8?hr IV) therapy initiated within 72?hr of development of initial symptoms decreases the likelihood of progressive varicella and visceral dissemination in high-risk patients. Treatment is continued for 7 days or until no new lesions have appeared for 48?hr. Delaying antiviral treatment until prolonged new lesion formation is evident is not advisable because visceral dissemination occurs during the same time period.
Antiviral drugs are effective for treatment of herpes zoster. In healthy adults, acyclovir (800?mg 5 times a day PO for 5 days), famciclovir (500?mg tid PO for 7 days), and valacyclovir (1,000?mg tid PO for 7 days) reduce the duration of the illness and the risk of developing postherpetic neuralgia; concomitant corticosteroid usage improves the quality of life in the elderly. In otherwise healthy children, however, herpes zoster is a less severe disease, and postherpetic neuralgia is rare. Therefore, treatment of uncomplicated herpes zoster in the child with an antiviral agent may not always be necessary, although some experts would treat with oral acyclovir (20?mg/kg/dose; maximum 800?mg/dose) to shorten the duration of the illness. Use of corticosteroids for herpes zoster in otherwise healthy children is not recommended.
In contrast, herpes zoster in immunocompromised children can be severe and disseminated disease may be life threatening. Patients at high risk for disseminated disease should receive acyclovir (500?mg/m2 or 10?mg/kg q 8?hr IV). Oral acyclovir is an option for immunocompromised patients with uncomplicated herpes zoster and who are considered at low risk for visceral dissemination.
The complications of VZV infection occur with varicella, or with reactivation of infection, more commonly in immunocompromised patients. In the otherwise healthy child, mild varicella hepatitis is relatively common but rarely clinically symptomatic. Mild thrombocytopenia occurs in 1–2% of children with varicella and may be associated with transient petechiae. Purpura, hemorrhagic vesicles, hematuria, and gastrointestinal bleeding are rare complications that may have serious consequences. Cerebellar ataxia occurs in 1 in every 4000 cases. Other complications, some of them rare, of varicella include encephalitis, pneumonia, nephritis, nephrotic syndrome, hemolytic-uremic syndrome, arthritis, myocarditis, pericarditis, pancreatitis, and orchitis.
Secondary bacterial infections of the skin, usually caused by Streptococcus and Staphylococcus, may occur in up to 5% of children with varicella. These range from superficial impetigo to cellulitis, lymphadenitis, and subcutaneous abscesses. An early manifestation of secondary bacterial infection is erythema of the base of a new vesicle. Recrudescence of fever 3–4 days after the initial exanthem may also herald a secondary bacterial infection. Varicella is a well-described risk factor for serious infections caused by group A streptococcus. The more invasive infections, such as varicella gangrenosa, bacterial sepsis, pneumonia, arthritis, osteomyelitis, and necrotizing fasciitis, account for much of the morbidity and mortality of varicella in otherwise healthy children. Bacterial toxin–mediated diseases (e.g., toxic shock syndrome) also may complicate varicella.
Encephalitis and acute cerebellar ataxia are well-described neurologic complications of varicella; morbidity from central nervous system complications is highest among patients younger than 5 yr or older than 20 yr of age. Nuchal rigidity, altered consciousness, and seizures characterize meningoencephalitis. Patients with cerebellar ataxia have a gradual onset of gait disturbance, nystagmus, and slurred speech. Neurologic symptoms usually begin 2–6 days after the onset of the rash but may occur during the incubation period or after resolution of the rash. Clinical recovery is typically rapid, occurring within 24–72?hr, and is usually complete. Although severe hemorrhagic encephalitis, analogous to that caused by herpes simplex virus, is very rare in children with varicella, the consequences are similar to herpes encephalitis. Reye syndrome of encephalopathy and hepatic dysfunction associated with varicella has become rare since salicylates are no longer routinely used as antipyretics ( Chapter 342 ).
Varicella pneumonia is a severe complication that accounts for most of the increased morbidity and mortality in adults and other high-risk populations, but pneumonia may also complicate varicella in young children. Respiratory symptoms, which may include cough, dyspnea, cyanosis, pleuritic chest pain, and hemoptysis, usually begin within 1–6 days after the onset of the rash. Smoking has been described as a risk factor for severe pneumonia complicating varicella. The frequency of varicella pneumonia may be greater in the parturient and may lead to premature termination of pregnancy.
Primary varicella has a mortality rate of 2–3 per 100,000 cases with the lowest case fatality rates among children 1–4 years and 5–9 years (approximately 1 death per 100,000 cases). Compared with these age groups, infants have a 4 times greater risk of dying and adults have a 25 times greater high risk of dying. Approximately 100 deaths occurred in the United States annually before the introduction of the VZV vaccine; the most common complications among people who died from varicella were pneumonia, CNS complications, secondary infections, and hemorrhagic conditions. The mortality rate of untreated primary infection in immunocompromised children is 7–14% and may approach 50% in adults. Varicella morbidity has declined in recent years as vaccine coverage has improved. It is expected that when data are available, a decline in mortality will also be apparent.
Neuritis with herpes zoster should be managed with appropriate analgesics. Postherpetic neuralgia can be a severe problem in adults and may persist for months, requiring care by a specialist in pain management.
VZV transmission is difficult to prevent because the infection is contagious for 24–48?hr before the rash appears. Infection control practices, including caring for infected patients in isolation rooms with filtered air systems, are essential. All health care workers should have documented VZV immunization or immunity. Susceptible health care workers who have had a close exposure to VZV should not care for high-risk patients during the incubation period.
Varicella is a vaccine-preventable disease. Live virus vaccine is recommended for routine administration in children at 12–18 mo of age. Older children, adolescents and adults without a history of VZV infection should also be immunized. Children 12 mo to 12 yr receive a single vaccine dose; adolescents and adults require 2 vaccine doses, a minimum of 4 wk apart. Live virus vaccine is contraindicated in children with cell-mediated immune deficiencies, although the vaccine may be administered to children with acute lymphoblastic leukemia who are in remission and who meet enrollment criteria under a research protocol, and the vaccine may also be considered for HIV-infected children with CD4% greater than 25%. Both these groups receive 2 doses of vaccine, 3 months apart. Administration of varicella vaccine within 4 wk of MMR vaccine has been associated with a higher risk of breakthrough disease; therefore, it is recommended that the vaccines either be administered simultaneously at different sites or be given at least 4 weeks apart. Vaccine virus establishes latent infection; however, the risk of developing subsequent herpes zoster is lower after vaccine than after natural VZV infection among immunocompromised children. Post-licensure data also suggest the same trend in healthy vaccinees. Post-licensure effectiveness

studies and ongoing studies of the persistence of immunity after vaccination, however, may ultimately demonstrate a need for children to receive a booster dose of vaccine.
Varicella-zoster immune globulin (VZIG) postexposure prophylaxis is recommended for immunocompromised children, pregnant women, and newborns exposed to maternal varicella. VZIG is distributed by FFF Enterprises, California. The dosage is 1 vial (125 units) for each 10?kg increment (maximum: 625 units) given intramuscularly as soon as possible but within 96?hr after exposure.
Newborns whose mothers develop varicella 5 days before to 2 days after delivery should receive one vial of VZIG. Adults should be tested for VZV IgG antibodies before VZIG administration because many adults with no clinical history of varicella are immune. VZIG prophylaxis may ameliorate disease but does not eliminate the possibility of progressive disease; patients should be monitored and treated with acyclovir if necessary. Immunocompromised patients who have received high-dose intravenous immune globulin (100–400?mg/kg) for other indications within 2–3 wk before the exposure can be expected to have serum antibodies to VZV.
Close contact between a susceptible high-risk patient and a patient with herpes zoster is also an indication for VZIG prophylaxis. Passive antibody administration or treatment does not reduce the risk of herpes zoster or alter the clinical course of varicella or herpes zoster when given after the onset of symptoms.
Vaccine given to normal children within 3–5 days exposure is effective in preventing or modifying varicella, especially in a household setting where exposure is very likely to result in infection. Varicella vaccine is now recommended for postexposure use, for outbreak control. Oral acyclovir administered late in the incubation period may modify subsequent varicella in the normal child. However, its use in this manner is not recommended until it can be further evaluated.


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