24. Varicella (chickenpox)

In temperate climates, winter-spring epidemics occur with peak incidence in preschool and early primary school ages (1–9 years). Around 90 percent of individuals have been infected by adolescence and fewer than 5 percent of adults are susceptible. The annual number of infections therefore approximates the birth cohort.[1, 2]

Transmission of the virus is less efficient in tropical climates. Adolescent and adult immigrants to New Zealand from such countries are more likely to be susceptible, placing them at risk of contracting chickenpox in their new environment. Being older, they are more likely to suffer severe disease.

The long incubation and high transmissibility of VZV conspire to maximise disruption to families: by the time the rash occurs a child will have been infectious for two days; any susceptible household members will then become unwell just as the first child recovers. This results not only in morbidity but also in financial consequences for parents missing work.

Crude hospitalisation admission rates in high-income countries range from around 2–6 per 100,000 population-year. Most of these admissions are children, consistent with the high incidence of varicella in children. Crude mortality rates ranged from 0.3–0.5 per million population-year with overall case fatality ratios of around 2–4 per 100,000 cases. Almost 90 percent of varicella hospital admissions occur in otherwise healthy and immunocompetent individuals.[1, 2]

VV has been introduced into childhood immunisation programmes overseas, including the US from 1995 and Australia from 2005, resulting in dramatic reductions in varicella morbidity, hospitalisations and mortality.[3, 4, 5] By 2005 in the US, vaccine coverage was approximately 90 percent and varicella incidence had declined by more than 90 percent. Herd immunity was observed outside of age groups targeted for vaccination.[1]

Following the introduction of VV onto the childhood schedule, exposure to wild-type virus decreases. It has been theorised that a lack of boosting may lead to an increase in zoster in older adults. However, studies that have investigated this issue have been unable to attribute any increase in incidence of zoster to the childhood VZV vaccine programme.[6, 7] Studies from the UK and Canada reported increases in zoster not associated with a vaccination programme, and some US data showed zoster rates were increasing prior to the initiation of their varicella vaccination programme.[8, 9]

Varicella is not a notifiable disease, so data is limited for uncomplicated varicella, but the epidemiology is likely to be as described above for temperate climates. With increasing participation in early childhood services, a greater proportion of infections may now be occurring in preschool-aged children. It is expected that zoster numbers will rise in New Zealand as the population ages.

Prospective nationwide surveillance of varicella in New Zealand children, conducted from November 2011 to October 2013, found that the incidence of varicella-related hospitalisation was 8.3 per 100,000 children per year – although this is likely to be a significant underestimate.[10] Māori and Pacific children were disproportionately affected, with an almost three- and four-fold increase in the relative risk of hospitalisation for varicella or its complications, respectively. Of the hospitalised children, 9 percent required ICU admission and most of them were previously healthy. Almost one-third of hospitalised children had multiple complications from varicella, and those with neurological complications were more likely to have ongoing problems at discharge.

A retrospective survey of admissions to the paediatric intensive care unit at Auckland’s Starship Children’s Hospital during 2001–2011 found 26 children admitted for varicella or its secondary complications.[11] The main admission reasons were neurological (38.5 percent) and secondary bacterial sepsis or shock (26.9 percent). Four children died (15 percent), three of whom were immunocompromised. A further eight children (31 percent) had ongoing disability at discharge, most having had no prior medical condition.

Based on overseas rates, it is estimated that up to one case of congenital varicella syndrome may be expected in New Zealand each year, although few have been reported.

In 2017, adults (aged 20 years and older) accounted for 25 percent of varicella related hospital admissions;[12] approximately one person per year dies from VZV infection, and most VZV-related deaths occur in adults.[13]

There are two live attenuated monovalent VVs registered (approved for use) and available (marketed) in New Zealand. Two quadrivalent live attenuated MMRV vaccines are registered but not currently available in New Zealand.

Funded vaccine

Monovalent VV

Single-dose varicella vaccination programmes have had a dramatic impact on the incidence of VZV infections,[14, 15, 16] hospitalisations [3, 4, 17] and serious outcomes,[5] particularly when high coverage rates are achieved. Indirect effects are also apparent. A 2014 systematic review of varicella vaccines found that a single dose of VV is moderately effective for preventing any severity of varicella (approximately 80 percent) in immune-competent individuals, highly effective for preventing moderate-severe disease (approximately 95 percent) and highly effective in preventing severe disease only (approximately 99 percent).[18] However, single-dose programmes are associated with outbreaks even among highly vaccinated groups.[19, 20]

The use of a second dose during outbreaks has been an effective strategy to prevent further cases. Catch‑ups for non-immunised groups without a previous history of varicella are also important. There is a significant reduction in breakthrough disease when two doses are given. After a second dose in children the immune response is markedly enhanced, with over 99 percent of children attaining an immune response thought to provide protection, and the geometric mean antibody titre is also significantly increased.

Over a 10-year period the estimated vaccine efficacy of two doses for prevention of any varicella disease is 98 percent (compared to 94 percent for a single dose), with 100 percent efficacy for the prevention of severe varicella. The likelihood of breakthrough varicella is reduced by a factor of 3.3.[21, 22] Because of this data, in 2006 the US authorities recommended a two‑dose strategy for varicella prevention, with the first dose at age 12–15 months and the second at age 4–6 years, as for MMR.[19, 21] A Hong Kong study recommended reducing the time between doses, to age 12 months and 18 months, to reduce breakthrough cases and outbreaks in preschools.[23]

The antigenic components of MMRV vaccines are non-inferior compared with simultaneous administration of MMR and VV,[24, 25] for both the first and second doses.

Herd immunity

In regions where universal varicella vaccination programmes have been implemented, significant declines in varicella cases and hospitalisation have been observed. These programmes also reduce circulating VZV and provide protection through herd immunity for those who are unable to be immunised, such as infants and immunocompromised individuals.

In the US, the annual average age-adjusted mortality rate for varicella was 0.05 per million population during 2008–2011, an 87 percent reduction from the pre-vaccine years.[26] In Canada between 2000 and 2007, a single dose of VV was introduced to the immunisation schedules of different provinces at 12 months of age; most provinces also included catch-ups for susceptible children at preschool or school. An ecological study of varicella-related hospitalisations in Canada between 1990 and 2010 found that hospitalisation rates decreased in all age groups, including infants and those aged 20–39 years.[27] Similar herd effects were seen in Germany, with declines in varicella cases and hospitalisations in infants and adolescents who were not eligible for VV.[28]

Duration of immunity

Varicella vaccination provides long-term but probably not lifelong immunity against VZV, in contrast to VZV natural infection. The duration of protection after a single dose of vaccine is difficult to study – especially if wild-type varicella continues to circulate liberally in the community, providing natural boosting and prolonging the duration of protection.[18] Many countries that initially introduced a single-dose vaccination programme have subsequently changed to a two-dose programme as the epidemiology of the disease has changed over time.

Transport according to the National Standards for Vaccine Storage and Transportation for Immunisation Providers 2017 (2nd edition).

The dose of monovalent VV is 0.5 mL, administered by intramuscular or subcutaneous injection in the deltoid area (see section 2.2.3).

Co-administration with other vaccines

Monovalent VV can be administered concurrently with other vaccines, but in a separate syringe and at a different site. If not administered concurrently, the vaccine must be separated from other live vaccines (eg, MMR, BCG) by at least four weeks.

From 1 July 2020, one dose of VV is funded for children at age 15 months. A second VV dose is not currently funded but may be purchased for those who wish to reduce the risk of breakthrough disease.

A catch-up dose of VV is funded for previously unvaccinated children turning 11 years old on or after 1 July 2017, who have not previously had a varicella infection (as determined by clinical history). This dose aims to protect those who have not become immune to varicella before adolescence, as disease in adolescents and adults can be more severe.

Two doses of VV at least six weeks apart, are recommended and funded for the special groups listed in Table 24.1 above from age 9 months. 

Immunocompromised (including immunosuppressed) individuals

The vaccine should not be given to immunocompromised individuals except under the direction and care of a specialist, following a suitable protocol[19] (see section 4.3).

Some clinical trials of the original vaccine formulations were conducted in immunocompromised children (with leukaemia in remission or with HIV infection on antiretroviral treatment). One study found that half the vaccinated children receiving maintenance chemotherapy developed a rash up to one month after vaccination (40 percent of these required acyclovir treatment), compared with 5 percent of those no longer on chemotherapy.[30] Despite this, the study concluded that the vaccine, Varivax, was safe, immunogenic and effective in these children.[30, 31]

Varicella immunisation of children with congenital T‑cell immune deficiency syndromes is generally contraindicated, but those with impaired humoral immunity may be immunised (see section 24.6.1 for further contraindications). Seek specialist advice.

Household contacts of immunocompromised individuals

Immunocompromised individuals are at highest risk of severe varicella and zoster infections.

Where such individuals cannot be vaccinated, it is important to vaccinate the non-immune household members and other close contacts (funded for household contacts) to provide ‘ring-fence’ protection (see sections 4.2, 4.3 and 24.7.1).

A single dose of VV is recommended for susceptible children who do not meet the eligibility criteria for funded vaccine (Table 24.1). A second dose may also be purchased for those who wish to reduce the risk of breakthrough disease.

VV in a two-dose schedule is recommended but not funded for the following groups:[19]

• adults and adolescents who were born and resided in tropical countries, if they have no history of varicella infection
• susceptible adults and adolescents (ie, those who have no prior history of chickenpox)
• susceptible individuals who live or work in environments where transmission of VZV is likely (see Table 4.9 for occupational groups)
• susceptible non-pregnant women of childbearing age
• susceptible international travellers[19]
• health care workers (see below)
• susceptible individuals who have been exposed to varicella (see section 24.8.3).

See section 24.8.1 for information about assessing susceptibility.

Health care workers

All health care workers should be immunised with VV if they are susceptible to varicella (not funded), particularly those within obstetric, paediatric and neonatal units, and those caring for immunocompromised children and adults. When a health care worker has a good history of prior varicella infection, no blood test is required.[32] If there is not a good history of varicella infection, a blood test to assess susceptibility will be necessary, as many individuals with no clinical history of varicella are immune (see section 24.8).

If a health care worker who has clinical contact with patients develops a rash as a result of the vaccine (around 5 percent), they must be excluded from contact with immunocompromised or other at-risk patients and allocated other duties, or excluded from their place of work, for the duration of the rash.

Varicella vaccines are contraindicated in pregnant women. Pregnancy should be avoided for at least four weeks after vaccination.[33] The vaccine’s safety for the fetus has not yet been demonstrated, although no congenital defects have been described following inadvertent administration to pregnant women.

A pregnant woman in the household is not a contraindication for immunisation of a child, and the vaccine can be administered to non-immune mothers who are breastfeeding.

Varicella vaccines are contraindicated for the following people:

• individuals with primary or acquired T-cell immune deficiency states – consult the child’s paediatrician for advice[33]
• individuals with blood dyscrasias, leukaemia, lymphomas of any type, or other malignant neoplasms affecting the bone marrow or lymphatic systems.
• individuals on high-dose steroids for more than two weeks (ie, children on 2 mg/kg per day or more of prednisone or its equivalent, or 20 mg per day if their weight is over 10 kg)
• individuals are receiving or who have recently received chemotherapy (consult with specialist)
• individuals with a family history of congenital or hereditary immunodeficiency, unless the immune competence of the potential vaccine recipient is demonstrated.
• individuals with a history of an anaphylactic reaction to a prior dose of VV or any component of the vaccine, including neomycin and gelatin.
• individuals with active untreated TB
• pregnant women – women should avoid pregnancy for at least four weeks after vaccination[33] (see section 24.5.4).

Because of the association between Reye syndrome, natural varicella infection and salicylates, the vaccine manufacturers advise against the use of salicylates for six weeks after VV is given. There has been no reported association between the vaccine and Reye syndrome, but avoidance of salicylates is recommended as a precaution,[33] and physicians need to weigh the theoretical risk of Reye syndrome from the vaccine against the known risk from varicella disease in children receiving long-term salicylate therapy. Children on low-dose aspirin following cardiac surgery would be more at risk of thrombosis from stopping their aspirin[34] than from the theoretical risk of Reye’s with VV.

If tuberculin testing has to be done, it should be carried out before or simultaneously with vaccination because it has been reported that live viral vaccines may cause a temporary depression (anergy) of tuberculin skin sensitivity.[35] As this anergy may last up to a maximum of six weeks, tuberculin testing should not be performed within that period after vaccination to avoid false negative results.

On the advice of their specialist, VV may be administered to:

• patients at least two years after bone marrow transplantation
• patients at least six months after completion of chemotherapy
• HIV-positive patients who are non-immune to varicella, with mild or moderate immunosuppression.

For suggested intervals between receipt of human normal immunoglobulin or other blood products and VV, see Table A6.1 in Appendix 6.

Antiviral medications with anti-VZV activity, such as acyclovir, valaciclovir and famciclovir, can interfere with the replication of the VZV strain in VV. It is recommended that antiviral medication be stopped at least 24 hours before vaccination and recommenced at least 14 days after vaccination.

A 2013 systematic review of varicella vaccines found that mild adverse events were the most frequently reported AEFIs.[36] This includes injection-site reactions such as pain, swelling and redness, which occurred in up to 28 percent of recipients. There was no increased risk of cerebellar ataxia, encephalitis or ischaemic stroke following vaccination. Post-marketing surveillance in the US found the rate of AEFIs to be 30 per 100,000 doses of VV, and the rate of serious AEFIs was less than 4 per 100,000 doses. Fever has been reported in 15 percent of healthy children following VV and 10 percent of adults.[33, 37]

Post-VV rash

In approximately 1–3 percent of immunised children, a localised rash develops, and in an additional 3–5 percent a generalised varicella-like rash develops.[33] These rashes typically consist of two to five lesions and may be maculopapular rather than vesicular; lesions usually appear 5–26 days after immunisation. Not all rashes can be attributable to the vaccine;[33] some may be due to exposure to wild-type virus, prior to vaccination.

Transmission of vaccine virus to contacts of vaccinated individuals

In healthy vaccine recipients, transmission of vaccine virus to contacts is exceedingly rare, documented in nine immunised people and resulting in 11 secondary cases. The documented risk exists only if the immunised person develops a rash.[33] Err on the side of caution and isolate the vaccine recipient if they are a household contact of an immunocompromised individual and a post-immunisation rash occurs. If an immunocompromised individual inadvertently comes in contact with a vaccine recipient who has a varicella-like rash, the administration of zoster immunoglobulin (ZIG) and/or acyclovir should be considered (see below).[33] Intravenous acyclovir may be required if symptoms develop.

Vaccine virus shingles

The Oka strain of VZV used in the available vaccines can establish latent ganglionic infection in vaccine recipients and later reactivate to produce clinical zoster (shingles). The risk of zoster is lower, and the clinical severity milder, in immunocompentent vaccine recipients than in naturally infected children. A cohort study in children with acute lymphoblastic leukaemia (who have a high rate of zoster in childhood) showed that vaccine recipients had less than one-fifth the zoster rate of their naturally infected counterparts.[30, 38] Some zoster lesions in vaccine recipients have been shown to contain wild-type virus, likely acquired prior to vaccination.[33]

Febrile seizures with MMRV vaccine

MMRV vaccines are not currently available in New Zealand. Compared with the use of MMR and VV at the same visit, use of MMRV vaccine requires one fewer injection but is associated with a higher risk of fever and febrile seizures 5 to 12 days after the first dose among children aged 12–23 months (approximately one extra febrile seizure for every 2,300–2,600 MMRV vaccine doses).[39]

After the second dose, there are no differences in incidence of fever, rash or febrile seizures among recipients of MMRV vaccine compared with recipients of MMR and VV.[39] There is no evidence of an association with increased febrile seizures when MMRV is given to toddlers as a second dose of MMR.[40] For example, in Australia, the first dose of MMR is given at 12 months and the second dose is given as MMRV at 18 months.

In general, a positive history of chickenpox can be taken as indicating immunity, provided there has not been an intervening bone marrow transplant or other immunosuppressive therapy. Recall of varicella or characteristic rash is reliable evidence of immunity. In people with no history or recall of the rash, 70–90 percent are found to be immune.[33] Consult with the local laboratory about the availability and interpretation of varicella serology.

Zoster immunoglobulin (ZIG) is a high-titre immunoglobulin available from the New Zealand Blood Service for passive immunisation of varicella in high-risk individuals. It is most effective if given within 96 hours after exposure, but may be have some efficacy if given up to 10 days post-exposure.[39, 41, 42, 43] ZIG should be given intramuscularly.[43] Intravenous immunoglobulin (IVIG) can be given when ZIG is unavailable.

For further information, see Starship Child Health guidelines.

The decision whether to offer ZIG depends on:[43]

• the likelihood that the exposed person is susceptible to varicella
• the probability that a given exposure to varicella will result in infection
• the likelihood that complications would develop if the person exposed is infected.

Contact (exposure) can be classified as follows:[43]

• household contact – infection is very likely to occur in a susceptible individual living with an infected contact
• playmate contact – more than one hour of play indoors with infected individual
• newborn infant contact – when the mother of a newborn infant develops chickenpox (but not shingles) from seven days before to seven days after delivery
• hospital contact – individuals in the same two-bed room or have face-to-face contact for longer than five minutes.

Provided exposure has occurred and susceptibility is likely, ZIG is recommended for:

• pregnant non-immune women (see section 24.8.6 below and discuss with an infectious diseases physician)
• newborn infants whose mother had onset of chickenpox (but not shingles) within seven days before or after delivery (see section 24.8.6)
• hospitalised premature infants whose mothers have no history of chickenpox, or who were born at less than 28 weeks’ gestation, or with birthweight less than 1,000 g, irrespective of maternal history
• immunocompromised individuals – discuss the use of ZIG with their specialists, as appropriate.

Dosage of ZIG

ZIG prepared by CSL Behring in Melbourne, derived from human plasma donated in New Zealand, is available in single vials containing 200 IU varicella-zoster antibody. The actual volume in the vial is stated on the label. The recommended dose is based on body weight and is shown in Table 24.2 below. ZIG should be given intramuscularly, not intravenously.[43]

VV may be used for post-exposure prophylaxis of susceptible individuals aged 9 months or older, if there are no contraindications to vaccine use[33] – see Table 24.3. Data from the US and Japan from household, hospital and community settings indicates that VV is effective in preventing illness or modifying varicella severity if used within three days, and possibly up to five days, of exposure.

In the event of an exposure:

• susceptible staff should be excluded from contact with high-risk patients from day 8 to day 21 after exposure to varicella (or shingles in an immunocompromised patient)
• hospital staff who have no history of chickenpox and who will be in contact with pregnant women or high-risk patients should be tested for varicella zoster antibodies; vaccination is recommended for those who are not immune or whose serostatus cannot be promptly determined.

Two doses of VV are funded for post-exposure prophylaxis of immune-competent in-patients who are susceptible to varicella (see section 24.8.3).

Parents/guardians should be advised that:

• infected children should be excluded from early childhood education services or school until fully recovered, or all lesions have crusted. Lesions from mild breakthrough disease in immunised children may not crust but these children should be excluded until no new lesions appear for 24 hours[33]
• immune-deficient children should be excluded from early childhood education services or school until three weeks after the last documented case.

Pregnant women are at higher risk of severe complications from varicella. If an immune-competent pregnant woman with no history of varicella or vaccination is exposed to varicella, it is recommended, where possible, that her varicella antibodies be assessed (Figure 24.1). If there is no evidence of immunity, two possible courses of action are available: either administer ZIG, or await the onset of symptoms and as soon as possible commence the administration of acyclovir, which is effective in this situation and now regarded as safe in pregnancy. Discuss the clinical circumstances with an infectious diseases physician before deciding on which course of action is best.

Intravenous acyclovir is recommended for the pregnant woman with severe complications of varicella. ZIG given to a pregnant woman within five days of delivery may not protect the fetus/neonate: the neonate should receive ZIG on delivery and may need treatment with acyclovir (Figure 24.2).

Figure 24.1: Management of pregnant women exposed to varicella or zoster

Figure 24.2: Management of infants from mothers with perinatal varicella or zoster

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