Referaat

HERPES ZOZTER DURING PREGNANCY

Guided by:
Dr.

By:
Dr. Deiki

PPDS 1 Obstetry and Gynaecology

Medical Faculty of Sebelas Maret University / dr. Moewardi Hospital Surakarta
2016
 CHAPTER I
INTRODUCTION

Herpes zoster (HZ) is characterised by a unilateral, painful, vesicular rash with a

dermatomal distribution. It is a manifestation of the reactivation of latent varicella-zoster virus
(VZV), which, as a primary infection, produces chickenpox (varicella). Although the rash is its
most distinctive feature, HZ is frequently not a benign disease; zoster-associated pain, both acute
and chronic, can be debilitating and poorly responsive to treat-ment once established. The proven
effectiveness of a live, attenuated VZV vaccine (Oka/Merck strain, Zostavax [Merck Sharp &
Dohme, distributed in Australia by CSL Limited; trade name used for product identification only,
and no endorsement is implied]) in reducing the incidence of and morbidity associated with HZ
and postherpetic neuralgia (PHN) is a major advance.1,2
The burden of illness from herpes zoster (HZ) and postherpetic neuralgia (PHN) in the
Australian community is high. The incidence and severity of HZ and PHN increase with age in
association with a progressive decline in cell-mediated immunity to varicella-zoster virus (VZV).
Antiviral medications (valaciclovir, famciclovir, aciclovir) have been shown to be effective in
reducing much but not all of the morbidity associated with HZ and PHN, but are consistently
underprescribed in Australia. Zoster-associated pain should be treated early and aggressively, as
it is more difficult to treat once established. Clinicians should be proactive in their follow-up of
individuals at high risk of developing PHN, and refer patients to a specialist pain clinic earlier,
rather than later. A live, attenuated VZV vaccine (Oka/Merck strain, Zostavax [Merck Sharp &
Dohme]) has proven to be efficacious in reducing the incidence of and morbidity associated with
HZ and PHN in older adults. The vaccines efficacy has been shown to persist for at least 4
years, but is likely to last a lot longer. Ongoing surveillance will determine the duration of
protection and whether a booster dose is required. Clinicians should consider recommending the
vaccine, which can be safely administered at the same time as the inactivated influenza vaccine,
to all immunocompetent patients aged 60 years or older. Clinicians should refer to theAustralian
immunisation handbookfor advice on the use of the live vaccine in immunosuppressed
individuals.1,3
Following a primary infection with the varicella-zoster virus (VZV), the virus can remain
latent in the dorsal root ganglia and might cause herpes zoster (HZ) upon reactivation. Herpes
zoster infection typically exhibits vesicular rash, pain, and itching in the dermatome distri-
bution. Patients might suffer from postherpetic neuralgia for months after the rash subsides.
Herpes zoster is contagious only while the patient has lesions and until the lesions crust.
Covering the lesions decreases transmission. Susceptible (nonimmunized) individuals might
contract primary varicella infection (chickenpox) by direct contact with the zoster lesion.4
Herpes zoster, which affects an estimated one in five people, is a painful, blistering
condition. It can show up at any time, but is especially alarming if it strikes during pregnancy.
Fortunately, shingles in pregnancy is rare. And, for most women who develop shingles during
pregnancy, the outlook is good.5
 CHAPTER II
HERPES ZOSTER1,6,7

A. Aetiology, virology and pathology

One of eight human herpes viruses, VZV infects 90% of the population by adulthood,
establishing latency within the dorsal root ganglia (see Box 1). Cell-mediated immunity is now
known to be more important than humoral immunity for protec-tion against VZV infection,
although VZV-specific antibody levels can be used as an index of vaccine efficacy (positive titres
46 weeks after vaccination indicate protection). Exogenous, circu-lating wild-type virus
episodically boosts adult T-cell immunity (eg, exposure to infected children) so that reactivation
usually occurs as a result of naturally waning cell-mediated immunity with age or induced
immunosuppression. PHN is currently thought to be the result of neuronal damage and scarring
to the affected dorsal root ganglion after the extensive inflammation of HZ.

B. Spectrum of illness and its complications

A prodrome characterised by pain and other localised skin sensa-tions (eg, burning,
tingling and itching), headache, photophobia, malaise and (rarely) fever typically precedes the
appearance of the zoster rash by 23 days (Box 2). The rash, often pruritic, spreads throughout
the affected dermatome, evolving through papular, vesicular (35 days) and crusting (710 days)
stages, taking 24 weeks to heal.
Acute pain accompanies the rash in 80% of individuals aged over 50 years, varying in
both nature (burning to lancinating) and severity. It may be accompanied by parasthesiae,
anaesthesia or allodynia (pain induced by touch, often from trivial stimuli such as clothing).
Although usually self-limiting, pain may persist beyond the resolution of the rash PHN,
defined as pain persisting for 90 or more days after the onset of pain or rash, can last months and
even years.
Zoster ophthalmicus (ranging from keratitis to the more severe iritis) is a relatively
common complication of HZ, affecting 10% 20% of patients. Rarer complications include
motor neurone and peripheral nerve palsies (eg, Bells palsy and Ramsay Hunt syndrome), as
well as meningitis, myelitis, vasculitis, paresis and urinary retention owing to visceral
involvement.

C. Diagnosis of herpes zoster

Herpes zoster is usually diagnosed clinically. Laboratory diagnosis (involving the
detection of VZV antigens or nucleic acid, or isolation of virus, from swabs of lesions, or by
VZV-specific IgM antibody tests) is recommended when the clinical picture is atypical or
complicated (eg, when there is persistent or recurrent rash, a single lesion, central nervous
system involvement or immunosuppression).

D. Management of herpes zoster

1. Antiviral medications
Antiviral therapy for HZ is currently underprescribed in Australia. Data from the
Restricted Pharmaceuticals Benefits Scheme for the period 19951999 indicate that only
 40% of all community cases of HZ were treated with antiviral drugs. The proportion of
this trend resulting from late presentations (beyond 72 hours) versus non-prescribing is
unclear. The GPRN database recorded an antiviral drug treatment rate of 61% for 2001
2005, suggesting a trend towards increased prescribing of antiviral medications (Lynne
Conway, Director, Health Economics, CSL Limited, per-sonal communication).
Aciclovir, valaciclovir and famciclovir have proven efficacy in managing acute HZ,
accelerating the resolution of acute pain and skin lesions, while reducing the duration and
possibly the inci-dence of PHN. Famciclovir and valaciclovir have replaced aciclovir as
the drug of choice because of their more favourable pharmacokinetic profiles and simpler
dosing regimens.
As antiviral drugs are most effective when started within 72 hours of rash onset,
early presentation should be encouraged. However, existing data suggest benefit might
extend beyond this time period, and antiviral therapy initiated at or shortly after 72 hours
should be considered if pain is severe or lesions are progressive.
Antiviral therapy is particularly indicated if the patient is aged over 50, is
immunocompromised, has ophthalmic zoster, or if PHN is more likely (Box 3). The
favourable riskbenefit profile of antiviral medications, however, means antiviral therapy
should be considered even for patients deemed at low risk of developing PHN and other
complications.
2. Corticosteroids
Therapy with oral corticosteroids (eg, 40 mg prednisolone daily for 7 days,
tapering to 5 mg daily over the next 2 weeks) can reduce symptoms in the
acute(inflammatory) phase of HZ, but only when used in combination with an antiviral
agent. Corticosteroids are recommended for patients over the age of 50 ifnot contraindi-
cated, and should be used with caution in patients with comor-bid conditions such as
diabetes. Corticosteroids are not effective in preventing or managing PHN.

3. Analgesics
Zoster-associated pain should be treated early and aggressively, asevidence
suggests it is more difficult to treat once established. As necessary, treatment should
ascend the analgesic ladder from paracetamol/non-steroidal anti-inflammatory drugs to
 codeine, morphine or oxycodone. The need for analgesia frequently escalates during the
acute period, so regular follow-up (every 23days) is recommended until pain is
controlled. Box 4 provides a guide for assessing acute pain severity and the presence of
neurological dysfunction.
4. When to refer
Patients with specific zoster syndromes (eg, ophthalmic and disseminated zoster),
and those with neurological dysfunction should be referred for appropriate specialist care.

E. Diagnosis and management of postherpetic neuralgia

Patients at high risk for developing PHN (see Box 3) should receive proactive follow-up
to enable the prompt diagnosis of PHN following HZ. However, there is little consensus
within Australia, or overseas, about how best to manage the pain of PHN. We present one
suggested algorithm in Box 5. A case vignette illustrat-ing the high psychosocial impact of
PHN is presented in Box 6.
F. Role of a live vaccine for the prevention of herpes zoster
The rationale behind the introduction of a HZ vaccine is to reduce the high medical and
psychosocial costs associated with HZ and its complications. The current therapies for HZ
and PHN have limitations, and are often used suboptimally in older patients, who bear the
overwhelming majority of the burden of illness associated with HZ. The close link between
the increasing incidence of HZ in older adults and the observed decline in VZV cell-mediated
immunity with age means that boosting VZV cell-mediated immun-ity through immunisation
also has a strong biological rationale.
In the United States Shingles Prevention Study (SPS), a double-blind, placebo-controlled,
multicentre trial involving 38 546 par-ticipants aged 60 years or over, a live, attenuated,
Oka/Merck strain, VZV vaccine (containing a viral titre 14 times higher than the current
varicella vaccine) significantly altered the natural history of latent VZV, preventing HZ in the
young old (6069 years) and either preventing or attenuating HZ in older partici-pants.
Overall, the vaccine reduced the burden of illness from HZ by 61.1% (P< 0.001) and reduced
its incidence by 51.3% (P< 0.001). The duration of pain and discomfort among partici-pants
with confirmed HZ was significantly shorter in the vaccine group (21 days v 24 days; P=
0.03), and the incidence of PHN was reduced by 66.5% (P<0.001).
The vaccine (Zostavax) is currently indicated in Australia for the prevention of HZ in
individuals aged 50 years and older, and for the prevention of HZ and PHN and reduction of
acute and chronic zoster-associated pain in individuals aged 60 years and older. An
application to the federal government for the vaccine to be listed on the publicly funded
National Immunisation Program is pending. As the only vaccine able to prevent the clinical
recurrence of a pre-existing latent viral infection (and which does not induce herd immunity),
Zostavax represents a unique case for National Immuni-sation Program funding. The
availability of this vaccine is stimulat-ing more accurate studies of the health care costs of
zoster and PHN, and vaccine cost-effectiveness analyses, especially to help appraise the case
for national funding. These should be discussed in depth in future publications when key data
are available.
Despite the success of the SPS, a number of uncertainties still surround the topic of HZ
vaccination. The following discussion aims to address some of these issues. However, where
evidence is lacking, clinicians should await the formal recommendations of the Australian
Technical Advisory Group on Immunisation.
1. Age at vaccination
Worldwide epidemiological data suggest that the ideal age for HZ vaccination
would probably be before 5055 years, the time at which the incidence of HZ begins to
increase exponentially. From a biological viewpoint, it is likely that a younger individual
would mount a greater immune response to the vaccine. This supports vaccinating
individuals 510 years earlier than currently indicated (ie, at 5059 years). Precautions or
contraindications to the vaccine are also likely to be less troublesome in a slightly
younger age group. The potential loss of environmental boosting of VZV cell-mediated
immunity after the introduction of universal varicella vaccination may mean that the age-
specific incidence curve for HZ shifts to a younger age group. This epidemiological
trend, should it eventuate, would also provide a strong case for vaccinating people at a
younger age.
However, as the duration of the vaccines effect is not yet known, early
vaccination may increase the likelihood that a booster dose is required in later years.
Vaccination at age 6065 years as part of a national program would be convenient, as the
vaccine could be given concomitantly with the influenza and pneumococcal vac-cines,
and still cover most older individuals at risk.
It is difficult to make a strong recommendation for a particular age group at this
time; Pharmaceutical Benefits Scheme/National Immunisation Program listings (decided,
in part, by age-specific cost-effectiveness analyses) are most likely to influence
prescribing behaviour in the immediate future.
2. Duration of protection
It is currently recommended that the zoster vaccine be given as a single dose.
Trial data indicate that the vaccines efficacy will persist for at least 4 years, with
plateauing at about 1 year. Without any evidence of waning immunity, we expect the
vaccines efficacy to endure much longer than this. The ongoing surveillance of SPS-trial
participants will show the total duration of protection that the vaccine affords and
whether a booster dose is required.
3. Concomitant administration
 In general, live vaccines are safe when administered before or after an inactivated
vaccine. In a double-blind, placebo-controlled trial of 762 participants aged 50 years or
older, the zoster vaccine induced a similar antibody response after 4 weeks when
adminis-tered concomitantly or non-concomitantly with the influenza vaccine. No safety
data exist on the concomitant administration of the zoster vaccine with the pneumococcal
(polysaccharide) or diphtheriatetanusacellular pertussis vaccines.
4. Use in immunosuppression
Live vaccines are usually contraindicated in immunosuppressed people.
Clinicians should refer to the Australian immunization handbookfor guidelines on
administering live virus vaccines to this patient group. In patients for whom HZ
vaccination is contrain-dicated, the priority should be early diagnosis of HZ and prompt
treatment with antiviral agents. The effectiveness of a killed vaccine for use in
immunosuppressed individuals is currently being explored.
The safety and efficacy of the zoster vaccine has not yet been established in adults
with HIV, with or without evidence of immunosuppression.
Immunocompetent individuals aged 60 years or less who are VZV seropositive
and expect to become immunocompromised in the future (eg, future organ transplant,
before chemotherapy, those with early HIV) may benefit from HZ vaccination. The
efficacy of the vaccine and its durability following the subsequent immuno-suppression
are, however, unknown. People who have been given immunosuppressive therapy but are
in remission, are between rounds of chemotherapy, or are having a break from
immunosup-pressive therapy, may also benefit from the vaccine. Research is ongoing in
this area.
5. Vaccination of varicella-zoster virus-nave individuals
The epidemiology of HZ in Australia is well described; clinicians can assume that
any long-term resident of Australia is VZV immune. The immune status of foreign-born
individuals cannot be assumed; VZV exposure has been reported to be as low as 40%
50% in some tropical countries.However, the zoster vaccine was safe when given to 125
subjects who had never had primary varicella infection.
6. Transmission of vaccine virus
 Experience with varicella vaccines suggests it is unlikely that the zoster vaccine
strain will be transmitted between people who have been vaccinated and susceptible
contacts. Although a much higher viral titre is used for zoster prevention, most
individuals will have residual specific antibody and (memory) T cells to varicella
vaccines. The risk of transmitting the attenuated vaccine virus to a susceptible individual
should be weighed against the risk of developing natural zoster that could be transmitted
to a suscept-ible individual. It is expected that the attenuated vaccine virus would respond
well to antiviral treatment.
7. Individuals with prior herpes zoster
The use and safety of vaccinating an individual who has had HZ in the distant
past (estimated to be about 15% of the target popula-tion) is currently being studied. The
time interval is likely to be important; the rationale behind vaccinating a 70-year-old
follow-ing an episode of HZ at age 63 is not compelling, but a strong argument could be
made for vaccinating the same individual if the HZ occurred at the age of 40. The US
Advisory Committee on Immunization Practices currently recommends vaccination
regard-less of prior history of HZ.

CHAPTER III
HERPES ZOSTER DURING PREGNANCY4,5,8,9,10

A prospective study reported on 474 women diag-nosed with HZ during pregnancy.The

474 women had 466 live births, 5 miscarriages, and 3 therapeutic abor-tions. There were 2
children with malformations, but no cases of congenital varicella syndrome (CVS) among the
live births and no serologic evidence of intrauter-ine infection. A smaller prospective report had
14 cases complicated with HZ with no adverse outcomes or CVS. There is a theoretical risk of
intrauterine infection fol-lowing HZ involving the T10 to L1 dermatomes (as sen-sory nerves to
the uterus originate from these segments) during pregnancy. However, no such reports have been
documented. There was a case of congenital malfor-mations consistent with CVS (limb
hypoplasia and skin scarring) in a child whose mother had disseminated zoster at 12 weeks of
gestation, highlighting the possi-bility of infection caused by maternal viremia. There is no
clinical or serologic evidence of VZV infection in infants whose mothers developed perinatal
zoster. Newborns do not appear to be at risk of infection if maternal zoster occurs near delivery.
If a susceptible pregnant woman (in any stage of preg-nancy) is exposed to VZV, passive
antibody prophylaxis with immunoglobulin preparation containing VZV immu-noglobulin G is
indicated within 96 hours of exposure. Herpes zoster infection during pregnancy is not associ-
ated with increased risk of congenital malformations above the general population baseline risk
or of CVS. Individuals with HZ should cover lesions in order to reduce the risk of transmitting
VZV to susceptible pregnant women.
Varicella zoster virus (VZV) is a DNA virus and a member of the herpesvirus family. It is
highly infectious and is transmitted by direct contact and through respiratory droplets. About
90% of infections are contracted in the first decade of life, and immunity to VZV is lifelong.
Morbidity and mortality are much higher among older persons who are newly exposed to VZV.
All women of reproductive age should be screened for immunity to VZV. Women who
did not have childhood "chickenpox" (or do not recall having had it) should be tested for serum
VZV immunoglobulin (Ig)G. Women of reproductive age who are not immune should be offered
varicella vaccine. Note, however, that this vaccine is contraindicated during pregnancy.
Therefore, pregnant women who are not immune to varicella should be educated to avoid
exposure to persons who have varicella or herpes zoster. Nonimmune pregnant women who have
been exposed to varicella should be offered varicella-zoster immune globulin (VZIG), preferably
within 72-96 hours post exposure. Prophylactic acyclovir, 800 mg orally 5 times daily for 5-7
days, is also effective in preventing the infection. Pregnant women who have been exposed and
are not immune should be counseled about the clinical manifestations of varicella that they may
experience, especially pneumonia and encephalitis.
Reactivation of latent VZV results in herpes zoster infection. This infection is less serious
than varicella secondary to the presence of maternal antibodies; however, it can be very serious
in immunocompromised patients. The infection manifests clinically as fever, malaise, and skin
rash. The rash is painful and is usually confined to a dermatome. Serious life-threatening
complications of the infection include pneumonia (up to 20% of pregnant patients) and
encephalitis (up to 1% of pregnant patients).
Pregnant women with herpes zoster symptoms should be treated with oral acyclovir,
unless hospital admission is warranted. Oral antiviral agents (acyclovir, valacyclovir, or
famciclovir) have been shown to significantly reduce herpes-related symptoms as well as the
duration, intensity, and prevalence of zoster-associated pain. According to Drugs in Pregnancy
and Lactation, Sixth Edition, famciclovir, a category C drug, has not been studied enough in
pregnant women. Valacyclovir, also a category C drug, is metabolized to acyclovir. Acyclovir is
the drug of the 3 that has been most extensively studied in pregnant women and is the agent most
commonly used to treat patients with VZV during pregnancy. All HIV and immunocompromised
women who are pregnant and are manifesting VZV infection should be admitted to the hospital
for intravenous acyclovir.
A pregnant woman who has been exposed to VZV before pregnancy should be reassured
that her fetus is safe. It is well documented in the literature that IgG antibodies are
transplacentally passed to the fetus providing the necessary immunity. These antibodies persist in
the newborns for up to 6 months of life. A pregnant woman manifesting VZV infection should be
counseled about the risk of viral transmission to the fetus and the risks of fetal anomalies. They
should also be informed that these risks are very low. The incidence of fetal anomalies after an
early exposure (before 20 weeks) is 1.2% to 2.0%. VZV infection of the fetus occurs primarily
via hematogenous dissemination across the placenta. This infection may lead to spontaneous
abortion, fetal demise, and varicella embryopathy (eg, limb hypoplasia, microcephaly, muscle
atrophy, cataracts, and mental retardation). Prenatal ultrasound and magnetic resonance imaging
have been used to document the extent of tissue damage in fetal varicella syndrome. Findings
include oligohydramnious, intrauterine growth restriction, hydrops, limb deformities, and
microcephaly.
Neonatal infection may occur in 10% to 20% of neonates whose mothers became acutely
infected from 5 days before delivery to 2 days after the delivery. It results from hematogenous
dissemination of the virus across the placenta in the absence of maternal antibodies. Infants
become symptomatic 5-10 days postpartum. The clinical picture may vary form skin lesions to
systemic illness, pneumonia, for example.
 In acutely infected mothers the delivery should be postponed 5-7 days to prevent the
spread of VZV to the neonate. If this is not possible, the neonate should be given VZIG
immediately after birth and should be isolated from the mother if the latter has skin lesions/rash
present.

Treatments can lessen the severity of shingles and reduce the risk of postherpetic
neuralgia. These include the antiviral drugs acyclovir (Zovirax), famciclovir (Famvir), and
valacyclovir (Valtrex). One of these medications must begin within a few days of a shingles
outbreak for best results. It's important to take it exactly as directed. Most are taken once daily
for several days. When taken as directed, these drugs should be safe during pregnancy.

In addition to the medications, there are over-the-counter (OTC) medications and self-help
measures for relieving shingles pain and itching and preventing infection. These include:
Cold compresses and cool baths to relieve blisters
Loose clothing and clean gauze coverings over affected areas to hasten healing of blisters
and prevent infection
Antihistamines (particularly Benadryl), oatmeal baths, and calamine lotion to reduce
itching
The OTC painkiller acetaminophen. Before taking any OTC medication, it's important to
speak with your doctor. Pregnant women should not take NSAIDs late in pregnancy.

Shingles Prevention: Reduce the Risk. The varicella-zoster virus is highly contagious.
If mother have not had chickenpox, it's important to avoid exposure to anyone known to have
the infection -- or even crowds where there may come in contact with the infection, particularly
if woman is pregnant. If woman already had chickenpox, she cannot catch shingles from
someone with chickenpox or shingles. Having chickenpox during pregnancy could potentially
lead to chickenpox infection or birth defects in the unborn child, depending on when they are
infected. Shingles, too, could potentially cause problems for the baby, but most experts agree the
risk is less than with chickenpox. In one large study, there was no evidence of fetal harm in
pregnant women who developed shingles. A blood test to check for antibodies to VZV can be
perform. If woman have the antibodies (indicating they have already had chickenpox infection),
they run the risk of shingles in the future, but they cannot catch shingles from someone else.
There is also a vaccine called Zostavax that can help prevent shingles. In clinical studies, the
vaccine reduced the overall occurrence of shingles by half. For people who were vaccinated and
got shingles anyway, the severity was dramatically reduced. But the time to get the vaccine is
before they get pregnant. The vaccine's manufacturer recommends waiting at least three months
after getting the vaccine before attempting to become pregnant.

Shingles Complications. Shingles can be quite painful. Many people

who see their doctor for shingles say it was the pain that ultimately led them
to seek treatment. Some report that the sensation of anything brushing
across the inflamed nerve endings on the skin is almost unbearable. Even
when the rash is gone, postherpetic neuralgia can persist, sometimes for
years. Shingles can cause other lasting complications as well. If it occurs on
the face, it can damage the eyes. Shingles of the eye can lead to scarring,
which can damage the vision. It can also lead to glaucoma, an eye disease
that can cause blindness later in life. Shingles can also cause hearing or
balance problems, as well as weakness of the muscles on the affected side of
the face. In rare cases, shingles can spread into the brain or spinal cord and
cause serious complications such as stroke or meningitis (an infection of the
membranes outside the brain and spinal cord). According to the CDC, more
than one-third of people who get shingles will develop serious complications.
People whose immune systems are suppressed because of medication or
diseases such as HIV run the greatest risk of complications. Complications
are also more common among people over age 60, which precludes women
of childbearing age.

CHAPTER IV
 CONCLUSION

The advent of a vaccine to prevent latent varicella reactivation marks an important

advance in the prevention of HZ and its sequelae. The vaccine has the potential to prevent a
major burden of disease among older Australians if adequate coverage can be achieved. Future
research will address the uncertainty about the vaccines safety and efficacy in currently
unstudied clinical settings (eg, immunosuppressed individuals, younger age groups) and show
whether a booster dose is required. Future vaccine develop-ment strategies may alter as the
epidemiology of VZV and HZ continues to evolve. This vaccine offers a new paradigm for
managing HZ immunisation followed by prompt antiviral therapy for break-through cases.

The incidence of shingles in pregnant women is very low. If woman are

planning to get pregnant and are concerned about shingles, consultation
about the possibility of the shingles vaccine is needed. If woman are already
pregnant, practice healthy habits and consult if there is any symptoms. Early
recognition and treatment will minimize the risk of complications for mother
and the baby.

Herpes zoster infection during pregnancy is not associ-ated with increased risk of
congenital malformations above the general population baseline risk or of CVS. Individuals with
HZ should cover lesions in order to reduce the risk of transmitting VZV to susceptible pregnant
women.
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