Zika Virus Infection Evaluation of Pregnant Women and Infants

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4/5/2016 Zika virus infection: Evaluation of pregnant women and infants

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Offi cial reprint from UpToDatewww.uptodate.com ©2016 UpToDate

Author Edward RB McCabe, MD, PhD

Section EditorsMartin S Hirsch, MDCharles J Lockwood, MD, MHCMDeborah Levine, MD

Deputy EditorsVanessa A Barss, MD, FACOG Elinor L Baron, MD, DTMH

Zika virus infection: Evaluation of pregnant women and infants

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2016. | This topic last updated: Apr 21, 2016.

INTRODUCTION — Zika virus is an arthropod-borne flavivirus transmitted by mosquitoes. This topic will discuss

issues r elated to Zika virus infection in pregnant women and congenitally infected newborns. Other issues related

to Zika virus infection are reviewed separately. (See "Zika virus infection: An overview".)

ACQUISITION OF INFECTION — Zika virus may be transmitted to humans via the following (see "Zika virus

infection: An overview", section on 'Transmission'):

Preventive measures are discussed below. (See 'Pr evention' below.)

There is no evidence to suggest that pregnant women are more susceptible to Zika virus infection than men or

nonpregnant women [1,2]. Transmission of Zika virus infection through breastfeeding has not been described [3,4].However, transmission of some other flaviviruses via breast milk can occur [ 5,6].

CLINICAL MANIFESTATIONS

Maternal infection — Clinical manifestations of Zika virus infection in pregnant women are the same as those in

nonpregnant adults. (See "Zika virus infection: An overview", section on 'Clinical manifestations'.)

There is no evidence to suggest that pregnant women experience more severe disease than nonpregnant women

[1,2]. However, viremia may persist longer in pregnant women than nonpregnant individuals [7].

Congenital infection — Zika virus infection in all trimesters has been associated with fetal abnormalities, so it

should be presumed that the risk for congenital infection exists throughout pregnancy [ 8,9].

Further study is needed to determine the rate of vertical transmission and the rate at which infected fetuses

manifest complications [10]. In a cohort including 88 pregnant women who presented to a Brazilian clinic with a

rash at 5 to 38 weeks of gestation, 72 women (82 percent) had a positive test for Zika virus infection [ 8]. Among

42 of these women who underwent ultrasonography, fetal abnormalities were detected in 12 (29 percent). Viremia

longer than typically observed may indicate fetal infection [7].

Vertical transmission of Zika virus from mother to fetus [1,4,11,12] has been associated with several sequelae

(table 1) [7,8,13-20]. Serious sequelae include:

®

®

Bite of an infected mosquito●

Maternal-fetal transmission (see 'Congenital infection' below)●

Sex (including vaginal, anal, and oral sex)●

Blood transfusion●

Organ or tissue transplantation●

Laboratory exposure●

Microcephaly – Zika virus infections have been confirmed in the cerebrospinal fluid (CSF) and serum of

newborns with microcephaly [13,15,16,21], although it is not known how many of the microcephaly cases are

●

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DIAGNOSIS — Case definitions for Zika virus infection have been developed by the World Health Organization;

these are the same in pregnant and nonpregnant individuals and are summarized separately. (See "Zika virus

infection: An overview", section on 'Diagnosis' and "Zika virus infection: An overview", section on 'Case

definitions'.)

ANTEPARTUM MATERNAL EVALUATION — Approaches to Zika virus diagnosis may vary depending onavailable resources; the approach outlined for pregnant women in the following sections may need to be tailored to

local circumstances.

In the first three months of 2016, over 3300 pregnant women in the United States who traveled to or moved from

areas with active Zika virus transmission were tested for Zika virus: 0.8 percent had confirmed Zika virus infection

and 64 percent of these women had at least one Zika virus-associated symptom [40]. Infection was confirmed in

2.9 percent of symptomatic women and 0.3 percent of asymptomatic women.

History — In areas with no known mosquito-borne Zika virus transmission (ie, no ongoing risk of exposure),

healthcare providers should determine whether the pregnant woman is at risk because of her travel or sexual

history by asking about:

caused by Zika virus infection [22,23]. (See 'Definition of Zika virus-related microcephaly' below.)

Between March 2015 and April 2016, more than 5000 cases of microcephaly were reported among newborns

born to Brazilian mothers with Zika virus infection; this represents a >20-fold increase in microcephaly

compared with previous years [14,24-30]. In one report including 574 cases of microcephaly in Brazil

between January 2015 and January 2016, the prevalence of microcephaly was significantly higher in 15

states with active Zika transmission than in 4 states without transmission (2.8 versus 0.6 cases per 10,000

live births) [31].

Birth defects were not recognized as a complication of Zika virus infection at the time of the outbreak in theYap Islands of Micronesia in 2007, perhaps because of the relatively small size of the population. Similarly,

no fetal abnormalities were identified initially during the French Polynesia outbreak in 2013 to 2014; however,

subsequent retrospective evaluations identified 19 cases of fetal or neonatal central nervous system

malformations or brainstem dysfunction [32,33], and retrospective polymerase chain reaction testing of

stored amniotic fluid was positive for Zika virus in some of these cases [34]. Further retrospective analysis

of the data from French Polynesia estimated a baseline microcephaly prevalence of 2 cases per 10,000

neonates and a risk of microcephaly associated with Zika virus infection rate of 95 cases per 10,000 women

infected in the first trimester [35]; based on these estimates, the risk of microcephaly associated with Zika

virus infection in the first trimester during that outbreak was approximately 1 percent.

During the current Zika outbreak, there have been a number of yet unsubstantiated theories about thepathogenesis of microcephaly [36]. However, the World Health Organization (WHO) and the United States

Centers for Disease Control and Prevention (CDC) concluded that the Zika virus causes microcephaly

[22,23].

Fetal loss and stillbirth – Zika virus RNA has been detected in the pathologic specimens of early and late

fetal losses [8,13,15].

●

Ocular abnormalities – Ocular abnormalities are common and include focal pigment mottling, chorioretinal

atrophy, and optic nerve abnormalities (hypoplasia and severe cupping of the optic disk) [ 37-39].

●

Other central nervous system abnormalities (eg, ventriculomegaly, global hypogyria, hydranencephaly

[complete or partial destruction of cerebral hemispheres with cerebrospinal fluid in the remaining cranialcavity]) [18,19,33]

●

Hydrops fetalis [18]●

Fetal growth restriction [8]●

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Women who meet one or both of these criteria or who live in an area with known Zika virus transmission should be

asked about symptoms consistent with Zika virus infection.

Women with no exposure to Zika virus — For pregnant women with no relevant epidemiologic exposure,

laboratory testing or fetal screening for Zika virus infection is not indicated [ 12].

Women with symptoms consistent with possible Zika virus infection — Pregnant women with clinical illness

consistent with Zika virus infection (two or more symptoms consistent with Zika virus infection [maculopapular

pruritic rash, arthralgia, conjunctivitis, or low-grade fever]) within two weeks of epidemiologic exposure should

have both laboratory testing and ultrasound examination [ 12,41,42]:

Asymptomatic women with possible but not ongoing exposure to Zika virus — Asymptomatic women with

possible exposure to Zika virus should have both laboratory testing and ultrasound examination:

The United States Centers for Disease Control and Prevention (CDC) maintains a clinical consultation service

(available 24 hours per day, 7 days per week) for healthcare providers evaluating and caring for pregnant women

and infants with possible Zika virus infection (telephone 1-800-CDC-INFO or email at [email protected]) [ 43].

Asymptomatic women with ongoing risk for Zika virus infection — Asymptomatic women with ongoing risk

for Zika virus infection should have both laboratory testing and ultrasound examination:

Previous residence in or travel to an area where mosquito-borne transmission of Zika virus infection has been

reported

●

Unprotected sexual contact with a person who resides in or has traveled to an area where mosquito-borne

transmission of Zika virus infection has been reported

●

For patients presenting


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EVALUATION OF FETAL LOSS AND STILLBIRTH — Fetal tissue testing is warranted for fetal losses in

women with history of Zika exposure, together with either symptoms consistent with Zika virus infection during or

within two weeks of exposure or findings of fetal microcephaly. In such cases, Zika virus reverse-transcription

polymerase chain reaction and histopathologic examination with immunohistochemical staining should be

performed on fetal tissues, including the umbilical cord and placenta [ 12,45].

SCREENING FOR FETAL INFECTION — Ultrasound is the major modality used to screen for fetal Zika virus

infection, but magnetic resonance imaging (MRI) is more sensitive [ 7].

Ultrasonography — Ultrasound findings associated with fetal Zika virus infection may be detected as early as 18to 20 weeks gestation in some cases [2,42,46,47]. The two major ultrasound findings suggestive of congenital

Zika virus infection are the following [2]:

Accurate assessment of gestational age early in pregnancy is important for establishing a diagnosis of

microcephaly late in pregnancy. (See "Prenatal assessment of gestational age and estimated date of delivery".)

The International Society of Ultrasound in Obstetrics and Gynecology (ISUOG) interim guidance on ultrasound for

Zika virus infection in pregnancy recommends a baseline ultrasound examination for women with Zika virus

exposure and symptoms, positive serology or proven Zika virus infection, or exposure and/or symptoms without

positive serology results [48].

The baseline examination should include routine biometry to detect microcephaly and assessment for intracranial

calcifications. The anatomic survey should also look for findings that may be associated with Zika virus infection

and which may occur in the absence of microcephaly and intracranial calcifications, including:

If the baseline examination is normal in these women, the ISUOG recommends serial ultrasound examinations

every four to six weeks, if possible.

If the baseline examination is abnormal, referral to a specialist for neurosonography of the fetal brain is

recommended. In the absence of microcephaly, if the head circumference is small or not enlarging appropriately,

MRI may detect abnormalities not visible on ultrasound and may be useful [7].

Amniocentesis — Zika virus reverse-transcription polymerase chain reaction (RT-PCR) positivity in amniotic fluid

is diagnostic of fetal viral exposure but not predictive of outcome. The indications for diagnostic amniocentesis,

the appropriate gestational age for testing, and the interpretation of the test are uncertain. Decisions regarding

amniocentesis should be tailored to individual clinical circumstances [49].

We suggest offering amniocentesis to women with either of the following:

Microcephaly (head circumference more than two standard deviations below the mean) – Microcephaly as an

isolated finding is not usually seen on ultrasound before the third trimester. (See 'Definition of Zika virus-

related microcephaly' below.)

●

Intracranial calcifications – Intracranial calcifications are sometimes evident in the second trimester but more

often in the third trimester.

●

Irregularly shaped ventricular margins●

Increased periventricular echogenicity●

Cystic lesions●

Intraventricular adhesions●

Callosal or vermian dysgenesis●

Small transcerebellar diameter ●

Enlarged cisterna magna●

Increased amount of cerebrospinal fluid around the brain●

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Timing — For women with characteristic sonographic findings of fetal Zika virus infection, amniocentesis upon

diagnosis and as early as 15 to 16 weeks is reasonable. In general, amniocentesis is not performed before 15

weeks because of an increased risk of pregnancy loss.

For women with positive or inconclusive Zika virus test results and a normal-appearing fetus, the optimal timing for

performance of amniocentesis is uncertain. We suggest six to eight weeks after maternal infection. The sensitivity

of amniocentesis for diagnosis of congenital Zika virus infection may be higher at ≥21 weeks than earlier in

pregnancy because, by analogy with other causes of congenital infection (such cytomegalovirus and Toxoplasma),

it is likely that Zika virus is not shed into amniotic fluid until sufficient time has elapsed following maternal viremia

for the virus to breach the placental barrier; this is six to eight weeks after maternal infection [50-52]. In addition,

fetal kidney development must be sufficiently advanced to excrete the virus into the amniotic fluid (fetal urine

production accounts for most of the amniotic fluid volume after 18 to 21 weeks of gestation). However,

amniocentesis this late in gestation may not allow adequate time to arrange termination of pregnancy if desired

because of positive results. Therefore, if amniocentesis is performed six to eight weeks after maternal infection

and false-negative results are suspected, a repeat amniocentesis later in gestation may be considered.

Interpretation — The sensitivity and specificity of Zika virus RT-PCR testing of amniotic fluid for diagnosis of

congenital infection are not known and likely depend on timing of amniocentesis after onset of maternal infection

[1]. A positive RT-PCR result on amniotic fluid should be considered suggestive of intrauterine infection [ 12]. If the

test was performed because of maternal laboratory findings or viral exposure and the fetus appears normal, it is

unknown whether a positive amniotic fluid RT-PCR result is predictive of a subsequent fetal abnormality and, if so,

what proportion of infants will have abnormalities.

If the RT-PCR is negative and the fetus is abnormal, evaluation for other causes of the fetal abnormalities should

be considered [46]. However, the duration of amniotic fluid PCR positivity is unknown [ 10].

PRENATAL CARE

Maternal treatment — There is no specific treatment for Zika virus infection. Management consists of rest and

symptomatic treatment including drinking fluids to prevent dehydration and administration of acetaminophen to

relieve fever and pain [53].

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided until dengue infection has been

ruled out to reduce the risk of hemorrhage. NSAIDs should also be avoided in pregnant women at ≥32 weeks of

gestation to minimize risk for premature closure of ductus arteriosus. (See "Inhibition of acute preterm labor",

section on 'Fetal side effects'.)

The World Health Organization has issued initial guidance on psychosocial support for patients and families

affected by Zika virus infection and associated complications [54].

Antepartum fetal monitoring — Infected fetuses are at risk for stillbirth. If antenatal testing is performed (eg,

nonstress test, biophysical profile) and results are abnormal, early delivery may be appropriate, depending on the

clinical scenario.

Nosocomial transmission — Transmission of Zika virus via occupational exposure in a healthcare setting has

not been described. Standard precautions are appropriate for protection of healthcare personnel and patients from

Zika virus infection in these settings [55]. (See "General principles of infection control", section on 'Standard

precautions'.)

NEWBORN EVALUATION — The approach to postnatal diagnostic evaluation for congenital Zika virus infection

may vary depending on available resources; where necessary, the approach outlined in the following sections may

Fetal microcephaly (three standard deviations below the mean for gestational age), intracranial calcifications,

and/or ventriculomegaly, regardless of maternal laboratory test results for Zika virus infection

●

Positive or inconclusive maternal laboratory test results for Zika virus infection●

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Diagnostic criteria for congenital infection — Congenital infection is defined as the presence of Zika virus RNA

in any of the samples collected, including amniotic fluid, placenta, umbilical cord, newborn serum, or newborn CSF

[62]. In addition, congenital infection may be established by the presence of Zika virus IgM antibodies in newborn

serum or CSF, with confirmatory neutralizing antibody titers that are ≥4-fold higher than dengue virus neutralizingantibody titers. Test results are inconclusive if Zika virus neutralizing antibody titers are


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If newborn cerebrospinal fluid (CSF) is obtained for any reason, CSF testing for Zika virus RNA (via RT-PCR) is

appropriate [64].

PREVENTION — There is no vaccine for prevention of Zika virus infection.

Pregnant women — To protect against Zika virus infection, pregnant women should:

In addition, pregnant women and clinicians should be aware that Zika virus is transmissible via blood products and

organ or tissue transplantation [71,72]. Issues related to donor screening are discussed separately. (See "Blood

donor screening: Medical history", section on 'Zika virus' and "Blood donor screening: Laboratory testing".)

Breastfeeding women — Breastfeeding women should take the precautions described above. Transmission of

Zika virus through breastfeeding has not been described, although the virus has been detected in breast milk.

Some have recommended that women continue to breastfeed [10,73,74]. Thus far, no developmental

complications have been observed in otherwise healthy children with postnatal Zika virus infection or exposure

[75,76].

Women planning pregnancy — There is no evidence that women who have had a prior Zika virus infection are at

risk of birth defects in future pregnancies. The United States Centers for Disease Control and Prevention (CDC)

recommends that women who have had a Zika virus infection should wait at least eight weeks after symptom

onset before attempting conception [77].

Outside areas of Zika virus mosquito transmission, the CDC has suggested that men with symptomatic Zika virus

infection (confirmed or suspected) wait at least six months before having unprotected sex and that asymptomatic

men with Zika virus exposure (via travel to mosquito transmission areas or sexual contact) wait at least eight

weeks before unprotected sex [78,79]. (See "Zika virus infection: An overview", section on 'Sexual transmission' .)

diagnostic of infection.

If the RT-PCR is negative and the mother is ≥4 days after the onset of symptoms, check Zika virus

immunoglobulin (Ig)M and neutralizing antibody titers. A positive test is presumptive of infection.

If the newborn is symptomatic and the mother is asymptomatic, check maternal Zika virus IgM and

neutralizing antibody titers.

●

Avoid travel to areas with mosquito transmission of Zika virus – Given an association between Zika

virus exposure during pregnancy and congenital microcephaly, pregnant women should avoid or consider

postponing travel to areas below 6500 feet (2000 meters) where mosquito transmission of Zika virus is

ongoing, unless the need for travel is essential [11,66-70].

●

The geographic distribution of Zika virus infection is discussed further elsewhere. (See "Zika virus infection:

An overview", section on 'Geographic distribution'.)

Updates regarding the geographic distribution of Zika virus may be viewed at the United States Centers for

Disease Control and Prevention website and the Pan American Health Organization/World Health

Organization website.

Adhere to mosquito protective measures (see "Zika virus infection: An overview", section on 'Mosquito

protection'). Use of EPA-approved insect repellants in pregnancy has no known harmful effects if used

according to directions. (See "Prevention of arthropod and insect bites: Repellents and other measures",

section on 'DEET'.)

●

Adhere to measures (abstinence or condoms) to protect from sexual transmission – Risk of sexual

transmission (vaginal, oral, anal), including the duration of risk, is reviewed separately. (See "Zika virus

infection: An overview", section on 'Sexual transmission' .).

●

Adhere to standard infection precautions. (See 'Nosocomial transmission' above.)●

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'Asymptomatic women with possible but not ongoing exposure to Zika virus' above.)

Following nonrecurrent exposure, asymptomatic pregnant women should have Zika virus IgM and

neutralizing antibody titers checked 2 to 12 weeks after the exposure.

•

For women with ongoing exposure, Zika virus IgM and neutralizing antibody titers are warranted at the

initiation of prenatal care. A positive test is diagnostic of infection. If the initial test is negative and

performed in the first or early second trimester, repeat testing at 18 to 20 weeks.

•

We agree with the International Society of Ultrasound in Obstetrics and Gynecology (ISUOG) interim

guidance on ultrasound for Zika virus infection in pregnancy, which recommends a baseline ultrasound

examination for women with Zika virus exposure and symptoms, positive serology or proven Zika virus

infection, or exposure and/or symptoms without positive serology results.

●

The baseline examination should include routine biometry to detect microcephaly and assessment for

intracranial calcifications and other abnormalities, which may be present without microcephaly.

If the baseline examination is normal, serial ultrasound examinations are repeated every four to six weeks, if

possible. (See 'Ultrasonography' above.)

We suggest offering amniocentesis to women with either of the following (see 'Amniocentesis' above):●

Fetal microcephaly (three standard deviations below the mean for gestational age), intracranialcalcifications, and/or ventriculomegaly, regardless of maternal laboratory test results for Zika virus

infection

•

Positive or inconclusive maternal laboratory test results for Zika virus infection•

Zika virus RT-PCR in amniotic fluid is diagnostic of fetal viral exposure but not predictive of outcome.

All newborns who warrant Zika virus laboratory testing should be evaluated within 24 hours of birth. These

infants include (see 'Laboratory evaluation' above):

●

Newborns with microcephaly or intracranial calcifications born to women with Zika virus exposure•

Newborns of mothers with positive or inconclusive laboratory test results for Zika virus infection•

The extent of newborn clinical evaluation depends on whether the newborn has had no exposure to Zika

virus, possible exposure to Zika virus, or findings suggestive of infection (table 3). (See 'Clinical evaluation

and follow-up of newborns' above.)

●

If the mother had relevant epidemiologic exposure within two weeks of delivery and the mother or newborn is

symptomatic, maternal and newborn laboratory testing are indicated. (See 'Evaluation of women and

newborns with peripartum Zika virus exposure' above.)

●

There is no specific treatment for Zika virus infection, and there is no vaccine for prevention. (See

'Prevention' above.)

●

To protect against Zika virus infection, pregnant women should (see 'Pregnant women' above):●

Avoid travel to areas with known mosquito transmission of Zika virus•

Adhere to mosquito protective measures•

Adhere to measures to protect from sexual transmission of Zika virus•

Adhere to recommendations regarding blood donation•

Adhere to recommendations for standard infection precautions•

Women with Zika virus exposure may breastfeed. Transmission of Zika virus through breastfeeding has not

been described, although the virus has been detected in breast milk. (See 'Breastfeeding women' above.)

●

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65. Centers for Disease Control and Prevention. Questions and Answers for Healthcare Providers Caring for Infants and Children with Possible Zika Virus Infection. http://www.cdc.gov/zika/hc-providers/qa-pediatrician.html (Accessed on February 22, 2016).

66. Centers for Disease Control and Prevention. CDC Newsroom: CDC adds countries to interim travelguidance related to Zika virus. http://www.cdc.gov/media/releases/2016/s0122-zika-travel-guidance.html(Accessed on January 25, 2016).

67. European Centre for Disease Prevention and Control. Rapid Risk Assessment: Zika virus disease epidemic:Potential association with microcephaly and Guillain-Barre syndrome (first update), 21 January 2016. ECDC,Stockholm 2016. http://ecdc.europa.eu/en/publications/Publications/rapid-risk-assessment-zika-virus-first-update-jan-2016.pdf (Accessed on January 26, 2016).

68. World Health Organization. WHO statement on the 2nd meeting of IHR Emergency Committee on Zika virus

and observed increase in neurological disorders and neonatal malformations.http://www.who.int/mediacentre/news/statements/2016/2nd-emergency-committee-zika/en/ (Accessed onMarch 09, 2016).

69. Centers for Disease Control and Prevention. CDC issues advice for travel to the 2016 Summer OlympicGames. http://www.cdc.gov/media/releases/2016/s0226-summer-olympic-games.html (Accessed onFebruary 29, 2016).

70. Cetron M. Revision to CDC’s Zika Travel Notices: Minimal Likelihood for Mosquito-Borne Zika VirusTransmission at Elevations Above 2,000 Meters. MMWR Morb Mortal Wkly Rep 2016.http://www.cdc.gov/mmwr/volumes/65/wr/mm6510e1er.htm (Accessed on March 14, 2016).

71. Musso D, Nhan T, Robin E, et al. Potential for Zika virus transmission through blood transfusiondemonstrated during an outbreak in French Polynesia, November 2013 to February 2014. Euro Surveill 2014;

19.72. Centers for Disease Control and Prevention. Zika virus: Transmission.

http://www.cdc.gov/zika/transmission/index.html (Accessed on February 03, 2016).

73. Pan American Health Organization. PAHO Statement on Zika Virus Transmission and Prevention.http://www.paho.org/hq/index.php?option=com_content&view=article&id=11605%3A2016-paho-statement-on-zika-transmission-prevention-&catid=8424%3Acontent&lang=en (Accessed on January 27, 2016).

74. World Health Organization. Breastfeeding in the context of Zika virus: Interim guidance, 25 February 2016.http://apps.who.int/iris/bitstream/10665/204473/1/WHO_ZIKV_MOC_16.5_eng.pdf?ua=1 (Accessed onFebruary 25, 2016).

75. Centers for Disease Control and Prevention. Question and Answers: Zika virus infection (Zika) andpregnancy. http://www.cdc.gov/zika/pregnancy/question-answers.html (Accessed on February 05, 2016).

76. Karwowski MP, Nelson JM, Staples JE, et al. Zika Virus Disease: A CDC Update for Pediatric Health CareProviders. Pediatrics 2016.

77. Centers for Disease Control and Prevention. Questions and Answers for Healthcare Providers Caring for Pregnant Women and Women of Reproductive Age with Possible Zika Virus Exposure.http://www.cdc.gov/zika/hc-providers/qa-pregnant-women.html (Accessed on April 15, 2016).

78. Petersen EE, Polen KN, Meaney-Delman D, et al. Update: Interim Guidance for Health Care ProvidersCaring for Women of Reproductive Age with Possible Zika Virus Exposure - United States, 2016. MMWRMorb Mortal Wkly Rep 2016; 65:315.

79. Oster AM, Brooks JT, Stryker JE, et al. Interim Guidelines for Prevention of Sexual Transmission of ZikaVirus - United States, 2016. MMWR Morb Mortal Wkly Rep 2016; 65:120.

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Topic 107211 Version 2.0


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GRAPHICS

Zika virus infection: Reports of clinical findings of infants and

fetuses

Citation Cases Imaging findings

Clinical findings

and/or laboratory

findingsBrasil P et al,

2016

88 pregnant

women

Fetal abnormalities seen in

29 percent of 42 US

performed (US performed

at 20 to 40 weeks).

Microcephaly, cerebral

calcifications,

ventriculomegaly, IUGR,

cerebellar and/or vermis

agenesis, mega cisterna

magna, oligohydramnios,abnormal middle cerebral

artery Doppler.

Fetal deaths (at 36 and 38

weeks of gestation).

Schuler-Faccini L

et al, 2016

35 infants with

microcephaly

CT and transfontanellar

cranial US performed;

findings included:

Brain calcifications,

mainly in the

periventricular,

parenchymal, and

thalamic areas and inthe basal ganglia.

Ventricular

enlargement

secondary to

cortical/subcortical

atrophy.

(Further study pending.)

Martines RB et al,

2016

Four infants; two

with

microcephaly who

died within 20hours of birth,

and two fetal

losses

(miscarriages at

11 and 13

weeks)

(None performed.) Placenta and infant brain

positive for Zika viral RNA

and antigens.

Mlakar J et al,

2016

One pregnancy

termination at 29

weeks

US at 29 weeks

demonstrated microcephaly

and intracranial

Zika virus detected in brain

via reverse-transcription

PCR testing and EM.

[1]

[2]

[3]

[4]


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calcifications; an earlier US

performed during the

second trimester did not

detect any abnormalities.

Calvet G et al,

2016

Two pregnant

women with

symptoms of Zika

virus infection in

first trimester

US at 22 weeks showed

microcephaly in both cases.

Amniotic fluid obtained at

28 weeks demonstrated

Zika virus RNA; Zika virus

RNA was not detectable in

blood or urine in either

case.

Sarno M et al,

2016

One stillbirth at

32 weeks

US in the second and third

trimesters demonstrated

severe microcephaly,

hydranencephaly,

intracranial calcifications,

destructive lesions of

posterior fossa, and hydrops

(hydrothorax, ascites,

subcutaneous edema).

Hydrops fetalis,

microcephaly, and

hydranencephaly.* Zika

virus RNA was detectable in

central nervous system

tissues and amniotic fluid.

Driggers RW et al,

2016

One maternal

infection at 11

weeks;

pregnancy

termination at 21

weeks

Fetal head circumference

decreased from the 47 to

24 percentile between 16

and 21 weeks of gestation.

Ventriculomegaly, cortical

thinning, hypoplastic corpus

callosum.

Zika virus RNA was

detected in maternal serum

at 16 and 21 weeks. Fetal

brain demonstrated diffuse

cerebral cortical thinning

and Zika virus was detected

by RNA and culture.

Hazin AN et al,

2016

23 infants with

microcephaly

CT findings:

Intracranial

calcifications (all

cases) mainly in

frontal and parietal

lobes; often at the

corticomedullary

junction.

Ventriculomegaly (all

cases); severe in

approximately half.

Global hypogyration of

the cerebral cortex(all cases); severe in

more than three-

fourths.

Abnormal white

matter hypodensity

(in all cases).

CSF was positive for Zika

virus IgM in seven out of

seven cases.

de Fatima Vasco

Aragao M et al,

23 infants with

microcephaly

CT/MRI findings:

Intracranial

CSF was positive for Zika

virus IgM in seven cases,

[5]

[6]

[7] th

th

[8]


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2016 calcifications (junction

between cortical and

subcortical white

matter in all cases,

basal ganglia,

periventricular,

brainstem,

cerebellum).

Simplified gyralpattern and other

cortical

malformations.

Ventriculomegaly.

Hypogenetic or

hypoplastic corpus

callosum

abnormalities.

Cerebellum or

brainstem hypoplasiaand enlarged cisterna

magna.

Decreased brain

volume.

Delayed myelination.

17 cases had no data.

US: ultrasound; CT: computed tomography; PCR: polymerase chain reaction; EM: electron microscopy;

MRI: magnetic resonance imaging; CSF: cerebrospinal fluid; IgM: immunoglobulin M; IUGR: intrauterine

growth restriction.

* Hydranencephaly is the absence or partial destruction of cerebral hemispheres with cerebrospinal fluid

in the remaining cranial cavity.

References:

1. Brasil P, Pereira JP Jr, Raja Gabaglia C, et al. Zika virus infection in pregnant women in Rio de

Janeiro - Preliminary report. N Engl J Med 2 016.

2. Schuler-Faccini L, Ribeiro EM, Feitosa IM, et al. Possible association between Zika virus infection

and microcephaly - Brazil, 2015. MMWR Morb Mortal Wkly Rep 2016; 65:59.

3. Martines RB, Bhatnagar J, Keating MK, et al. Notes from the field: Evidence of Zika virus infection

in brain and placental tissues from two congenitally infected newborns and two fetal losses -

Brazil, 2015. MMWR Morb Mortal Wkly Rep 2016; 65:159.

4. Mlakar J, Korva M, Tul N, et al. Zika virus associated with microcephaly. N Engl J Med 2016;

374:951.

5. Calvet G, Aguiar RS, Melo AS, et al. Detection and sequencing of Zika virus from amniotic fluid of

fetuses with microcephaly in Brazil: a case study. Lancet Infect Dis 2016.

6. Sarno M, Sacramento GA, Khouri R, et al. Zika virus infection and stillbirths: A case of hydrops

fetalis, hydranencephaly and fetal demise. PLoS Negl Trop Dis 2016; 10:e0004517.

7. Driggers RW, Ho CY, Korhonen EM, et al. Zika virus infection with prolonged maternal viremia and

fetal brain abnormalities. N Engl J Med 2016.

8. Hazin AN, Poretti A, Di Cavalcanti Souza Cruz D, et al. Computed tomographic findings in

microcephaly associated with Zika virus. N Engl J Med 2016.

9. de Fatima Vasco Aragao M, van der Linden V, Brainer-Lima AM, et al. Clinical features and

9


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neuroimaging (CT and MRI) findings in presumed Zika virus related congenital infection and

microcephaly: retrospective case series study. BMJ 2016; 353:i1901.

Graphic 107662 Version 2.0


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Contributor Disclosures

Edward RB McCabe, MD, PhD Nothing to disclose. Martin S Hirsch, MD Nothing to disclose. Charles JLockwood, MD, MHCM Consultant/Advisory Boards: Celula [Aneuploidy screening (No current products or drugsin the US)]. Deborah Levine, MD Nothing to disclose. Vanessa A Barss, MD, FACOG Nothing to disclose.Elinor L Baron, MD, DTMH Nothing to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multi-level review process, and through requirements for references to be provided

to support the content. Appropriately referenced content is required of all authors and must conform to UpToDatestandards of evidence.

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Zika Virus Infection Evaluation of Pregnant Women and Infants