Two Infants with Presumed Congenital Zika Syndrome, Brownsville, Texas, USA, 2016–2017

Abstract

Since 2007, Zika virus has spread through the Pacific Islands and the Americas. Beginning in 2016, women in Brownsville, Texas, USA, were identified as possibly being exposed to Zika virus during pregnancy. We identified 18 pregnant women during 2016–2017 who had supportive serologic or molecular test results indicating Zika virus or flavivirus infection. Two infants were evaluated for congenital Zika syndrome after identification of prenatal microcephaly. Despite standard of care testing of mothers and neonates, comparative results were unreliable for mothers and infants, which highlights need for clinical and epidemiologic evidence for an accurate diagnosis. A high index of suspicion for congenital Zika syndrome for at-risk populations is useful because of current limitations of testing.

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Full text

Since 2007, Zika virus has spread through the Pacic Is-
lands and the Americas. Beginning in 2016, women in
Brownsville, Texas, USA, were identied as possibly being
exposed to Zika virus during pregnancy. We identied 18
pregnant women during 2016–2017 who had supportive se-
rologic or molecular test results indicating Zika virus or a-
vivirus infection. Two infants were evaluated for congenital
Zika syndrome after identication of prenatal microcephaly.
Despite standard of care testing of mothers and neonates,
comparative results were unreliable for mothers and infants,
which highlights the need for clinical and epidemiologic evi-
dence for an accurate diagnosis. A high index of suspicion
for congenital Zika syndrome for at-risk populations is use-
ful because of current limitations of testing.
Zika virus is an arbovirus and avivirus transmitted by
Aedes aegypti and Ae. albopictus mosquitoes, vec-
tors that also transmit other arboviruses, such as dengue
virus and chikungunya virus. Zika virus was discovered in
the Zika Forest of Uganda in 1947 in rhesus and macaque
monkey populations (http://www.who.int/emergencies/zi-
ka-virus/timeline/en/). Until 2007, only 14 cases of human
infection were reported in Asia and Africa (1). However,
outbreaks of infection with Zika virus occurred on Yap Is-
land, Micronesia, in 2007 and in French Polynesia in 2013,
aecting ≈31,000 persons (2). Zika has spread rapidly in
the Americas since 2015 and has been associated with
hundreds of conrmed microcephaly cases in Brazil, Co-
lombia, and Puerto Rico (2–7). In April 2016, the Centers
for Disease Control and Prevention (CDC) conrmed evi-
dence that supported the causal relationship between Zika
virus infection prenatally and microcephaly, in addition to
other brain abnormalities, and described what has become
known as congenital Zika syndrome (2,8–11).
In the United States since June 2017, there have been
5,335 travel-associated cases and 227 locally transmitted
cases of infection with Zika virus in southern Florida and
Brownsville, Texas (4). A total of 2,364 pregnant women
(972 completed pregnancies) with laboratory evidence of
Zika virus infection in the United States have been report-
ed to CDC; the Zika-related birth defect risk among these
women has been estimated to be 1 in 10 women (12,13).
In November 2016, local transmission was conrmed by
health authorities in Brownsville, and screening for Zika
virus in asymptomatic pregnant patients and testing for
Zika virus in symptomatic patients began (14,15). This
screening was quickly followed in December 2016 by iden-
tication of pregnant women with supportive laboratory
evidence of Zika virus infection in the Brownsville area.
Cases
Eighteen cases of possible Zika virus infection in pregnant
women were identied by screening and testing of symp-
tomatic patients living in Brownsville during December
2016–May 2017. Twelve case-patients had laboratory
evidence of Zika virus infection: positive PCR results for
serum (8), serum and urine (3), or placenta (1). One case-
patient had plaque reduction neutralization test (PRNT)
results consistent with recent Zika virus infection, and 5
case-patients had PRNT results consistent with recent a-
vivirus infection. Fifteen women had delivered their babies
as of July 14, 2017; the remaining women had estimated
dates of delivery through early 2018. Two pregnant women
in this cohort had ndings consistent with congenital Zika
syndrome. Neonatal and infant follow-up is ongoing for
women who delivered up to this point. We report the prena-
tal and neonatal outcomes for 2 infants who had congenital
Zika syndrome.
Case-Patient 1
Case-patient 1 was born to a 23-year-old woman (G1P1)
who spent the rst 4 months of her pregnancy in Matamoros,
Mexico. She received prenatal Zika testing while residing
there, and results were negative. She moved to Browns-
ville, where she received prenatal care at 28 weeks’
gestation. She was screened for Zika virus by serum IgM
Two Infants with Presumed
Congenital Zika Syndrome,
Brownsville, Texas, USA, 2016–2017
Ashley Howard,1 John Visintine,1 Jaime Fergie,1,2 Miguel Deleon1
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 24, No. 4, April 2018 625
1All authors contributed equally to this article.
2Current aliation: Texas A&M University College of Medicine,
Bryan, Texas, USA.
Author aliation: Driscoll Children’s Hospital, Corpus Christi,
Texas, USA
DOI: https://doi.org/10.3201/eid2404.171545

SYNOPSIS
testing; results were negative. She was referred for maternal
fetal medicine at 36 weeks’ gestation because of suspected
microcephaly. The fetus was found to have microcephaly:
head circumference (HC) 251 mm, which was 5 SD below
the mean value. The mother denied having any symptoms
of Zika virus infection (rash, fever, malaise, arthralgia, or
conjunctivitis). At 37 weeks’ gestation, transvaginal fetal
neuroimaging was performed; results showed calcications
in the cortical white matter–gray matter junction, but no
calcications were observed in the thalami (Figure 1, panel
C). On the basis of ultrasonographic ndings, a maternal
repeat Zika virus IgM test was performed and showed a
positive result at 37 weeks’ gestation. PRNT results were
consistent with recent avivirus infection (Zika and den-
gue PRNT titers >1,280) (16). A TORCH (toxoplasmosis,
rubella cytomegalovirus, herpes simplex virus, and HIV)
panel did not show evidence of recent infections, and re-
sults of a cell-free fetal DNA screening were negative.
An elective primary cesarean delivery was performed
at 39 weeks’ gestation. APGAR scores for the baby were
9 at 1 min and 9 at 5 min. At initial examination, the neo-
nate had a vesicular generalized rash, overriding sutures,
and microcephaly. The initial HC of the infant was 29 cm,
which was 2.63 SD below the mean value for term male
newborns. Birthweight was 2.62 kg (4.76 percentile), and
birth length was 45 cm (3.2 percentile). On further ex-
amination, mild craniofacial disproportion with narrow
and laterally depressed frontal bone and mild retrognathia
was seen. No limb contractures were observed (Figure 1,
panel A).
626 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 24, No. 4, April 2018
Figure 1. Term male infant (case-patient 1) with presumed congenital Zika syndrome, Brownsville, Texas, USA, 2016–2017. A)
Microcephaly on the day of birth. Head circumference was 29 cm, which is 2.63 SDs below the mean value for term male newborns.
Craniofacial abnormalities present are mild narrow and laterally depressed frontal bone and mild retrognathia. B) Generalized pustular
melanosis rash. C) Prenatal transvaginal ultrasonographic (midsagittal plane) image at 37.2 weeks’ gestation, showing calcications
at the gray matter–white matter junction. Head circumference was 251 mm. D) Sagittal T2 magnetic resonance image on day of life 1,
showing severe microcephaly, frontal lobe polymicrogyria, and hypoplastic corpus callosum. E) Axial T2 magnetic resonance image
on day of life 1, showing severely hypoplastic cerebral hemispheres and corpus callosum. Symmetric frontal lobe polymicrogyria and
simplied gyral pattern in the occipital and temporal lobes are present. F) Axial computed tomography image on day of life 3, showing
small bilateral brain hemispheres and hypogyration of the cerebral cortex. Areas of punctate calcication located at the subcortical and
gray matter–white matter junctions of the frontal, parietal, and occipital lobes are present. A, anterior; AFL, anterior left; FPL, posterior
left; HAR, anterior right; L, left; LHA, left anterior; P, posterior; PHR, posterior right; R, right; RFP, right posterior.

Presumed Congenital Zika Syndrome, Texas, USA
The newborn was transferred to the neonatal intensive
care unit (NICU) at Driscoll Children’s Hospital (Corpus
Christi, TX, USA) on day 1 of life. Because of a general-
ized vesicular rash, concern for herpes simplex virus in-
fection prompted treatment with acyclovir for the rst 2
days of life. The rash was diagnosed as neonatal pustular
melanosis; it faded by day 1 of life and disappeared by day
2 of life (Figure 1, panels A, B). Zika virus testing was
performed on day 1 of life. Zika virus PCRs were per-
formed for serum, urine, and cerebrospinal uid (CSF); all
results were negative. Zika virus IgM testing was ordered
for serum and CSF, but the test for CSF was not performed
by the state laboratory because of a negative PCR result
for CSF. Serum was positive for Zika virus IgM, which
is consistent with probable congenital Zika virus infection.
Results of placental testing by reverse transcription PCR
for the Zika virus nonstructural protein 5 gene were posi-
tive. Test results for dengue and chikungunya viruses were
negative. Additional TORCH testing was performed, and
results were negative for herpes simplex virus, cytomega-
lovirus, syphilis, HIV, Toxoplasma spp., and parvovirus.
The neonate passed the initial newborn hearing screen
and had a pediatric ophthalmologic examination on day 1
of life, during which a small left subconjunctival hemor-
rhage was identied (17,18). Initial head ultrasonography
on day 1 of life showed parietal calcications and pachygy-
ria. Follow-up magnetic resonance imaging showed frontal
lobe polymicrogyria, bilateral dystrophic calcications, and
severe microcephaly (Figure 1, panels D, E). Computerized
tomography was performed on day 3 of life for better charac-
terization of calcications and showed bilateral small brain
hemispheres with hypogyration of the cerebral cortex. Areas
of punctate calcication were observed at the subcortical and
gray matter–white matter junctions of the frontal, parietal,
and occipital lobes (Figure 1, panel F). A prominent occipi-
tal bone was observed with overlapping of the region of the
lambdoid suture and prominent bony ridging at the region
of the coronal sutures. Partial fusion of the inferior aspect
of coronal sutures and asymmetric closure of the temporal
sutures were also observed. There was no ventriculomegaly.
The infant was in the NICU for 9 days. During that
time, the infant had poor feeding and required an orogastric
tube to assist with feeds until day 7 of life. The CDC rec-
ommended electroencephalogram (EEG) testing because
of new information concerning development of seizures
in 30%–50% of infants with congenital Zika syndrome;
the EEG result was unremarkable (19,20). Microarray and
microcephaly gene panel were tested; all showed negative
results. A screening echocardiogram showed results con-
sistent with reference transitional neonatal cardiac changes.
Results of thyroid function testing, complete blood count,
and a comprehensive metabolic panel (CMP) were all with-
in reference ranges.
The infant was discharged on day 9 of life. At
discharge, he had an HC of 30 cm, which was 3.16
SD below the mean value for term male newborns with
microcephaly.
Case-Patient 2
Case-patient 2 was born to an 18-year-old woman (G1P1)
who lived in Brownsville. She reported weekly travel to
Matamoros, Mexico, during the early stages of her preg-
nancy. She denied any viral symptoms of rash, fever, mal-
aise, arthralgia, or conjunctivitis. She was screened by her
obstetrician for Zika virus at 23 weeks’ gestation by a PCR
for serum; results were positive. Results were negative for
a Zika virus PCR for urine and serum Zika virus IgM. At 28
weeks’ gestation, fetal ultrasonography was performed for
growth and anatomy evaluation. The fetus had microceph-
aly and was referred for maternal fetal medicine evaluation.
The HC of the fetus was 203 mm at 29 weeks’ gestation,
which was 4−5 SD below the mean value. Coarse calci-
cations were observed in the basal ganglia and thalami by
transabdominal and transvaginal fetal neuroimaging (Fig-
ure 2, panels C, D). The TORCH panel did not show evi-
dence of recent infections.
A planned primary cesarean delivery was performed
at 39 weeks’ gestation. APGAR scores were 9 at 1 min
and 9 at 5 min. At initial examination, the neonate had a
prominent sagittal ridge, overriding sutures, and severe
microcephaly (Figure 2, panel A). Initial head circumfer-
ence was 26.5 cm, which was 6.23 SD below the mean
value for term female newborns. Birthweight was 2.39
kg (2.21 percentile), and birth length was 41.5 cm (<0.01
percentile). Further examination showed excess scalp
skin (Figure 2, panel B) and craniofacial disproportion
with narrow and laterally depressed frontal bone (Figure
2, panel A). Upper limb contractures were also observed
(Figure 2, panel A).
The patient was transferred to the NICU at Driscoll
Children’s Hospital on day 1 of life, and Zika virus testing
was performed the same day. Results of Zika virus PCRs
were negative for serum, urine, and CSF. IgM serum was
negative for Zika virus. Testing for Zika virus IgM was or-
dered for serum and CSF, but the test for CSF was not per-
formed by the state laboratory because of a negative PCR
result for CSF. Test results were negative for dengue virus
and chikungunya virus. Additional TORCH testing was
performed, and results were negative for CMV, syphilis,
HIV, Toxoplasma spp., and parvovirus. The infant passed
the initial newborn hearing screen and had a pediatric oph-
thalmology examination performed on day 1 of life; no eye
anomalies were identied (17,18).
Initial ultrasonography of the head on day 1 of life
could not be completed because the anterior fontanelle
was too small. Magnetic resonance imaging showed
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 24, No. 4, April 2018 627

SYNOPSIS
microcephaly with enlarged extraaxial spaces, large bilat-
eral parenchymal cysts in the posterior parietal and occipi-
tal lobes, an overall smooth gyral pattern, dysgenesis of
the corpus callosum, and 5 small bilateral choroid plexus
cysts (Figure 2, panels E, F).
The infant was in the NICU for 28 days, during which
daily examinations showed intermittent tremors, hyperto-
nia, and an exaggerated Moro reex. Upper bilateral wrists
continued to be contracted in the exed and ulnar deviated
positions and required physical therapy intervention. The
infant had to be fed by an orogastric tube because of poor
feeding until she was able to be transitioned to ad libitum
feeds on day 25 of life. Because of excessive irritability
and crying, the infant was given phenobarbital on day 16 of
life. In addition, an EEG was performed because of tremor
activity; results were uneventful. Screening echocardio-
gram results were consistent with standard transitional
neonatal cardiac changes. Abdominal ultrasonography was
performed and results were unremarkable. Results were
negative for a microarray and microcephaly gene panel
testing. Results of thyroid function testing, complete blood
count, and a comprehensive metabolic panel were all with-
in reference ranges.
The infant was discharged on day 27 of life. She had
an HC of 27 cm, which was 7.42 SD below the mean value
for term females.
Discussion
Making a diagnosis of congenital Zika syndrome is chal-
lenging, despite testing and imaging available in a well-
resourced area, such as the United States, which empha-
sizes the role of clinical and epidemiologic circumstances
as critical pieces for a presumptive diagnosis. Diagnosis is
needed not only epidemiologically, but also longitudinally
628 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 24, No. 4, April 2018
Figure 2. Term female infant (case-patient 2) with presumed congenital Zika syndrome, Brownsville, Texas, USA, 2016–2017. A)
Microcephaly on the day of birth. Head circumference was 26.5 cm, which is 6.23 SDs below the mean value for term females.
Craniofacial disproportion with narrow and laterally depressed frontal bone is seen. Upper wrist contractures are present, more
apparent on the right, with ulnar deviation. B) Redundant scalp skin with multiple rugae. C) Transabdominal ultrasonography image
of the axial transthalamic plane at 37 weeks’ gestation, showing coarse bilateral calcications in the thalami. D) Transvaginal
ultrasonography image of the coronal section at 37 weeks’ gestation, showing coarse calcications in the thalami. E) Sagittal T2 turbo
spin echo magnetic resonance image on day of birth, showing microcephaly, dysgenesis of the corpus callosum, and a small bilateral
choroid plexus cyst. F) Axial T2 turbo spin echo magnetic resonance image on day of birth, showing microcephaly with enlarged extra-
axial spaces and a smooth gyral pattern. Large bilateral posterior parietal and occipital lobe parenchymal cysts are present. AFL,
anterior left; FLP, left posterior; HRA, right anterior; LHA, left anterior; PHR, posterior right; R, right; RFP, right posterior.

Presumed Congenital Zika Syndrome, Texas, USA
for follow-up of associated problems with congenital Zika
virus infection, which have been reported as a constella-
tion of malformations and clinical symptoms involving the
brain, craniofacial defects, nervous system, eyes, and limbs
(3,5–9,12,19–24).
Both infants reported in our case series had nd-
ings of congenital Zika syndrome (Figures 1, 2). Results
of neuroimaging performed prenatally for both infants
were consistent with the presence and degree of micro-
cephaly observed postnatally (25). Calcications identi-
ed prenatally in case-patient 1 had consistent postnatal
distribution at the subcortical white matter–gray matter
junction. Case-patient 2 had changes in the presence of
calcications seen during prenatal ultrasonography that
were not present by postnatal imaging. In addition, pre-
natal diagnosis of arthrogryposis was not made because
of spontaneous movement of all extremities on prenatal
ultrasonographic images. This limitation illustrates that
the spectrum of congenital Zika syndrome cannot be fully
assessed until further postnatal assessment and highlights
the need for advanced neuroimaging.
However, despite the neonatal diagnosis of congeni-
tal Zika syndrome, results for maternal testing were not
consistent. The rst case-patient had maternal laboratory
ndings of probable avivirus infection that was not iden-
tied until the third trimester. The rst IgM screening (at
28 weeks’ gestation) might have shown a false-negative
result, or the infection might have occurred later. How-
ever, even without denitive evidence of maternal Zika
virus infection at the time of delivery, the neonate showed
a positive result for Zika IgM in serum, and a subsequent
placental test showed a positive result, which conrmed
maternal infection.
Maternal diagnosis for case-patient 2 was conrmed
with positive PCR results for serum at 23 weeks’ gestation.
However, despite this newborn displaying more severe fea-
tures of congenital Zika syndrome postnatally (redundant
scalp skin, bilateral upper arm arthrogryposis, smaller head
size, and extrapyramidal symptoms), results of serum test-
ing for Zika virus infection were negative.
In conclusion, results for these 2 case-patients indi-
cate the complexity and challenges of screening and diag-
nostic testing for congenital Zika syndrome and illustrate
the need for clinical ndings and epidemiologic history.
We advise a high index of suspicion for congenital Zika
syndrome for at-risk populations on the basis of current
limitations of testing.
About the Author
Dr. Howard is a physician and member of the South Texas Zika
Task Force Team, Driscoll Children’s Hospital, Corpus Christi,
TX. Her primary research interests are congenital, arboviral, and
emerging infections.
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Address for correspondence: Ashley Howard, Driscoll Children’s
Hospital, 3533 S. Alameda St, Corpus Christi, TX 78411, USA; email:
ashley.howard@dchstx.org
630 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 24, No. 4, April 2018