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diagnosis during the acute phase is nucleic acid amplication testing (NAAT).
However, this test may produce a false negative in the active phase, since viraemia
may be only transient. NAAT has FDA approval for emergencies where ZIKV
infection is suspected and suitable samples include serum, plasma, whole blood,
urine, and cerebrospinal or amniotic uid [8].
Quantication of IgM by serology is possible after just 7days of the patient
being symptomatic. However, the absence of IgM specic for ZIKV is not proof
that the virus is absent as the stage at which IgM begins to be synthesized varies
from patient to patient. Testing too soon may be falsely negative if the synthesis of
IgM has not yet properly begun. Likewise, a delayed test may appear falsely negative due to the immune system decreasing the synthesis of IgM as the infection
resolves. Another complication is that IgM synthesis potentially continues for a
maximum of 12weeks following ZIKV infection, and thus, a positive result may
represent acute infection or persistence of the immune response beyond the acute
phase. There is cross-reactivity with IgM specic to other aviviruses, such as yellow fever, dengue, Japanese encephalitis, and West Nile fever, which may cause
false positivity to occur. The serological tests for ZIKV are suitable for the following specimens: blood (whole, serum, or plasma) and cerebrospinal uid (CSF) [8].
If there is a suspicion that serological false positivity has occurred due to crossreaction with IgM for other aviviruses, plaque reduction neutralization tests
(PRNTs) may be used. PRNTS can quantify the levels of immunoglobulin specic
for several aviviruses, notably Zika and dengue. The CDC employs the following
criteria for test positivity: for serum, a titer of at least 10 for 90% plaque reduction,
whereas for CSF a titer of at least 2. If the titer for ZIKV neutralizing immunoglobulins is at least four times above that for other aviviruses, the diagnosis is
conrmed. PRNT can be used to distinguish ZIKV infection from other aviviruses
and can retrospectively conrm the diagnosis even if more than 3 months have
elapsed since the acute infection. However, if PRNT is employed more than 1 year
after the episode, it may be difcult to interpret the result. A study in Florida found
that 27% of cases still had raised IgM titers more than a year after the initial viral
episode, and PRNT could not differentiate Zika from dengue [8].
At the time of writing, there have been no positive NAATs for ZIKV infection in
the continental United States since September 2017, nor in other US territories since
May 2018. The low prevalence of Zika does, however, mean that false positivity of
Zika testing is more probable [8].
For cases of suspected Guillain-Barré syndrome, the recommendation of the
WHO is to employ the Brighton criteria [24].
M. Dilber et al.
11.8 Laboratory Investigations
Initial clinical diagnosis and laboratory conrmation of ZIKV infection is difcult
to achieve in a timely fashion [8].
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11.8.1 Serology
Laboratory conrmation of suspected ZIKV infection depends on detecting and
isolating viral RNA with the NAAT and is performed on serum. NAAT is most
sensitive in the rst 7days of symptoms, when the level of viraemia is elevated.
Following the rst 7days, detection of specic IgM and neutralizing immunoglobulins is possible with an ELISA assay [25]. Following a negative NAAT, IgM
serology is advised, irrespective of the timing of specimen submission to the laboratory [8].
If NAAT serology is positive less than a week after the patient becomes symptomatic, this result implies an acute ZIKV infection. A positive result, however,
needs to be conrmed by extracting RNA a second time from the specimen to repeat
the NAAT procedure. On the other hand, if both NAAT serology and IgM levels are
normal in a patient whose symptoms are of less than 1 week’s duration, ZIKV infection is unlikely [8].
IgM levels in the normal range in a patient who has been symptomatic for
between 1 week and 12days imply ZIKV is not present [8]. Where IgM levels are
equivocal, IgM serology should be performed once again or use made of PRNT testing [8]. Cases where IgM levels are raised but NAAT is negative should be investigated further using PRNT testing [8].
In patients who have previously experienced Zika or a similar avivirus, or who
have undergone vaccination, the criterion generally used to distinguish immunoglobulins specic to ZIKV from cross-reacting, other immunoglobulins, that is, a
titer at least four times higher on PRNT, does not apply [8].
Where IgM serology points to ZIKV or dengue infection, or the results are
unclear, PRNT results should be interpreted as follows [8]:
• If the PRNT titer to one particular avivirus is at least 10 and the PRNT to other
aviviruses is below 10, that particular avivirus is the likely pathogen respon-
sible for infection.
• PRNT titers that are lower than 10 show that the virus to which those immuno-
globulins are specic is not the cause of the infection.
• PRNT titers for a variety of aviviruses that are simultaneously above 10 may be
interpreted as the patient responding to a recent infection with some sort of
avivirus.
The tables that follow are based on the CDC guidance on how to interpret diagnostic tests for dengue or Zika. The guidance applies to patients who present with
characteristic clinical ndings following exposure to a source of the virus and can
be used in all patients, including those who are pregnant [8].
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M. Dilber et al.
11.9 Congenital ZIKV Infections
11.9.1 Congenital Anomalies, Including Microcephaly
Despite the general mildness of ZIKV infections, an area of signicant concern is
the occurrence of congenital anomalies caused by vertical transmission of ZIKV.A
spike in the frequency of congenital microcephaly was noted in Brazil 6 months
after an epidemic of ZIKV, the level being 20 times higher than usual. The background rate of microcephaly was 2in 10,000 live births. However, for 2015, 1248
potential cases of microcephaly were noted [14, 26], with 4810 potential cases notied in January 2016. Of the cases reported, 270 underwent diagnostic conrmation,
but in 462 cases, the criteria for microcephaly were not met [26].
A number of anomalies affecting the eyes have been linked to babies with congenital microcephaly, where fetal ZIKV was believed responsible. The anomalies
include absent foveal reex, mottled areas of pigment on the macula, chorioretinal
thinning, and hypoplasia of the optic nerve, which presents as the double-ring
sign [14].
It is important to be cautious, however, about interpreting these ndings, given
the potentially inaccurate data regarding the frequency of microcephaly in the past,
which may lead to a spurious impression that congenital abnormalities have
increased [26].
A Brazilian study dened microcephaly as a head circumference smaller than the
mean, adjusted for sex and gestational age, by a minimum of 2 standard deviations.
When 35 cases of microcephaly across the whole of Brazil and occurring between
August and October 2015 were examined in detail, it was ascertained that all the
mothers had had some degree of exposure to Zika, while pregnant, either through
residing in an affected area or by visiting there [27]. Of the 35 cases examined, 27
represented severe microcephaly occurring in isolation from any other form of congenital anomaly. It was recently reported from Brazil that ZIKV RNA was present
in amniotic uid, the placenta, or the fetus in cases involving congenital anomalies
of the nervous system [8, 26].
11.9.2 ZIKV Tests inPregnancy
Expectant mothers who present with symptoms of Zika infection and a history indicating exposure should be tested for ZIKV with molecular techniques and serology.
Serum and urine should be tested using NAAT, accompanied by serological quantication of IgM.The specimens should be gathered no later than 12 weeks after
symptoms began. Interpretation of the results of these investigations should follow
a diagnostic protocol, allowing Zika and dengue infections to be differentiated from
each other [8]. One such diagnostic protocol suitable for use in suspected cases of
congenital acquisition is the one developed by the CDC [8].
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11.9.3 Congenital ZIKV andAuditory Impairment
Congenital ZIKV infection puts the infant at risk of auditory impairment. In cases
where the initial audiological screen does not detect any abnormality, regular follow- up screening is needed, since auditory impairment may present insidiously and
gradually worsen, as is noted with other causes of congenital viral infection [28].
The most fully characterized congenital anomaly found in cases of ZIKV is
microcephaly [17, 18]. This malformation seems to mostly affect the nervous system. Imaging of the brain reveals calcied regions between the cortex and subcortex, malformed cortex, and pachygyria or agyria [17, 18, 29]. Alongside its effects
on the nervous system, there appear to be abnormalities of the eyes [30] and musculoskeletal system [31]. One Brazilian study looked at 23 newborn infants with
microcephaly who were believed to have contracted congenital ZIKV.As a result of
otoacoustic testing, 9% were found to have hearing loss, albeit this was not conrmed by other examination [29]. The diagnosis of Zika was made in these cases by
exclusion of competing diagnoses, since specic testing was not feasible due to the
circumstances of the study.
It is well known that congenital infections of various types cause auditory impairment, such as cytomegalovirus (CMV), rubella, toxoplasmosis, herpes simplex, and
syphilis. In such cases, auditory impairment generally affects both ears, is of sensorineural type, and is of very great or profound severity. In many cases, hearing loss
does not become evident at birth, but may progressively deteriorate or uctuate
[32, 33].
Fetal infection with ZIKV and auditory loss in the early years of childhood
appear to be connected. However, for this potential association to be better understood, future research will need to control for potentially confounding variables,
such as the presence of microcephaly. Furthermore, children exposed in utero to
ZIKV should be followed up for lengthy periods in order to identify auditory impairment occurring after a protracted delay [34].
The location of the neurological insult, which causes deafness following Zika
infection, is still unknown. Studies where the inner ear was imaged have failed to
note any potential structural defect. It is worth bearing in mind, nonetheless, that
there is often no apparent abnormality of the cochlea in children with auditory
impairment caused by other infections acquired in utero. Thus, it is wrong to assume
that the absence of apparent anatomical abnormality means no hearing loss will
occur. Indeed, a child who received a cochlear implant following congenital viral
infection, despite no demonstrable anatomical injury to the inner ear, was reported
to demonstrate benet. His behavior changed, with more independence-seeking,
positive responses to auditory stimuli, smiles when the device was activated, greater
interest in music, and being able to respond to sound at an intensity of 30dB [35].
The explanation for this response is that the auditory nerve and auditory pathways
of the central nervous system must have remained functional, with auditory loss
attributable to cochlear dysfunction. The same conclusion had already been proposed in a study of infants exposed in utero to ZIKV and whose auditory function
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M. Dilber et al.
was assessed by measuring otoacoustic emissions, although without a formal diagnosis being made [29, 36].
Infants who present with signs of congenitally acquired ZIKV infection should
be thoroughly assessed clinically, and appropriate investigations should be undertaken. The US CDC has published guidelines on optimal practice in managing such
patients. The usual workup includes complete physical examination, recording of
growth parameters, ongoing observation of development, and audiological screening in accordance with the advice of the American Academy of Paediatrics, which
suggests neonatal auditory function testing at the time of birth. The ideal technique
for this purpose is automated auditory brain stem response testing [8].
Additionally, the following investigations may be valuable [8]
• Ultrasound of the central nervous system
• A complete ophthalmological assessment within the initial month of life, by a
specialist with expertise in evaluating and treating infants
• If the child passes neonatal screening by otoacoustic emissions testing, but no
other investigations were performed at that stage, automated auditory brain stem
testing should be undertaken within the initial month of life.
Involvement of a specialist with knowledge on care of infants is also
recommended.
Patients with congenitally acquired Zika syndrome should also be closely followed up for potential complications, and any such issues call for timely investigation [17].
• An infant who has distressed breathing or goes into respiratory failure and been
placed on ventilatory support may be unable to restart breathing when the venti-
latory is withdrawn, due to paralysis of the diaphragm.
• Dysphagia or choking, coughing or gasping while feeding, or very slow feeding
is indications for a swallowing assessment.
• If there are any indications of raised intracranial pressure (such as raised head
circumference, irritability, or vomiting), postnatal hydrocephalus should be sus-
pected. Imaging of the central nervous system is required.
Care should be taken that such children receive preventative interventions routinely, are fully vaccinated, and are under regular pediatric follow-up. The advice
about performing auditory brain stem response (ABR) testing has changed. It used
to be recommended that ABR measurement be repeated at age 4–6months in children with congenital ZIKV infection. The assumed low probability of developing
auditory impairment after a delay in such cases makes this test unnecessary.
Furthermore, infants who lack evidence of congenital ZIKV infection, but where
there is laboratory conrmation of maternal infection or a history of exposure to an
area where Zika is endemic, require careful follow-up in a pediatric clinic. If the child
subsequently shows any indications of congenital Zika syndrome, he or she should be
referred to a subspecialty clinic to advise on further assessment and treatment [17].
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11.10 Pharmacotherapy
In the rst instance, bed rest and plentiful uids are recommended. If the patient
becomes pyrexial or complains of pain, paracetamol may be administered. Itching
and an exanthem are treated with an antihistamine. Nonsteroidal anti-inammatory
drugs (NSAIDs) should not be administered if the diagnosis of Zika has not been
conrmed. The reason for this avoidance is that these drugs may cause hemorrhage
in patients with dengue and is a risk factor for Reye’s syndrome in children [37].
According to WHO guidelines, patients who develop Guillain-Barré syndrome
should receive high level supportive care. There should be regular physical examination of the nervous system, checking of vital signs and careful monitoring of
breathing, since respiratory failure may supervene or a thrombotic event occur. In
cases where the symptoms swiftly deteriorate or where the patient can no longer
walk, immunoglobulin treatment should be administered intravenously or plasma
exchange performed [24]. Specialist involvement is required if ZIKV occurs in
pregnancy or where the patient is a child with congenital Zika syndrome [8].
No medications are specically licensed by the FDA for the treatment of ZIKV
infections. There are, however, several drugs currently being evaluated as potential
treatments for Zika [2, 10, 38]. The agents currently being developed either directly
inhibit various stages in viral replication or inhibit cellular processes involved in the
viral life cycle. Examples of the former are nucleoside analogues and polymerase
inhibitors, including those acting on RNA-dependent RNA polymerase, such as
sofosbuvir and galidesivir, while examples of the latter are inhibitors of purine or
pyrimidine synthesis or drugs that interfere with viral entry into cells. There have
been encouraging results so far from a number of studies, both invitro and invivo.
There are some agents that are already licensed by the FDA for other indications that
may be of benet in combating ZIKV.Examples include interferon (which exhibits
antiviral actions invitro), Chloroquine and Meoquine (licensed in treating malaria
and with low teratogenicity potential throughout pregnancy), Ivermectin (an antiviral), and Azithromycin (licensed as an antibacterial but may also reduce infectivity).
These agents are potentially effective against ZIKV, but further research is needed to
establish how safe and efcacious they are. The development of anti- Zika medications faces the difculties that any agent needs to have the ability to cross both the
blood–brain barrier and the placenta but have low teratogenicity. One further constraint is that any new agent needs to be affordable by patients who are mostly found
in low- or middle-income countries within the tropics or subtropics [39].
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18. Schuler-Faccini L, Ribeiro EM, Feitosa IML, etal. Possible association between Zika virus
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19. Weaver SC, Costa F, Garcia-Blanco MA, Ko AI, Ribeiro GS, Saade G, etal. Zika virus: history, emergence, biology, and prospects for control. Antivir Res. 2016;130:69–80.
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Hearing Loss inNeonates Exposed
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toHerpes Simplex Virus
GülsümİclalBayhan, AyşeEnginArısoy,
andArmandoG.Correa
12.1 Introduction
Although neonatal herpes simplex virus (HSV) infections primarily develop due to
transmission of the virus from the mother’s genital tract during delivery, it can also
develop as a result of viremia in the intrauterine period [1]. The essential factor in
determining mother-to-child transmission is the classication of the infection in the
mother. Compared to the risk of transmission from mother with primary infection,
transmission from mother to newborn with recurrent infection is very low; the presence of antibodies in the mother is a protective factor for the newborn [1]. The
absence of HSV symptoms and signs in the mother does not exclude the diagnosis
of congenital HSV because even if the mother is asymptomatic, virus shedding may
continue [2, 3].
Symptomatic fetal HSV is an infrequent clinical entity, while it can cause signicant morbidity and mortality [4, 5]. A high index of suspicion is required for early
diagnosis, especially in the absence of skin lesions.
12
G. İ. Bayhan (*)
Section of Pediatric Infectious Diseases, Ankara City Hospital, Ankara Yıldırım Beyazıt
University, Ankara, Türkiye
e-mail: gibayhan@gmail.com
A. E. Arısoy
Division of Neonatology, Department of Pediatrics, Faculty of Medicine, Kocaeli University,
Kocaeli, Türkiye
e-mail: arisoyaengin@yahoo.com
A. G. Correa
Division of Academic General Pediatrics, Department of Pediatrics, Baylor College of
Medicine, and Section of International and Destination Medicine, Texas Children’s Hospital,
Houston, TX, USA
e-mail: acorrea@bcm.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_12
163
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G. İ. Bayhan et al.
12.2 Etiology
Herpes simplex viruses are enveloped, double-stranded DNA viruses of the
Herpesviridae family and are highly prevalent among humans. There are two types
of HSV: HSV-1 and HSV-2 [6]. Herpes simplex virus-1 is usually related to labial
herpes and HSV-2 to genital herpes. However, either virus can be present in areas
other than their familiar territories [6, 7]. Herpes simplex virus-2 is the leading
cause of HSV infection in newborns, while HSV-1 can also occur after the neonatal
period [8, 9].
12.3 Epidemiology andTransmission
The incidence of neonatal HSV infection is reported as 1in 3200–10,000 live births
[10]. This wide range in incidence is due to the prevalence of genital HSV infection
in different parts of the world. Since 2000, an increasing incidence of severe neonatal HSV infection has been reported [11]. Herpes simplex viruses are most commonly transmitted by contact at birth from the maternal genital tract; however, they
can also be transmitted by ascending route from ruptured or intact amniotic membranes. More rarely, HSV can be transmitted by the transplacental intrauterine
route [6].
Despite the general opinion that HSV-1 causes oral infections and HSV-2 causes
genital infections, HSV-1 is the cause of 40% of genital herpes cases in some populations. Both HSV-1 and HSV-2 can infect the newborn [4, 10, 12]. It has been
reported that congenital HSV infection develops not only in association with genital
HSV infection but also due to the maternal viremia caused by HSV gingivostomatitis [13].
12.4 Pathogenesis andImmunity
Herpes simplex virus penetrates the human body through the oral, genital, or conjunctival mucosa or cutaneous injury, infecting the sensory nerve endings. Following
primary infection, HSV migrates to the dorsal root ganglion in a retrograde manner
via the axonal bers. Then HSV remains dormant in the sensory ganglia with reactivation potential [2]. Herpes simplex virus-1 usually remains dormant in the trigeminal and/or sacral ganglions, while HSV-2 usually remains dormant in the sacral
ganglion [1]. After the latent period, HSV-1 and HSV-2 may reactivate. Reactivation
can cause asymptomatic infection causing only viral shedding or recurrent symptomatic disease. Genital infection caused by HSV-2 recurs more frequently than
caused by HSV-1 [6].
Denitions of primary, non-primary rst-episode, and reactivation infection for
the different types of maternal infection are used. In primary infection, the mother
has experienced a recent infection with HSV-1 or HSV-2 without a history of being
infected with the other type. In non-primary rst-episode infection, the mother is
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