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12 Hearing Loss inNeonates Exposed toHerpes Simplex Virus
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infected with one of the HSV virus types, mostly with HSV-2, but has antibodies
against the other type [14]. Reactivation is when the dormant virus wakes up and
results in infectious HSV on mucosal or skin surfaces as detected by the polymerase
chain reaction (PCR) test or cultures [14, 15].
The virus can be transmitted to the newborn transplacentally due to viremia during primary infection. Recurrent maternal infection can also result in congenital
HSV [15, 16]. The probability of developing congenital HSV is higher after primary
infection than reactivation or a non-primary rst episode [2, 15]. The transmission
rate from the mother to the baby is more than 50% in primary HSV infection and
can go up to 60% when the infection occurs close to birth. The transmission risk is
less than 3% in non-primary infection and less than 2% with reactivation in the rst
half of pregnancy. This variance is due to the difference in genital viral load and
maternal antibodies. The protective antibodies present in the mother may protect the
newborn and limit the disease during reactivation [17].
Less than one-third of women with a primary infection during pregnancy are
symptomatic. After the rst attack, cervical scatter can continue asymptomatic for
as long as 2months [14]. The person may be asymptomatic during reactivation;
ulcers do not constantly occur in these cases, as some present only with vaginal
discharge. Therefore, the absence of HSV symptoms and signs in the mother does
not exclude congenital HSV, and virus scatter can occur even when the mother is
asymptomatic [2, 3].
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12.4.1 Herpes Simplex Virus Transmission totheFetus
Herpes simplex virus transmission to the fetus may occur by the transplacental route
in the intrauterine period (congenital or in utero infection) or by the ascending route
in the perinatal period (perinatal infection) [5].
Congenital infection is an extremely rare condition that develops due to maternal
viremia resulting from primary HSV infection during pregnancy [11]. Congenital
HSV infection’s estimated incidence is 1in 250,000 deliveries, representing less
than 5% of neonatal HSV cases. Peripartum transmission is much more common
(85%); the neonate is exposed to the virus in the birth canal during labor. Ten percent of neonatal HSV infections are acquired postnatally [5, 8, 18, 19].
Congenital and perinatal transmitted infections have different clinical presentations [5]. Intrauterine transmission can occur due to viremia developing after oral,
genital, or skin lesions. Perinatal transmission can occur with or without ruptured
amniotic membranes. Neonatal HSV infection was also reported in infants born by
cesarean section with intact amniotic membranes. Congenital HSV infection is
more likely to result in encephalomalacia, ventriculomegaly, calcications, and
microcephaly than perinatally acquired disease [19].
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12.5 Clinical Manifestations
12.5.1 Congenital (In Utero) Herpes Simplex Virus Infection
Intrauterine-acquired HSV infection is an extremely rare condition. The typical
triad of congenital HSV infection is chorioretinitis, microcephaly or hydranencephaly, and active skin lesions together with skin scarring [18]. However, this triad is
seen in less than one-third of the patients. Congenital HSV infection manifests with
signs and symptoms within the rst 2 days of life [18]. Death occurs within the rst
month of life in 60% of babies with intrauterine HSV infection [20].
The most common nding in congenital HSV infection is skin anomalies [13].
The skin manifestations may be localized or widespread and consist of skin ulcers,
erosions, scars, and mucocutaneous vesicles; corneal or retinal damage is also common [21, 22]. Central nervous system (CNS) ndings in newborns with in utero
HSV infection may include microcephaly, microphthalmia, cerebral hemorrhage,
anencephaly, intracranial calcications, hydrocephalus, ventriculomegaly, porencephaly, encephalomalacia, corpus callosum agenesis, and cerebellar anomalies [5,
10]. Possible ndings of congenital HSV infection are presented in Table12.1.
12.5.2 Perinatal Herpes Simplex Virus Infection
Symptoms may appear at birth or within the rst 6weeks [5]. The prognosis is good
with early diagnosis and treatment; however, the risk of progression to encephalitis
and disseminated disease is high if treatment is delayed. The condition can be insidious and nonspecic in early [5, 24].
Table 12.1 Possible ndings of
congenital herpes simplex virus
(HSV) infection
Fetal death
Premature birth
Intrauterine growth retardation
Hydrops fetalis
Limb hypoplasia
Skin anomalies
Heart anomalies
Herpetic keratitis, retinitis, retinal scar
Cardiomegaly, pericardial effusion
Hepatomegaly, elevated liver
enzymes, liver calcication, liver
necrosis
Splenomegaly
Hyperechogenicity in the intestines
Adopted from Refs. [3, 5, 10, 13, 18,
20, 21, 23]
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There are three types of neonatal HSV infection
• Disease localized to the skin, eyes, and mouth (SEM)
• Central nervous system (CNS) disease (with or without SEM involvement)
• Disseminated disease (may include the symptoms and signs of the rst
two groups)
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12.5.2.1 Skin, Eyes, andMouth (SEM) Disease
Skin, eyes, and mouth (SEM) disease constitutes 45% of neonatal HSV infections
[18]. It appears in the rst 2weeks and is most commonly localized to the skin,
eyes, and mouth. Skin lesions may be individual vesicles, large bullous lesions, and
desquamation. Eye involvement may be asymptomatic; however, keratoconjunctivitis, chorioretinitis, cataracts, and permanent vision loss are also possible. The prognosis of SEM disease is excellent when antiviral treatment is started early. Still, the
condition can progress to CNS and/or disseminated diseases if not diagnosed and
treated [1, 5].
12.5.2.2 Central Nervous System Disease
This form represents 30% of neonatal HSV infections [18]. It can result from retrograde viral spread from the nasopharynx and olfactory nerves or hematogenous
spread in newborns with disseminated disease. Central nervous system disease can
present with a bulging fontanel, lethargy, irritability, seizures, tremors, and body
temperature imbalance [14]. The patients usually become symptomatic on the
8–17th day of life. Two-thirds of the cases have concomitant skin lesions. The probability of sequelae in the long term is high [24].
12.5.2.3 Disseminated Disease
Disseminated HSV disease form constitutes 25% of neonatal HSV infection cases,
and a sepsis-like clinical picture with multiple organ failure is common [14, 18].
Two-thirds of the babies have concomitant skin lesions. However, skin vesicles do
not occur in more than 20% of newborns with disseminated disease [14].
Disseminated HSV disease may present with signs of hepatic, pulmonary, and neurologic dysfunction or failure [1]. Table12.2 summarizes the signs and symptoms
of neonatal disseminated HSV disease.
The neonatal disseminated HSV disease diagnosis is often delayed by mimicking bacterial sepsis [18]. In a newborn presenting a sepsis-like clinical picture with
thrombocytopenia, elevated liver enzymes, disseminated intravascular coagulation
(DIC), and cerebrospinal uid (CSF) pleocytosis, disseminated HSV disease should
also be suspected [6, 16]. It has the worst prognosis among neonatal HSV disease
forms in terms of mortality, with a mortality rate of 80%. However, the mortality
rate decreases to 30% with timely treatment [13].
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Table 12.2
manifestations of neonatal
disseminated herpes simplex
virus (HSV) disease
The
Fever or hypothermia
Lethargy
Apnea
Pneumonia, hemorrhagic
pneumonia
Myocarditis
Hepatitis, acute liver failure
Central nervous system (CNS)
involvement
Necrotizing enterocolitis
Neutropenia, thrombocytopenia
Disseminated intravascular
coagulation (DIC)
Adopted from Refs. [3, 18]
12.6 Diagnosis
Early ndings are indistinct and nonspecic, especially in disseminated disease
[11]. In the absence of skin lesions, diagnosing neonatal HSV infection can be troublesome and maybe late [14]. The maternal history is usually not helpful because
there is no history of genital ulcers in 80% of the cases [2, 3, 14]. Newborns with
disseminated HSV infection often appear at 1 week old with signs and symptoms
that mimic neonatal sepsis. The patient may experience fever or hypothermia, irritability, lethargy, and respiratory distress and rarely present with fever only. In
advanced neonatal disseminated HSV disease, fever is usually absent, and hypothermia is predominant [11, 25, 26].
In newborns, SEM disease presents with skin vesicles in 80% of patients; in the
absence of vesicles, the infection is localized to the eye and/or oral mucosa. More
than half of the neonatal disseminated or CNS HSV disease accompanied skin
lesions. However, skin lesions may not be present on admission [6]. Newborns with
a sepsis-like clinical picture, meningoencephalitis, progressive pneumonia, severe
hepatic dysfunction, or DIC should be tested for HSV infection, and empiric antiviral therapy should be initiated [6, 11, 27–30]. Herpes simplex virus should also be
considered in newborns with fever, vesicular rash, and abnormal CSF ndings in the
rst 3weeks of life, especially when a history of seizures is present [6].
12.7 Laboratory Features
The diagnosis of HSV infection is made with PCR, surface viral culture, and direct
immunouorescence tests. Serology does not help diagnose neonatal HSV infection
at presentation.
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12.7.1 Surface Viral Culture
Surface viral culture is the gold standard for diagnosing neonatal HSV infection [2].
The material can be aspirated from unruptured vesicular lesions, swabs from the
oor of ruptured vesicles, and the conjunctiva, mouth, nasopharynx, or anus [14, 31].
A single stick is used to take a surface swab. Swab samples from the mouth,
nasopharynx, conjunctiva, and anus can be taken with a single swab, starting from
the conjunctiva and ending at the anus. The swab is then placed in a viral transport
medium. Viral culture aims to determine the presence or absence of proliferating
virus instead of localizing the virus. Positive cultures result 12–24h after birth,
indicating viral replication and suggesting infection, not contamination at birth.
This is the most critical information from such cultures, except for CNS involvement. A moistened cotton swab should be preferred because a calcium alginateimpregnated swab inhibits virus growth. Surface viral cultures are transferred on ice
with the appropriate transport medium [5, 14].
Every patient with neonatal HSV infection should have a conjunctival HSV culture and an ophthalmologic examination, regardless of the type of disease [6, 11].
12.7.2 Polymerase Chain Reaction (PCR) Test
The polymerase chain reaction test is used for HSV deoxyribonucleic acid (DNA)
detection in CSF and blood samples. Viremia can occur in all three forms of neonatal HSV disease and is detectable by PCR.The polymerase chain reaction test is
precious in the diagnosis of HSV encephalitis. The sensitivity and specicity of
PCR in CSF for the diagnosis of neonatal HSV infection are 75–100% and 71–100%,
respectively [14]. A negative CSF PCR result does not exclude CNS involvement;
as a result, it can also be negative in the early stages [6]. In patients with a strong
presumption of CNS HSV disease but CSF PCR tests are negative more than once,
a histopathological survey and viral tissue culture of the brain biopsy specimen is
the most reliable investigation to diagnose HSV encephalitis [6]. Cerebrospinal
uid viral culture is usually negative in patients with HSV CNS disease [6].
Some authors report that PCR is acceptable if cultures from the surface swab are
not possible. However, studies on PCR in newborn surface swab samples are inadequate [14]. Using the PCR assay on surface swabs or scraping samples has not
been evaluated, but skin PCR should be used in addition to (and not in place of) a
surface culture, the gold standard. False-negative results are possible [14].
12.7.3 Direct Immunofluorescence Antibody (DFA) Test
The test provides fast results, but the sensitivity is 60–80%. A scraping sample from
the skin lesions is used. The test reliability increases if the sample is taken appropriately but is not as sensitive as culture. Therefore, samples negative for DFA must be
conrmed with another test [11, 32].
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12.7.4 Other Tests
Serology does not help diagnose neonatal HSV infection but helps diagnose and
classify maternal disease. Cross-reactions and false positivity are commonly seen
with serology.
The cytological changes on Papanicolaou (Pap) stain or the Tzanck test are not
specic, as these changes are also seen with cytomegalovirus (CMV) and varicellazoster virus (VZV). The sensitivity of these tests varies with the pathologist’s experience [5].
Complete blood count and liver function tests, especially alanine aminotransferase (ALT), are recommended in neonates with suspected congenital HSV infection
[11, 14].
All newborns with suspected HSV infection, including SEM disease, should
undergo lumbar puncture. CSF results may be normal at the onset of the disease.
However, typically mononuclear cell pleocytosis, normal or slightly low glucose,
and a slightly increased protein level are detected [5, 14]. In contrast to general
knowledge, erythrocytes do not increase signicantly in the CSF in CNS disease;
HSV PCR should also be studied in the CSF sample [14].
Blood and CSF cultures should be taken to exclude bacterial sepsis, one of the
most frequently confused diagnoses. Although most newborns with HSV infection
have a negative blood culture, there may be a possibility of positive blood culture
results due to bacterial co-infection [8].
12.7.5 Cranial Imaging
Cranial imaging is recommended for all infants with neonatal HSV infection, irrespective of disease category [23]. Initially, it may be normal, but this does not rule
out neonatal HSV infection. Magnetic resonance imaging (MRI) is recommended
because of the highest sensitivity among the imaging modalities. As a disadvantage,
it requires sedation to avoid motion artifacts. Therefore, cranial computed tomography (CT) or ultrasonography sufce for cranial imaging in neonatal HSV infection
[6]. Multifocal involvement is common. The temporal, frontal, and parietal lobes’
gray and white matters and the brain stem may be involved [5]. The basal ganglia
and cerebellum are other potential sites to be involved. Patchy involvement of the
parenchyma and meningeal enhancement can be present. Other imaging ndings in
CNS HSV infection include parenchymal brain edema, cortical thinning or atrophy,
encephalomalacia, hemorrhage, ventricular enlargement, and scattered calcications [5, 33].
12.7.6 Electroencephalogram (EEG)
All newborns with suspected CNS involvement of HSV infection should undergo an
EEG.The result is often abnormal in the very early stages of the disease. Focal or
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multifocal periodic epileptiform discharges on EEG are characteristic even before
abnormalities are seen on CT or MRI [14].
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12.7.7 Evaluation ofHearing
All infants with HSV infection should undergo routine audiological screening [34].
12.8 Neonates Exposed toHerpes Simplex Virus
andHearing Loss
One of the sequelae of HSV encephalitis in infants and children is sensorineural
hearing loss (SNHL) [35]. In HSV encephalitis, hearing loss (HL) is rare, and when
present, it is bilateral, severe, and associated with severe neurological complications
[36]. Herpes simplex encephalitis typically involves the temporal lobes. Bilateral
temporal involvement may lead to cortical deafness. Kaga etal. [35] described four
children with HSV encephalitis, with only mild-moderate SNHL but severe auditory agnosia due to bilateral auditory cortex lesions. Animal studies have also indicated that HSV infection may cause HL and vestibular symptoms. Following HSV-1
or HSV-2 infection, it has been shown that brosis of the scala tympani and vestibule, loss of outer hair cells, and atrophy of the stria vascularis and tectorial membrane occurred [36, 37]. In animal studies, viral antigens were detected in the
cochlea and viral capsids in cochlear nerve bers [36, 37]. In animal studies,
changes in temporal bone structures caused by HSV infection have been reported to
resemble those observed in humans who suddenly develop SNHL [37–39].
Due to the potential for HSV encephalitis to adversely affect hearing in infants
and children, intrauterine and perinatal HSV infections are considered risky conditions in permanent congenital, delayed-onset, or progressive HL in childhood.
However, the incidence of immediate and delayed-onset SNHL in children after
exposure to HSV is unknown [34]. In addition to the fact that congenital HSV is a
rare congenital infection, few studies have evaluated congenital HSV cases regarding HL.The current leading pediatric infectious diseases textbooks have no information about HL in congenital HSV infection [5, 6, 18].
The three studies in the literature evaluating audiometric ndings in newborns
with HSV infection included 20, 58, and 13 cases [12, 16, 40]. In the study, which
included 20 symptomatic neonatal HSV cases, audiological evaluations were performed in the postnatal period, at 2–75months, with a median of 32.5months [40].
Half of the patients had CNS involvement, 13 had psychomotor retardation, and 11
had visual abnormalities. Sensorineural HL has been detected in two infants,
although patients are severely affected in other respects.
The other study included 58 neonatal HSV cases followed up until the second
month of life [12]. Among the cases with neonatal HSV infection in this study,
62.5% had HSV-1; among those, the HSV type was determined. While 60% of the
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cases had localized infection, the rest had disseminated or CNS disease. Hearing
loss was not detected in any of the patients.
The third study included 13 newborns with intrauterine-acquired HSV infection
[16]. The presence of HSV infection was conrmed in all cases by culturing the
virus in skin or brain biopsy specimens. All patients infected with HSV-2 had multisystemic involvement, and 92% had CNS abnormalities. Four of the patients died
in infancy due to complications caused by HSV disease. Hearing loss was detected
in three (33%) of nine living children [16].
A review described SNHL after neonatal HSV infection in ve case reports following disseminated HSV-2 infections. The patients had apparent clinical sequelae,
and comorbid conditions were present. There were no reported cases of delayedonset SNHL after perinatal infection [34].
Although it has been reported that HSV-1 infection is associated with encephalitis and HL in newborns at a higher rate than HSV-2, there is not enough data to
reach a denite conclusion on this issue [36, 41]. Hearing loss is associated with
severe neurological complications; however, it is also rare following HSV-1
infection.
Hearing loss caused by neonatal HSV infection can be bilateral or unilateral [36].
Herpes simplex virus causes HL via neuronal damage to the cochlea and CNS
[36]. However, the relationship between HSV infection and HL is not clearly
known [33].
Newborns with congenital or perinatal HSV infection should undergo a screening hearing test before hospital discharge. At least one additional audiological evaluation is recommended by 24–30months of age to detect HL early.
G. İ. Bayhan et al.
12.9 Treatment
All neonates with HSV should be treated, regardless of the clinical ndings.
Newborns with HSV disease are administered intravenous (IV) acyclovir at 60mg/
kg/day. The patients with disseminated or CNS HSV disease are treated for 21days
and those with SEM disease for 14days [14].
Currently, acyclovir is used in the treatment of HSV encephalitis. Early treatment is associated with a better prognosis [35]. The CSF HSV-PCR test is highly
sensitive for the diagnosis, but false-negative results can also be obtained, albeit
rarely. Therefore, if clinical and radiologic ndings suggest HSV encephalitis, acyclovir treatment should be continued [8, 42]. At the end of IV acyclovir treatment, a
lumbar puncture should be repeated for CSF PCR for HSV.If CSF PCR is still positive for HSV, IV acyclovir treatment is given for one more week, and the CSF PCR
for HSV is repeated at the end of the week. Parenteral acyclovir therapy should be
extended at 1-week intervals until CSF PCR negativity for HSV is achieved [18].
Delayed acyclovir treatment is associated with a poorer prognosis. Before acyclovir
treatment, the case fatality rate of HSV encephalitis was 70%; however, even with
efcient antiviral treatment, >35% of patients still suffer from severe sequelae or
death [8, 42, 43].
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After completion of parenteral acyclovir treatment for acute disease, better neurodevelopmental outcomes and less recurrence of the skin lesions have been reported
with oral acyclovir suppression therapy [44]. Regardless of neonatal HSV disease
classication, oral acyclovir treatment should be administered for 6 months. The
oral dose of acyclovir is 300mg/m2/dose, 3 times a day. The dose should be adjusted
according to the current weight by monthly monitoring. During the treatment
period, absolute neutrophil counts must be done at weeks 2 and 4, then monthly
after starting suppression therapy [6, 18, 44]. There are no studies on the use of
valacyclovir for more than 5days in young infants, so this is not an appropriate
alternative to suppressive therapy [6].
Infants with ocular HSV involvement should be given parenteral acyclovir with
a topical ophthalmic drug (1% triuridine, 0.1% iododeoxyuridine, or 0.15% ganciclovir) [14].
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12.10 Prognosis
In utero HSV infection prognosis is poor, and 60% of these cases die in the rst
month of life [20]. The prognosis of HSV SEM disease is very good with early treatment; however, three-quarters of patients progress to disseminated disease if left
untreated [1]. Central nervous system HSV disease has a high probability of longterm sequelae [24]. Disseminated disease has the worst prognosis among neonatal
HSV disease forms with the highest mortality; however, with timely treatment, the
mortality rate drops to 30% [13].
12.11 Prevention ofNeonatal Herpes Simplex Virus Infection
For women with active, recurrent genital herpes, the American College of
Obstetricians and Gynecologists (ACOG) recommends antiviral suppression therapy at or after 36weeks of gestation [45]. However, neonatal HSV disease has also
been reported in infants of mothers given antiviral prophylaxis [6].
In newborns born to mothers with active genital lesions at birth, the classication
(primary infection, rst-episode non-primary infection, and reactivation) of the
mother’s HSV infection should be evaluated. In this way, the risk status of the newborn can be estimated [6].
12.12 Conclusion
Herpes simplex virus transmission can occur from mother to child during the intrauterine or perinatal period. Both HSV-1 and HSV-2 can lead to neonatal HSV infection. Although skin lesions are a signicant sign of HSV infection, they may not
always be found. Congenital and neonatal HSV infections may cause unilateral or
bilateral HL, although the frequency is not clearly known. Hearing loss in neonates
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with HSV infection may develop due to neuronal damage in the CNS or cochlea.
Newborns with HSV infection should undergo screening hearing tests before hospital discharge and thereafter.
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