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24 Viral Meningitis inChildren andHearing Loss
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24.14.3 Varicella-Zoster Virus (VZV) andHearing Loss
Varicella-zoster virus is a double-stranded enveloped DNA virus member of the
Herpesviridae family. Varicella-zoster virus causes varicella (chickenpox) as a primary infection and herpes zoster (shingles) as reactivation of the latent virus staying
in the sensory nerve ganglia. Hearing loss after herpes zoster infections is generally
related to herpes zoster oticus or Ramsey Hunt syndrome, a well-known complication of the latent VZV infection within the geniculate ganglion. However, this complication is usually seen in advanced ages and immunocompromised patients.
Pediatric herpes zoster infection rarely causes sudden HL without other neurologic
involvements and recovers entirely within weeks to months [94]. Sudden HL may
be the rst symptom of chickenpox before the typical rash [95]. There are only a
few case reports of VZV meningitis and HL in children. Schwab and Ryan [96]
reported a previously healthy 5-year-old girl with VZV meningitis presented with
fever, headache, and rash. She had a history of vaccination against VZV at 3 years
of age. Cerebrospinal uid was positive for VZV by PCR.Mild-to-moderate right
SNHL was demonstrated at 6 weeks after discharge. The hearing ultimately returned
to normal after 2 years. Hearing loss has a better prognosis than mumps and measlesrelated HL in VZV infections.
24.14.4 Influenza andHearing Loss
Inuenza viruses are single-stranded RNA virus members of the Orthomyxoviridae
family. There are four types of inuenza viruses, but only inuenza A and B viruses
cause seasonal epidemics in humans, especially in winter. Temporary HL is common during inuenza. Middle ear effusion and Eustachian tube dysfunction due to
congestion frequently cause mild HL and return to normal after congestion dissipates. Veltri etal. [97] studied the viral etiology in idiopathic sudden HL using viral
serologic methods. Inuenza virus group B was found in 14 patients (18%) and
inuenza group A3in six (8%), respectively, but no information was reported about
the type of HL.However, there are rare case reports in which HL was severe and
permanent. Alsanosi etal. [98] reported a 2-year-old girl and a 3-month-old boy
presented with sudden bilateral HL during a febrile illness. Inuenza A (H1N1) was
detected by PCR testing, and oseltamivir was used in both patients. Audiologic
assessment showed severe and permanent SNHL.No comment was made on the
pathogenesis of HL in these cases.
24.14.5 Epstein–Barr Virus (EBV) andHearing Loss
The EBV is a DNA virus member of Herpesviridae, also known as human herpesvirus 4. The primary infection mostly occurs in infants and children; the virus
becomes latent in the body. The CNS complications of primary EBV are rare
(0.5–7.5%), and EBV meningitis usually occurs after the reactivation of the latent
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virus [99, 100]. Epstein–Barr virus reactivation in latently infected B cells occurs by
activation from abnormal lymphoid follicles in the CNS (chronic CNS inammation) or transplantation into the CNS from latently infected memory B cells [101,
102]. Miyashita etal. [103] reported a 42-year-old man who presented with fever,
headache, and liver dysfunction. Blood and CSF PCR tests were positive for EBV,
and the patient was diagnosed with aseptic meningitis. Unilateral SNHL developed
in the right ear after 20days of disease onset. Hearing improved after corticosteroid
therapy. The authors presumed that the HL was due to eighth cranial nerve neuritis
related to the extension of inammation from the meninges [103]. In the literature,
there is no case report with the diagnosis of EBV meningitis who developed HL in
children. Epstein–Barr virus-associated HL was presented in systemic EBV infections, mostly in adults [104, 105].
B. Kara et al.
24.14.6 West Nile Virus (WNV) andHearing Loss
West Nile virus is a neurotropic single-stranded RNA virus of the genus Flavivirus
[59]. It circulates between insect vectors, mainly mosquitos and birds. West Nile
virus was rst isolated in Uganda in 1937 and then caused disease outbreaks
throughout North America, Europe, the Middle East, and East Asia. West Nile Virus
infection outbreaks are usually seen in the summer. Patients with WNV infection
are generally asymptomatic, and only 20% of immunocompetent patients are symptomatic, mainly presenting with u-like symptoms. Advanced age and immunosuppression are risk factors for severe neuroinvasive WNV diseases such as meningitis,
meningoencephalitis, and rarely cochlear–vestibular impairment.
A 57-year-old woman with myasthenia gravis presented with meningoencephalitis, accid paralysis, and moderate SNHL; WNV infection was diagnosed
[106]. Her hearing and motor function improved gradually after supportive treatment. The authors postulated that the neuroinvasive disease was enhanced by
immunosuppressive drugs to treat myasthenia gravis. Acute-onset quadriplegia
and bilateral SNHL were reported in a 41-year-old HIV-positive man with severe
WNV meningoencephalitis [107], but this patient’s hearing outcome details were
not reported. Casetta etal. [108] described a 55-year-old previously healthy man
with WNV neuroinvasive disease presenting with acute accid paralysis and
bilateral SNHL.Three months later, audiological examinations showed no recovery in hearing.
Weatherhead etal. [109] followed up patients with WNV meningoencephalitis.
After 1–3years, they found hearing abnormalities in 16 of 35 patients (46%), and
only ve patients had a history of some HL before WNV infection. A 45-year-old
man presented with bilateral moderate-to-severe SNHL and accid paralysis due to
WNV meningoencephalitis [110]. This patient was aggressively treated with oral
corticosteroids, and HL improved utterly. Parrino et al. [111] reported two cases
with SNHL and balance abnormalities caused by WNV, one of them was diagnosed
with meningoencephalitis. The hearing and balance abnormalities of these patients
gradually improved after 6months.
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Acute accid paralysis seems to be a frequent clinical presentation of neuroinvasive WNV infection, and SNHL can accompany neurological pictures in WNV
infection. Hearing loss due to neuroinvasive WNV infection usually recovers spontaneously, but permanent SNHL is not an unexpected nding.
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24.14.7 Lassa Fever (LF) andHearing Loss
Lassa fever (LF) is a viral hemorrhagic fever endemic to West Africa caused by the
Lassa virus, a member of the Arenavirus family. Lassa fever primarily transmits to
humans via contact with food or home stuff contaminated with infected Mastomys
rats’ urine or feces. Human-to-human transmission is rare. The case fatality rate of
LF is approximately 15–20% [112]. It has been reported that chronic HL develops
in one-third of LF survivors [113–115]. The prevalence of HL in LF is much more
common than in other viruses causing HL [59]. Hearing loss may be unilateral or
bilateral. Vertigo and balance abnormalities are also common among LF survivors.
Hearing loss usually occurs during the convalescent phase of the disease, within
5–22 days after the end of the acute episode [112]. The proposed pathogenetic
mechanisms of LF-associated HL are direct viral invasion, immune-mediated damage, vasculitis, and ribavirin, the only available antiviral agent for LF [112].
However, several studies have found no relationship between HL and ribavirin treatment in LF [116–118]. Cashman etal. [119] proposed a mechanism of autoimmune
vasculitis as the cause of sudden-onset SNHL following LF.This theory was supported by studies showing histopathological changes in blood vessels of non-human
primates infected with the Lassa virus resembling histopathological ndings of
polyarteritis nodosa [119, 120].
24.14.8 Enteroviruses andHearing Loss
Enteroviruses are small RNA viruses belonging to the genus of Picornaviruses.
There are many types of enteroviruses, such as echovirus, coxsackievirus, and
poliovirus. Children are more susceptible to enteroviral infections. Enteroviral
infections cause u-like illnesses or no symptoms, mostly in summer and fall. Nonpolio EVs are the leading cause of viral meningitis worldwide. Enteroviral meningitis is usually a benign and self-limited disease without sequela but rarely
complicates with HL.Mentel etal. [121] reported high rates of PCR positivity for
EVs in acute SNHL patients in contrast to a control group. However, only two case
reports in the literature show a relationship between enteroviral meningitis and
SNHL.Schattner etal. [122] reported a 27-year-old man with sudden-onset severe
SNHL and aseptic meningitis caused by EV infection diagnosed with CSF PCR
testing. The patient was treated with high-dose corticosteroids, and a dramatic
improvement in hearing was observed at 10days. The authors commented that EV
infections might be associated not only with aseptic meningitis but also with viral
cochleitis.
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Enteroviruses can cause aseptic meningitis in immunocompromised patients.
Recently, a 67-year-old woman with a history of mantle cell lymphoma on rituximab therapy presented with severe SNHL several months after a chronic febrile
illness [123]. Cerebrospinal uid examination showed mild mononuclear pleocytosis, low glucose, and normal protein levels, and the PCR test was positive for EV
RNA.The auditory function of the patient showed limited improvement at follow up, and she became a candidate for the cochlear implant.
B. Kara et al.
24.14.9 Herpes Simplex Virus Type 1 (HSV-1) andHearing Loss
Herpes simplex virus type 1 is a double-stranded DNA virus member of the
Herpesviridae family [124]. The relationship of the Herpesviridae family to congenital or acquired sudden-onset HL has been known for a long time [59, 97, 125].
Herpes simplex virus type 1 infections may cause HL following primary infection
or reactivation of the latent virus [126, 127]. There are also some case reports associated with HSV-1 meningitis or encephalitis [124, 125]. Herpes simplex virus type
1 infection-related HL is usually bilateral and severe [59]. Loss of outer hair cells
and atrophy of the stria vascularis and the tectorial membrane have been shown in
animals infected with HSV-1, and viral antigens were found within cochlear nerve
bers [59, 128]. Steroids are usually used in addition to antiviral agents to treat
HSV-1-related HL, but a complete recovery is not common [129]. In cases without
improvement, hearing aids or cochlear implantation can be used depending on the
severity of HL.
24.14.10 Human Immunodeficiency Virus (HIV) andHearing Loss
Human immunodeciency virus is a retrovirus consisting of two identical singlestranded RNAs grouped within the Lentiviruses. It causes both congenital and
acquired HL [59]. Bentivi etal. [130] systematically reviewed 26 articles that identied an association between HIV infection and HL and found a statistically signicant relationship between these parameters with an odds ratio of 5364. Hearing loss
in HIV-infected children ranges between 6% and 84%, but most studies reported a
prevalence of 20–30% [131, 132]. In a study of 370 HIV-positive children in Uganda
(mean age 38months, range 6months to 5years), 33% developed HL [133]. Hearing
loss can be unilateral or bilateral and conductive, sensorineural, or mixed in HIV
infections [59]. Conductive HL is more frequent than sensorineural or mixed HL in
HIV-infected children [132]. Htapcak et al. [131] reported the type of HL among
380 children with HIV infection, and HL was identied as conductive in 82%, sensorineural in 14%, and mixed in 4%.
24 Viral Meningitis inChildren andHearing Loss
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Recurrent otitis media, otitis externa, acquired aural atresia, cholesteatoma, formation of aural polyps, and malignancy are the most common causes of CHL in
patients with HIV infection [134]. Also, SNHL is more common in HIV-infected
adults. Central and peripheral auditory system damages, opportunistic infections
with VZV (herpes zoster oticus), CMV, HSV, toxoplasmosis, tuberculosis, cryptococcus, and syphilis, and ototoxic medications, mainly gentamicin, streptomycin,
and antiretroviral drugs, may cause SNHL [59, 132]. Rarely, SNHL may be the only
presenting symptom of HIV infection [135]. Sensorineural HL in HIV-infected
patients is usually mild to moderate and predominantly includes high frequencies
[136]. Human immunodeciency virus-infected patients with mild-to-moderate
SNHL may benet from hearing aids. Cochlear implantation may treat patients with
severe to profound SNHL [137].
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24.14.11 Severe Acute Respiratory Syndrome Coronavirus 2
andHearing Loss
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a singlestranded RNA virus member of the Coronaviruses family and the cause of the
COVID-19 pandemic. Coronavirus disease 2019 is a respiratory and vascular
disease, but CNS involvement is not rare. De Luca et al. [138] systematically
reviewed the 19 articles that identied an association between SARS-CoV-2 and
hearing impairment/sudden SNHL.All patients (age range 18–84years) tested
positive for COVID-19, and all had SNHL; additionally, four had tinnitus, two
had vertigo, and two had nausea or vomiting. The authors concluded that hearing
function might be affected by SARS-CoV-2 infection and proposed that the etiopathology might be related to a central and/or peripheral involvement of the auditory pathways. Tufatulin et al. [139] reported 87 children aged 5 months to
17years who had conrmed COVID-19 disease had no HL or central auditory
processing disorders. It seems that COVID-19- related hearing impairment is not
common in the pediatric age group. However, Saki etal. [140] reported two
cochlear-implanted children presented with sudden speech sound perception
problems during COVID-19 disease. No evidence exists that maternal COVID-19
disease causes HL in infants [141]. As a result, auditory impairment can appear
in patients with COVID-19. Children presented with sudden or gradual deterioration of speech during the pandemic, including cochlear- implanted children,
should be investigated for COVID-19.
Clinical features of viral infections associated with acquired HL are summarized
in Table24.2.
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Treatment of hearing
Duration between
symptom onset and
loss
Responsive to
corticosteroids
Severe and permanent
SNHL cases may be
candidates for cochlear
hearing loss
During the course of
acute infection
In immunocompromised
cases, infectious
symptoms may persist,
implantation
Responsive to
corticosteroids
and HL can occur in the
chronic process
20days after
symptom-onset
Antiviral agents and
corticosteroids; rare
During the course of
acute infection
complete recovery
Cochlear implantation
may be helpful in severe
SNHL
Hearing aids for
mild-to-moderate SNHL
During the course of the
disease
B. Kara et al.
Cochlear implantation
for severe to profound
SNHL
Meningitis
Enteroviral cochleitis?
Type of hearing
loss Pathogenesis of hearing loss
Bilateral
SNHL
Frequency of hearing
loss
positivity for
enteroviruses in acute
SNHL patients
Only two reported
Disease or -causative
viruses
Table 24.2 Clinical features of viral infections associated with acquired hearing loss
Enteroviruses (EVs) High rates of PCR
EBV meningitis (primary or
reactivation of the latent
virus)
Eighth cranial nerve neuritis
Loss of outer hair cells?
Unilateral
SNHL
cases with enteroviral
meningitis and SNHL
Extremely rare
Not reported in
Epstein-Barr virus
(EBV)
Mostly bilateral
children
Relatively common in
Herpes simplex
Atrophy of stria vascularis
and tectorial membrane?
HSV-1 meningitis
HSV-1 encephalitis
Recurrent otitis media, otitis
externa, acquired aural atresia,
SNHL
primary HSV-1
infection or
reactivation of the
virus-1 (HSV-1)
Unilateral or
bilateral
latent HSV-1 virus
infection
20–30% (6–84%) in
HIV-infected children
Human
immunodeciency
cholesteatoma, formation of
aural polyps, and malignancy
for conductive HL
Central and peripheral
auditory system damages,
opportunistic infections,
ototoxic medications, and
antiretroviral drugs for SNHL
Conductive,
sensorineural, or
mixed HL
virus (HIV)
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Treatment of hearing
loss
specialist consultation
for conductive HL
Hearing aids for
mild-to-moderate cases
of SNHL
Cochlear implantation
for severe to profound
cases of SNHL
Ribavirin
Persistent SNHL in
one-third of survivors;
Duration between
symptom onset and
hearing loss
During febrile illness Ear nose and throat
5–22days after the end
of the acute disease
hearing aids or cochlear
implantation may be
helpful according to the
severity of hearing
impairment
Hearing aids for
mild-to-moderate SNHL
Cochlear implantation
During the course of the
disease
for severe to profound
SNHL
No effective treatment
4 days before to 18days
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Early cochlear
implantation may be
helpful in bilateral HL
after the appearance of
salivary gland swelling
Middle ear effusion or
Eustachian tube dysfunction
in temporary HL
Not known in cases with
permanent SNHL
Type of hearing
loss Pathogenesis of hearing loss
Bilateral
Conductive in
temporary HL
and SNHL in
permanent cases
Frequency of hearing
loss
common
Severe and permanent
HL rare
Disease or -causative
viruses
Inuenza viruses Temporary HL
Direct viral invasion
Immune-mediated damage
Autoimmune vasculitis
Ribavirin adverse effect?
Bilateral or
unilateral
SNHL
other viruses
Lassa fever (LF) More common than
Degeneration of the organ
Corti and stria vascularis
Cellular inltration of the
cochlea
Otosclerosis?
Otitis media
Meningoencephalitis
Bilateral
SNHL
Conductive HL
in cases with
otosclerosis
with bilateral deafness
due to severe-
profound SNHL
before widespread
vaccination
Measles 4–9% of all cases
Invasion of auditory structures
Meningitis or
meningoencephalitis
Mostly unilateral
SNHL
Permanent HL 1/1000
to 1/20,000
Mumps Transient HL 4%
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Treatment of hearing
Duration between
symptom onset and
loss
Systemic or
intratympanic
corticosteroids may be
hearing loss
During the active phase
and recovery
helpful
Cochlear implantation
may be performed in
severe and persistent
cases
Symptomatic
Before the typical rash or
Complete recovery
within weeks and
months
Probable spontaneous
recovery
during the active phase
of chickenpox
During the course of
neuroinvasive WNV
May respond to
corticosteroids
Cochlear implantation
may be helpful in rare
permanent SNHL
disease
B. Kara et al.
Type of hearing
Frequency of hearing
Disease or -causative
Table 24.2 (continued)
Involvement of central
auditory pathways or cochlea
loss Pathogenesis of hearing loss
bilateral
SNHL
loss
Rare in children Unilateral or
viruses
Severe acute
respiratory syndrome
coronavirus 2
(SARS-CoV-2)
Herpes zoster oticus
Latent VZV infection within
the geniculate ganglion
VZV meningitis
WNV meningitis
WNV meningoencephalitis
Cochlear–vestibular
SNHL
Rare Mostly unilateral
Varicella-zoster virus
(VZV)
SNHL
Rare Bilateral
West Nile virus
(WNV)
impairment
HL hearing loss, PCR polymerase chain reaction, SNHL sensorineural hearing loss
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24.15 Viral Vaccines andHearing Loss
24.15.1 Mumps Vaccine
The mumps vaccine rarely carries a risk for HL.A 7-year-old girl who developed
unilateral HL 13days after mumps vaccination was reported [142]. Another patient
with a sudden unilateral total loss of cochleovestibular function following the
mumps vaccine has been reported [143]. Bilateral HL was reported in a 5-year-old
girl 18days after mumps and measles-rubella vaccinations were administered separately. Corticosteroid treatment was inefcient in this patient, and after applying
cochlear implantation to the right ear in third month of the disease, the hearing was
improved [144].
Sporadic meningitis cases began to be reported after the administration of mumps
vaccination in the UK in 1988. Urabe strain was used at that time, and the association of meningitis with vaccine strain was evidenced by nucleotide sequence.
Mumps meningitis developed 18days after measles–mumps–rubella (MMR) vaccination in two cases [145]. In Russia, among aseptic meningitis patients vaccinated
against mumps by monovaccines or divaccines (mumps–measles) containing
Leningrad-3 (L-3) strain in the previous 30days before disease onset, only seven
cases with HL were detected during 2009–2019 [146]. However, the incidence of
vaccine-induced HL and meningitis is lower than that of natural infection.
24.15.2 Measles Vaccine
The widespread use of live measles virus vaccination has dramatically reduced the
mortality and morbidity of measles. However, transient and mild local and systemic
adverse effects may be seen following vaccination. Hearing loss is an infrequent
complication of measles vaccination. There are rare case reports of who developed
SNHL after measles or MMR vaccines; however, an association between the measles vaccine and HL is not clear and which component of the MMR vaccine is
responsible for HL needs to be proven [142, 147–150].
24.15.3 Influenza Vaccine
A 17-year-old girl developed sudden bilateral HL, dizziness, nausea, and bilateral
tinnitus 14h after the H1N1 inuenza vaccination. The patient’s hearing improved
after oral prednisolone and vitamin B complex therapy, and pure tone audiometry
showed a hearing threshold of 30dB in both ears after 1month of treatment [151].
Recently, Kolarav etal. [152] reported a 79-year-old diabetic woman presented with
acute bilateral HL, vertigo, impaired balance, and left-sided temporal headache 2
days after seasonal inuenza vaccination (H1N1 and H3N2). Otolaryngological
examination and neuroimaging of the patient were found normal, and audiometry
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showed SNHL on both sides. The hearing adverse effects could be speculated due
to thimerosal or gentamycin within the vaccine, but both were in trace amounts in
the inuenza vaccine to cause ototoxicity.
B. Kara et al.
24.15.4 Hepatitis B Vaccine
An 11-year-old boy complained of sudden left HL, tinnitus, vertigo, and nausea
after 48h of the second hepatitis B vaccine (HBV) dose [153]. A marked left SNHL
was present after 2years. In adults, Biacebe and Bonls [154] reported a 42-yearold man with right uctuant SNHL and tinnitus after the second dose of HBV, and
Davanipour etal. [155] reported a 37-year-old woman with unilateral SNHL and
tinnitus. Tinnitus regressed, and hearing thresholds were normalized within
6months in both patients [154, 155]. The exact mechanism of HL could not be
explained in these cases. It was emphasized that it could be related to autoimmunity,
but extensive immunological examinations were not performed.
24.15.5 Rabies Vaccine
Rabies is a fatal disease and can be prevented with prompt administration of the
rabies vaccine and rabies immunoglobulin. Several formulations and dosing
schedules exist for rabies vaccines. Rabies vaccines produced in animal nervous
tissue were used in the past with a high incidence of neurological complications,
predominantly acute peripheral neuropathy [156]. Nowadays, the human diploid
cell vaccine (HDCV), puried chick embryo cell vaccine (PCECV), and puried
Vero cell rabies vaccine (PVRV) are available worldwide and replaced the oldtype vaccines [157, 158]. These vaccines are inactivated, and adverse effects are
primarily local reactions at the injection site and mild systemic signs such as
headache, fever, myalgia, arthralgia, nausea, weakness, and rare systemic hypersensitivity reactions [159–163]. Case reports of neurological complications such
as Guillain–Barre syndrome, acute disseminated encephalomyelitis, and facial
paralysis with new-type rabies vaccines have rarely been reported; however, no
evidence of causality exists [157, 164]. Cases of HL after rabies vaccine administration have also been rarely reported. An 11-year-old boy developed unilateral
HL after the rst dose of PCECV progressed with repeating doses but responded
to systemic corticosteroids [165]. A 33-year-old man developed profound suddenonset unilateral SNHL with tinnitus and vertigo within 24h of administering the
second dose of PVRV [166]. Sensorineural HL was also reported after HDCV in
an 11-year-old boy [167]. These cases had no history of upper respiratory infection, systemic illness, ototoxic medication, trauma, and normal otoscopic
examination.
Characteristics of viral vaccines associated with HL are summarized in
Table24.3.
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