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H. Maraş Genç et al.
reactivation [37]. The prevalence of congenital CMV infection is reported as
0.58–0.67%. Higher maternal seroprevalence, low socioeconomic status, and
younger maternal age are associated with higher rates of congenital CMV infection
[38, 39]. In utero transmission at an earlier gestational age has the most signicant
risk for neurologic sequelae with respect to intrapartum and postpartum transmission [40]. Approximately 10% of fetuses who acquire CMV will have clinical signs,
and an additional 10–15% will develop late-onset sequelae. Infants with congenital
CMV infection may be asymptomatic or have varying signs, including microcephaly, developmental delay, leukodystrophy, polymicrogyria, intracranial calcication, cataract, chorioretinitis, petechiae, hepatosplenomegaly, and hemolytic anemia.
Hearing loss is the most common long-term sequela of congenital CMV infection, and CMV is the leading acquired cause of SNHL in children [3, 41]. In a systemic review, 12.6% of newborns with congenital CMV infection had SNHL,
observed in one-third of symptomatic children and one out of 10 asymptomatic
children [39]. Approximately 3–5% of patients with congenital CMV infection will
develop bilateral moderate to profound SNHL.It is estimated that among pediatric
cases of bilateral moderate to profound SNHL, 15–20% are attributable to congenital CMV [42]. SNHL can manifest months or years after birth.
Fowler etal. [43] evaluated 307 children with asymptomatic congenital CMV
infection and reported that 7.2% developed SNHL during follow-up. Among children with SNHL, further hearing deterioration was observed in 50% and delayedonset SNHL in 18%. Newborn hearing screening will miss these patients, and
continuous monitoring is recommended in patients with congenital CMV infection. A recent study consisting of 92 congenital asymptomatic CMV cases detected
during hospital-based screening reported that the prevalence of SNHL at the age
of 18years was 25% [44]. After 5 years of age, the rate of SNHL development did
not signicantly differ between infected and uninfected children. Bilateral HL,
more severe involvement, and progression are more common in symptomatic
patients [3, 39]. Hearing loss in CMV may be directly due to viral components or
associated with the host’s immune response. Human and guinea pig studies have
shown the inammation of the cochlea and the presence of viral particles in the
inner ear [45].
Treatment with ganciclovir or valganciclovir followed by prolonged prophylactic courses of antiviral medication is recommended in symptomatic neonates since
this treatment has been shown to improve audiologic and neurodevelopmental outcomes. At present, antiviral therapy for asymptomatic infants with congenital CMV
infection has not been shown to improve hearing outcomes [41, 46]. Currently, there
is no treatment for CMV in pregnant women. CMV-specic hyperimmune globulin
therapy for pregnant women with primary CMV infection has been studied in large
trials but has not been proven to be efcacious and should be restricted to research
studies only [47, 48]. No effective vaccine is available against this virus. Strategies
for primary infection prevention include encouraging frequent handwashing and
avoiding saliva or urine of children aged <6 years [3]. A universal screening
approach at birth is recommended in some countries because early recognition of
congenital CMV will allow closer follow-up and early intervention for HL [49].
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25.11.2 Rubella Virus Infection
The rubella virus, belonging to the Togaviridae family, is the causative agent of
rubella disease, also known as “German measles” [50]. It is usually a self-limited disease characterized by fever and rash. However, if the infection occurs just
before conception or in the rst trimester of pregnancy, it may result in congenital
rubella syndrome (CRS) in up to 90% of cases. Congenital rubella syndrome is
characterized by stillbirth or birth defects, including SNHL, cataracts, microphthalmia, chorioretinitis, glaucoma, microcephaly, congenital heart disease, and hepatosplenomegaly [51]. Hearing loss is the most common sequela, with up to 90%
of CRS cases having SNHL [52–54]. Hearing loss is usually detected in affected
babies at six to 12months, although it may be present at birth.
Congenital rubella syndrome is a leading cause of a vaccine-preventable disease.
In the pre-vaccine era, CRS was seen in 0.8–4 per 1000 live births [55]. After vaccination policies, rubella and CRS have been eliminated in the majority of the
European region, Western Pacic countries, and American Health Organization
Region [56]. However, CRS cases still occur, especially in regions where vaccination coverage is low [57, 58]. Therefore, it is recommended that women should
undergo antibody screening before pregnancy, and rubella vaccination is applied if
necessary [57].
25.11.3 Toxoplasmosis
Toxoplasma gondii is a protozoan that infects both humans and animals. The seropositivity of T. gondii varies between countries, and 10–90% of the population is
infected. Human infection can result from ingestion or handling raw or undercooked
meat containing tissue cysts, contact with cats, or consuming food contaminated by
oocysts passing from infected cat feces [58, 59]. In immunocompetent healthy
adults, it is usually a self-limiting disease. In immunosuppressed patients, such as
those with HIV or congenital infection, T. gondii can cause severe disease.
Congenital toxoplasmosis occurs following maternal transmission, after acute primary infection within 3 months of conception or pregnancy. It can result in abortion, neonatal death, chorioretinitis, hydrocephaly, intracranial calcication,
developmental delay, epilepsy, rash, hepatosplenomegaly, and sepsis-like illness
[59, 60]. Epidemiologic studies have documented that children with SNHL have
increased seroprevalence of T. gondii [61, 62]. In a systematic review, the preva-
lence of SNHL was reported as 0–26% in patients with congenital toxoplasmosis.
The prevalence of toxoplasmosis-associated SNHL was 28% in the untreated group
and 12% in those treated with antiprotozoal therapy before 2.5months of age [63].
Toxoplasma gondii has been detected in infected children’s inner ear and brain
[61]. The temporal bone histopathological samples obtained from the autopsy of
three cases with congenital toxoplasmosis revealed parasites in the stria vascularis,
spiral ligament, saccular macula, or internal auditory canal. However, one of the
cases had intact neurosensory elements presenting with the loss of spiral ganglion
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cells, possibly due to meningoencephalitis. The authors concluded that HL in congenital toxoplasmosis could be sensorial, neural, or sensorineural [64].
Antiparasitic treatment with a combination of folinic acid is recommended
for symptomatic and asymptomatic infants diagnosed with congenital toxoplasmosis [60]. For pregnant women with acute toxoplasmosis, spiramycin is recommended in the rst trimester, after which the treatment depends on the
presence of fetal infection. A combination of pyrimethamine, sulfadiazine, and
folinic acid should be offered for women in cases where a fetal infection has
been conrmed [65]. The treatment of toxoplasmosis in immunocompetent people is generally not recommended except for ocular involvement [66]. Prevention
strategies include avoiding exposure to undercooked meat, untreated water, cat
feces, and soil [60].
H. Maraş Genç et al.
25.11.4 Zika Virus Infection
Zika virus is an arbovirus that belongs to the Flaviviridae family. It is a mosquitoborne virus rst isolated from a monkey in the Zika forest in Uganda. It was identied in humans in 1952. Zika virus is also transmitted from mother to fetus or
through sexual contact, transfusion of blood products, organ transplantation, or
laboratory exposure [67]. Most people with Zika virus infection are asymptomatic.
Symptomatic cases usually have mild complaints, including fever, rash, conjunctivitis, myalgia, and headache. However, in 2015, after an outbreak of rash illness in
Brazil, the Zika virus was associated with Guillain–Barré syndrome and congenital
microcephaly [68]. Intrauterine encephalitis was conrmed in a case report, demonstrating Zika virus particles in the brain of an electively aborted microcephalic fetus
[69]. Microcephaly in congenital Zika virus infection is generally severe. Other
common ndings are a partially collapsed skull, hydrocephaly, subcortical calcications, abnormal gyral patterns, and cerebellar hypoplasia. The additional ndings
of congenital Zika virus infection include microphthalmia, optic atrophy, visual
impairment, SNHL, epilepsy, hypertonia, and extrapyramidal involvement [70].
Sensorineural HL is reported in 5.8% of patients with microcephaly. Children
with congenital Zika virus infection should be followed up for hearing function,
even with normal initial screening tests [71]. There is no treatment or vaccination
for Zika virus infection. Prevention is based on avoiding travel to areas where the
virus is seen and protective measures against sexual transmission and mosquito
bites [72].
25.11.5 Lymphocytic Choriomeningitis Virus (LCMV) Infection
Lymphocytic choriomeningitis virus is a rodent-borne pathogen that belongs to
the Arenaviridae family. Humans can be infected through exposure to the secretions of house mice, rats, and hamsters. The symptoms range from mild to severe.
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Most cases are mild and may be overlooked. Severe infections include meningitis
and encephalitis, or a congenital syndrome may occur [73]. Lymphocytic choriomeningitis virus infection can result in abortion during pregnancy or severe neurologic sequelae, including microcephaly, hydrocephaly, pachygyria, intracranial
calcication, chorioretinitis, and HL.The mortality is approximately 35% in congenitally infected children, and 70% of these cases present with neurological
sequelae [74].
In contrast to other TORCH infections, such as CMV and rubella, visual impairment and microcephaly are more common than HL in LCMV infection. There is
currently no efcient antiviral therapy [74]. Hearing loss in LCMV infection can be
profound to severe. The severity of HL can vary between ears [3].
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25.12 Congenital andAcquired Infections Causing
Hearing Loss
25.12.1 Syphilis
Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum. The disease course follows primary, secondary, latent, and tertiary stages
over 10years in infected individuals. During pregnancy, maternal transmission to
the fetus results in congenital syphilis. Early congenital syphilis is dened as the
onset of clinical symptoms before 2 years of age, while late congenital syphilis is
dened if the symptoms occur after 2 years. Untreated maternal syphilis leads to
abortion, prematurity, intrauterine growth retardation, and long-term sequelae,
including fever, hepatomegaly, lymphadenopathy, bone marrow suppression, maculopapular rash, rhinitis, condyloma lata, and bone lesions. Neurological sequelae
include acute syphilitic leptomeningitis and chronic meningovascular syphilis
resulting in cranial nerve palsies. Late ndings of congenital syphilis result from
persistent inammation and scarring of tissues [75, 76]. Sensorineural HL in congenital syphilis occurs as a late nding, generally presenting with sudden onset,
bilateral, profound HL between 8 and 10years of age. Accompanying vestibular
symptoms are usually absent [77].
Neurosyphilis refers to the infection of the CNS by T. pallidum. It can occur at
any time after the initial infection. Hearing loss during syphilis is called otosyphilis,
associated with neurosyphilis or isolated abnormality. In a study of 329 patients
with syphilis and CSF abnormalities, 50.5% had normal hearing, 4.6% had isolated
low-frequency loss, 28.3% had isolated high-frequency loss, and 16.7% had both
low- and high-frequency loss. The authors found that older age and CSF pleocytosis
increased the likelihood of HL and impaired hearing recovery after treatment [78].
In adults, SNHL is usually asymmetric, uctuating, and accompanied by tinnitus
and vertigo [78]. Penicillin therapy is effective for all stages of syphilis. Screening
of pregnant women for syphilis is recommended [76].
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H. Maraş Genç et al.
25.12.2 Human Immunodeficiency Virus (HIV) Infection
The human immunodeciency virus is a retrovirus that causes acquired immune
deciency syndrome (AIDS), a sexually transmitted disease, but vertical transmission from mother to fetus can also occur. The human immunodeciency virus preferentially infects CD4+ T cells, consequently leading to immunosuppression and
resulting in opportunistic infections. In HIV infection, involvement of the neurological system includes meningoencephalitis, ADEM, cranial neuropathies, polyneuropathy, movement disorders, and seizures [79]. Neurological abnormalities can
be attributed to primary infection with HIV, opportunistic infections, and adverse
events associated with treatments. In a study of 78 HIV-infected children, 46 had
neurological abnormalities in the form of pyramidal tract signs in 33, hemiparesis
in ve, peripheral neuropathies in four, visual impairment in 18, and hearing impairment in ve [80].
Hearing loss in HIV-infected patients may be associated with the direct action of
the virus in the auditory system and the auditory complications of opportunistic
infections, such as syphilis, toxoplasmosis, and HSV or ototoxic drugs. Hearing
loss may be conductive, sensorineural, mixed, unilateral or bilateral, sudden or progressive [3, 81, 82]. In a study of 23 HIV-infected children, otitis was the most com-
mon opportunistic infection (61%) [81]. Audiometric tests revealed type B curves in
67% and type A curves in 11%. In another study including 23 HIV-infected children, conductive HL was found in six children and SNHL in two. Most patients with
conductive HL had a history of otitis media. Audiologic abnormalities were more
common in children with prolonged HIV-1, higher viral loads, or lower CD4+ cell
counts [83]. Therefore, regular hearing screening is recommended for patients with
HIV infection.
25.12.3 Herpes Simplex Virus (HSV) Infection
Herpes simplex virus 1 and HSV-2 are encapsulated, double-stranded deoxyribonucleic acid (DNA) viruses of the Herpesviridae family and are highly prevalent
among humans. Herpes Simplex Virus-1 is typically associated with labial herpes,
and HSV-2 with genital herpes. However, either virus can be present in areas other
than their typical territories [84]. After the initial infection, the virus remains within
the nerve cells in a latent state. Usually, viral reactivation is asymptomatic or limited
to epithelia. Rarely, it can result in severe infections, such as encephalitis [85].
Herpes simplex virus 2 is the leading cause in newborns, while HSV-1 can also
occur after the neonatal period [1, 2]. Herpes simplex encephalitis is one of the most
common causes of neonatal encephalitis. It can be acquired prenatally, perinatally
(most common), and postnatally. Neonatal HSV infection may present in three
forms: localized infection to the skin, eye, and mouth (SEM); encephalitis; and disseminated disease. Encephalitis may be seen in both SEM disease and disseminated
HSV.Hence, any neonate with suspected HSV disease, even those with isolated
SEM disease, should have blood and CSF PCR tests for HSV.
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Herpes simplex encephalitis is the most common cause of sporadic encephalitis.
Typical neuroradiological involvement includes the mesio-temporal and orbitofrontal lobes and insular cortex. Extratemporal involvement can also occur. 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. 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 [1, 86, 87].
Autoimmune encephalitis may occur after HSV encephalitis. In a prospective study
including 51 patients with HSV encephalitis, 27% had developed autoimmune
encephalitis. Of the patients with autoimmune encephalitis, 64% had N-methyl-Daspartate receptor (NMDAR) antibodies, and 36% had other neuronal antibodies [88].
In HSV encephalitis, HL is rare, and when present, it is bilateral, severe, and
associated with severe neurological complications [3]. In a review, SNHL after neonatal HSV infection was described in ve case reports following disseminated
HSV-2 infections. The patients had apparent clinical sequelae, and comorbid conditions were present. There were no reports of delayed-onset SNHL following perinatal infection [89].
Herpes simplex encephalitis typically involves the temporal lobes. Bilateral temporal involvement may lead to cortical deafness. Kaga etal. [90] described four
children with HSV encephalitis, with only mild–moderate SNHL but severe auditory agnosia due to bilateral auditory cortex lesions. Currently, acyclovir is used in
the treatment of HSV encephalitis. Early treatment is associated with a better prognosis [86].
Herpes simplex viruses may also cause HL in the setting of infections other than
encephalitis. In a cohort of 232 patients with idiopathic sudden SNHL, two subgroups with HSV immunoglobulin (Ig) M seropositivity and seronegativity were
compared [91]. No signicant difference was found between the patients with and
without HSV reactivation in prognosis. In another survey, including 1054 children
referred to the clinic suspected of hearing impairment, a high prevalence of HL was
found in those with HSV infection. It was noted that 82 (8%) children had a positive
IgM test for HSV-1, and 8 (0.8%) had a positive IgM test for HSV-2. Hearing
impairment was bilateral in 46 cases, profound in 7, moderate to severe in 23, and
mild in 16 [92].
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25.13 Acquired Infections Causing Hearing Loss
25.13.1 Measles
Measles is caused by the measles virus, which belongs to the Paramyxoviridae family. It is a highly contagious vaccine-preventable disease characterized by fever,
cough, nasal congestion, conjunctivitis, rash, and runny nose. It has been eliminated
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in high-income countries; however, it has started to reappear due to vaccine hesitancy. Mortality is usually related to respiratory or neurological complications.
Neurological complications include primary measles encephalitis, acute postinfectious encephalomyelitis, subacute sclerosing panencephalitis (SSPE), and
measles inclusion body encephalitis. Encephalitis occurs in up to one in every 1000
patients. Treatment is usually supportive. Prevention with the vaccine is vital since
there is no specic treatment. Vitamin A supplement is associated with decreased
morbidity and mortality [93, 94].
The measles virus can cause HL.Before vaccination, 5–10% of patients with
profound HL were associated with measles [95]. Measles is still a common cause of
HL in areas with low vaccination rates. Hearing loss in measles may be associated
with otitis media, a common complication of measles, or it can follow encephalitis.
Hearing loss associated with the measles virus is usually bilateral and moderate to
profound in severity [3, 96].
H. Maraş Genç et al.
25.13.2 Mumps
Mumps disease is caused by the mumps virus belonging to the Paramyxoviridae
family. Patients clinically present with a prodromal phase, including fever, headache, and myalgia, followed by parotitis. Complications include orchitis, pancreatitis, aseptic meningitis, encephalitis, and deafness. Cerebrospinal uid
pleocytosis occurs in nearly half of patients that usually have mild meningeal
signs and no other signs of meningitis. Manifest meningitis occurs in 1–10%, and
encephalitis occurs in 0.1% of patients with mumps infection [95, 97]. Before
vaccination, mumps was one of the leading causes of meningoencephalitis [2]. In
Japan, where the mumps vaccination coverage is low, Ohfuji etal. [98] reported
the incidence of complications (per 1000 mumps cases) as 6.6 for orchitis, 5.8 for
meningitis, 1.3 for deafness, 0.5 for pancreatitis, and 0.3 for encephalitis in the
period from 2005 to 2017.
Hearing loss associated with mumps is usually unilateral, mild to severe, and
sensorineural. Rarely profound bilateral HL occurs. Hearing loss may also be seen
in asymptomatic patients. In Israel, HL was detected in 3.5% of 79 patients with
mumps meningoencephalitis [99]. Kanra et al. [100], who investigated whether
patients with meningoencephalitis were more prone to HL, found that HL was more
severe in these patients than in mumps cases without meningoencephalitis. Children
with unilateral HL may remain undiagnosed; therefore, patients with mumps infection should be screened with audiological tests [101].
25.13.3 Varicella-Zoster Virus (VZV) Infection
Varicella-zoster virus belongs to the Herpesviridae family. It is a neurotropic virus
that causes lifelong infection in the trigeminal and dorsal root ganglia. Vaccination
plays an important role in the prevention of VZV infection. Primary infection results
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in varicella infection, also known as chickenpox. Varicella is highly contagious and
characterized by vesicular lesions throughout the body. Herpes zoster results from
the reactivation of the latent virus [102]. Both varicella and herpes zoster can cause
neurological complications, including encephalitis, cerebellitis, ADEM, myelitis,
and vasculopathy [103]. Neurological manifestations may be present in the absence
of rash, and the risk is higher in immunocompromised patients. Encephalitis incidence is 0.3 per 1000 patients with chickenpox, and the case fatality rate is 17%. In
patients with herpes zoster, the rate of encephalitis is 0.5–5% [2]. Diagnosis is conrmed based on the intrathecal synthesis of VZV antibodies and/or the CSF VZVPCR test. If skin lesions are present, VZV-PCR from the lesion would also be
diagnostic. Patients usually respond to acyclovir; steroid treatment may be considered additionally [102, 103].
Among neurological complications, cranial neuropathies can occur, and the
facial nerve is the most commonly affected cranial nerve [102]. Ramsay Hunt syndrome or herpes zoster oticus is caused by the reactivation of VZV in the geniculate
ganglion and results in ear pain, ipsilateral peripheral facial nerve palsy, and a vesicular rash on the ear or oral mucosa. Vestibulocochlear nerve involvement can also
occur due to the proximity of the geniculate ganglion to the eighth cranial nerve,
leading to SNHL, tinnitus, nausea, vomiting, and vertigo [104]. In a study evaluating 120 patients with Ramsay Hunt syndrome, 24% had abnormal hearing, and 23%
had vertigo [105]. There was no correlation between facial palsy and HL.The overall incidence of residual HL was 5%. Factors associated with a poor prognosis for
hearing recovery were older age, retrocochlear HL, presence of vertigo, more severe
initial HL, HL within speech frequency ranges, and male gender [105]. A combination of antiviral agents, including acyclovir, valacyclovir, or famciclovir, and steroids, is recommended. If possible, treatment should be started within the rst
3days [103].
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25.13.4 West Nile Virus (WNV) Infection
West Nile virus, a member of the Flaviviridae family, is the most common cause of
arthropod-borne encephalitis in the United States of America (USA) [1]. West Nile
virus is distributed throughout Africa, Europe, North America, the Middle East, and
West Asia. It is transmitted to humans by mosquitoes, usually Culex species. Birds
are the hosts of the WNV. Most cases of WNV infection are asymptomatic.
Approximately 20% of infected people develop West Nile fever. Clinical ndings
include fever, malaise, headache, myalgia, lymphadenopathy, and rash. Less than
1% of patients with WNV infection develop neurological complications, e.g., meningitis, encephalitis, and myelitis [106]. Older age and immunocompromised status
are associated with higher morbidity and mortality [107, 108].
Hearing loss associated with WNF infection is reported rarely. It may be transient or permanent [108–110]. In a study designed to analyze long-term complications in patients with WNV infection, among the 35 patients with WNV encephalitis,
hearing abnormalities were found in 16 (46%), of whom ve had developed these
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abnormalities prior to WNV infection [111]. The authors commented that it was
impossible to differentiate whether HL was related to WNV infection, secondary to
previous HL, or age-related abnormality in these patients. The treatment of WNV
infection is mainly supportive. Protection against mosquito bites is recommended
for prevention [106].
H. Maraş Genç et al.
25.13.5 Dengue Virus Infection
Dengue virus is an arbovirus belonging to the Flaviviridae family. Dengue disease
is endemic to tropical and subtropical regions and transmitted to humans by Aedes
mosquitoes. Infection with the Dengue virus may be asymptomatic or cause fever,
rash, headache, myalgias, and hemorrhagic fever [112]. Neurological involvements
associated with the Dengue virus include encephalopathy, encephalitis, and
Guillain–Barre syndrome [113]. Treatment is supportive. Prevention measures
include mosquito control and vaccination. A tetravalent dengue vaccine comprising
four recombinant, live, attenuated viruses (CYD-TDV) is currently licensed in several countries [114].
Hearing loss in dengue disease is rarely reported. In a prospective study, among
10 patients with dengue disease, three had HL, and one was asymptomatic. Although
they had mild SNHL, there was no improvement [115].
25.13.6 Lassa Virus Infection
Lassa fever is caused by the Lassa virus that belongs to the Arenaviridae family. The
disease is endemic in West Africa. It is transmitted through direct contact with
rodent feces or urine or by inhaling aerosolized rodent excretions. Human-to-human
transmission occurs due to exposure to the virus through blood, urine, feces, or
bodily secretions. Approximately 80% of patients are asymptomatic. Symptomatic
patients present with fever, cough, sore throat, and chest pain. Severe cases can
develop facial swelling, pulmonary edema, HL, and bleeding from mucosal sites.
The disease may progress to multiorgan failure. The mortality rate is reported as
1–15% [116].
Encephalitis, meningitis, or encephalopathy is seen in 15% of cases [117].
Diagnosis is established by PCR-based or antibody-based tests against the Lassa
virus [118]. Ribavirin is the recommended treatment, and early initiation is associated with a better prognosis [117].
The most common neurological complication of Lassa fever is SNHL, reported
in up to one-third of patients [119]. Hearing loss usually occurs in the recovery
phase, suggesting that it is caused by an immunological response rather than direct
viral damage. Hearing loss can be unilateral or bilateral, and recovery is achieved in
less than half of the cases. There is no correlation between the occurrence of HL and
the severity of the disease [117, 119].
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25.13.7 Severe Acute Respiratory Syndrome Coronavirus 2
(SARS-CoV-2)
In 2019, a novel coronavirus, severe acute respiratory syndrome coronavirus 2
(SARS-CoV-2), was identied in Wuhan after a cluster of pneumonia cases. The
disease was responsible for the coronavirus disease of 2019 (COVID-19), which
spread rapidly, causing a global pandemic. As of today, it has caused more than
6,500,000 deaths globally [120]. Especially in the pediatric population, most cases
are asymptomatic or have mild respiratory symptoms. Encephalitis and HL are
rarely reported in patients with COVID-19 [121]. Data regarding HL associated
with COVID-19 are sparse. There are case reports of HL in patients with COVID-19
[122, 123]. Mustafa etal. [124] investigated the audiological prole of 20 asymptomatic COVID-19 cases and reported that the high-frequency pure-tone thresholds
and transient evoked otoacoustic emissions were worse in the COVID-19-positive
group. Kilic etal. [125] performed SARS-CoV-2 PCR testing on ve patients with
sudden SNHL and found positivity in one patient. More data are needed to determine if SARS-CoV-2 affects HL.
25.13.8 Cryptococcosis
Cryptococcosis is an invasive fungal infection caused by Cryptococcus neoformans
or Cryptococcus gattii. It is transmitted by inhaling yeasts through soil contaminated with bird feces [1]. Cryptococcus neoformans is more common and has a
worldwide distribution; however, C. gattii has also been increasingly reported in
Pacic Northwest and causes illness in immunocompetent hosts at a greater rate
than C. neoformans [1, 126].
Cryptococcal meningoencephalitis is a common opportunistic infection and typically causes subacute or chronic presentation in contrast to viral and bacterial
encephalitides [1]. Patients with HIV are at the highest risk of developing the disease. Other immunosuppressive states with an increased risk of cryptococcal meningoencephalitis include chronic steroid use, history of solid organ transplant, and
organ failure [127]. Diagnosis is conrmed by demonstrating cryptococci based on
CSF Indian ink evaluation, cryptococcal antigen testing, PCR testing, and fungal
culture analysis. The treatment includes a combination of amphotericin B and ucytosine. Increased intracranial hypertension is seen in most patients before or after
therapy and should be treated aggressively [126, 127].
Hearing loss is a complication of cryptococcal meningoencephalitis. It is usually
bilateral, progressive, stable, or uctuating. It may involve the cochlear or neural
component. In a study consisting of 11 immunocompetent children with cryptococcal meningitis, only one (9%) patient had HL [128]. In another study, of the 26
HIV-negative cryptococcal meningitis cases, eight (30.8%) had SNHL [129].
Among the seven survivors, hearing improved in three, stabilized in two, and progressed in two. In a recent study analyzing the audiologic complications of
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