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21 Bacterial Meningitis inChildren andHearing Loss
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Recurrent Meningitis, Congenital
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Defects, andHearing Loss
BurcuBursal Duramaz, ÖzlemÇakıcı, andFatmaLevent
22.1 Introduction
Recurrent meningitis (RM) is dened as two or more episodes of meningitis weeks
to months apart with full recovery between events. This is in contrast to recrudescence or relapse of meningitis, which represents the persistence of the initial infection due to treatment failure [1]. Recurrent meningitis is rare in children, but a
thorough examination is often necessary to identify the underlying cause.
Recurrences can occur with bacterial, viral, and noninfectious causes of meningitis,
but most cases are bacterial [2]. Known etiologies of RM also include cranial anatomical defects, such as skull fractures, chronic parameningeal infections, recurrent
benign lymphocytic meningitis, antibody or complement deciency, and
hyposplenism [1].
22
B. Bursal Duramaz (*)
Section of Pediatric Infectious Diseases, Kanuni Sultan Süleyman Training and Research
Hospital, University of Health Sciences, İstanbul, Türkiye
e-mail: burcubursal@hotmail.com
Ö. Çakıcı
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine,
Kocaeli University, Kocaeli, Türkiye
e-mail: zlmckc@gmail.com
F. Levent
Division of Pediatric Infectious Diseases, Department of Pediatrics, School of Medicine,
Texas Tech University, Lubbock, TX, USA
e-mail: fatma.levent@ttuhsc.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_22
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B. Bursal Duramaz et al.
22.2 Etiology andEpidemiology
Bacterial meningitis mostly occurs when bacteria reach the choroid plexus via the
blood and invade the cerebrospinal uid (CSF). The main predisposing conditions
associated with RM are congenital and acquired anatomical defects, immunodeciencies, and chronic parameningeal infections. Epidermoid, dermoid, and neuroenteric cysts, heterotopic brain tissue, dermal sinus tracts, Mondini dysplasia, and
other congenital inner ear malformations (IEMs) and asplenia are among the signicant congenital anatomical defects. Head injury and neoplasia are the most commonly acquired predisposing anatomical conditions [3–7]. Congenital
immunodeciencies include complement, immunoglobulin (Ig), subclass, and
interleukin-1 receptor-associated kinase 4 (IRAK-4) deciencies. Human immunodeciency virus (HIV) infection is an example of acquired immunodeciency.
Streptococcus pneumoniae is the most common cause of recurrent bacterial meningitis (RBM) in patients with underlying structural defects or immune deciencies.
The second most common cause is Neisseria meningitidis, primarily associated
with complement deciency. Haemophilus inuenzae type b (Hib) associated with
RBM has become very rare with the widespread use of the conjugate Hib vaccine.
The intracranial spread of bacteria usually causes recurrent pneumococcal meningitis due to the direct association of CSF with an extracranial source. Patients with
dermal sinus have a greater risk for recurrent Staphylococcus aureus meningitis.
Also, a connection between the subarachnoid space and the intestine increases the
likelihood of RBM with gram-negative bacteria such as Escherichia coli. Oral
streptococci, enterococci, Proteus spp., Klebsiella spp., and group B streptococcus
were rarely reported as causes of RBM [2].
In a study evaluating cases with a diagnosis of RBM, S. pneumoniae was reported
as the causative agent in 310 (56.6%) of 548 culture-proven meningitis cases. In the
same study, N. meningitidis was the second most common cause, and complement
deciency was found in 123 (92%) of 134 patients with meningococcal meningitis
attacks. In patients with other culture-proven meningitis, H. inuenzae (6.9%),
E. coli (4.2%), S. aureus (2.4%), Salmonella spp. (1.8%), Proteus spp. (0.9%),
enterococci (0.5%), Klebsiella pneumoniae (0.4%), and streptococci (group A,
group B, group D, and viridans streptococci [1.8%]) were detected [1].
In the study of Driel etal. [8], the characteristics of recurrent bacterial and fungal
meningitis and the distribution of causative organisms in the Netherlands were evaluated. Data for patients with bacterial meningitis were prospectively collected
nationwide from 1988 to 2005. Of the 19,163 episodes, 450 attacks of bacterial
meningitis were detected. Two hundred and two patients (1.1% of all patients) experienced 11 episodes of bacterial meningitis during the study period. Of these
patients, 169 (84% of patients with RBM) had two, 25 (12%) had three, 5 (3%) had
four, two (1%) had ve, and one had seven episodes. Of the 202 patients, 178 (88%)
had experienced a second episode of bacterial meningitis ≥28weeks after the previous episode, whereas 24 patients (12%) had experienced another episode <28weeks
after an earlier episode. The authors found that RBM occurred more often in male
patients than female patients. In an adult study, 34 (4.8%) recurrent episodes were
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Table 22.1 Predisposing
conditions and congenital
temporal bone anomalies
associated with recurrent
bacterial meningitis
Mondini dysplasia
Stapedial anomalies
Klippel–Feil syndrome
Pendred syndrome
Petromastoid stula
Widened cochlear
aqueduct
Hyrtl ssure
found in 696 patients with bacterial meningitis, and the annual incidence of RM was
0.12 cases per 100,000 individuals [9].
Tebruegge and Curtis [1] identied 363 cases of RM reported in 144 articles
between 1998 and 2007. Of these cases, 214 (59%) were due to anatomical problems, 132 (36%) were immunodeciency, and 17 (5%) were related to parameningeal infections. Regarding gender distribution, there was a slight elevation in males
compared to females (1.2:1) [1].
Recurrent bacterial meningitis has been estimated to occur in 4–9% of all patients
with community-acquired bacterial meningitis [1, 9]. Risk factors associated with
RM are, in part, age-dependent. The most common risk factors are congenital anatomical defects in children, whereas remote head trauma or CSF leakage in
adults [10].
Various congenital defects in the skull’s bone structure in patients may cause
CSF leakage, which may cause RM.Adriani etal. [9] dened head trauma, CSF
leakage, and immunodeciency as predisposing causes in 26 of 34 episodes in their
study. The congenital anomalies in the temporal bone are noted in Table22.1. Inner
ear anomalies in the temporal bone were detected in 21% of patients with idiopathic
sensorineural hearing loss (SNHL) [11].
Mondini dysplasia and other congenital IEMs cause most RBM cases (55 out of
363 cases) [1]. Because of the existing cranial and spinal anatomical defects, it may
be easier for pathogenic organisms to enter the subdural and subarachnoid spaces.
The predisposition to develop bacterial meningitis in Mondini is due to the connection between the CSF spaces and the middle ear, connected to the nasopharynx
through the Eustachian tube. The organisms that cause meningitis are usually those
that colonize the nasopharynx.
22.3 Pathogenesis
Recurrent bacterial meningitis results from defects or imperfections of host defense
mechanisms, allowing bacteria to reach the central nervous system (CNS) or a
defect in the external covering of the leptomeninges and skull. Various cranial and
spinal anatomical defects may facilitate the migration of pathogenic organisms into
the intradural and subarachnoid spaces. These pathological entry pathways are in
the anterior cranial base (frontal, ethmoid, and sphenoid bones) and temporal bone
in the skull. Congenital neural tube defects are most common in the lumbosacral
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region and may also occur in the cervical and thoracic spine. Encephalocele and
glioma are risk factors for RM [12–14].
An otorhinolaryngologic cause was found in up to 33% of RM [15]. Congenital
inner ear abnormalities provide connections between the middle ear cavity and
CSF. Anatomical abnormalities of the middle and inner ear mainly include oval
window stula, round window stula, nasal defect, Hyrtl ssure, the roof defect of
the Eustachian tube, and a defect in the middle wall of the epitympanum anterior to
the semicircular canals. In these patients, CSF rhinorrhea may be indistinguishable
from normal nasal discharge, or a middle ear effusion may mistakenly be diagnosed
as otitis media. Also, CSF may be swallowed by owing through the Eustachian tube.
Children with RM are generally evaluated with computed tomography (CT)
because intracranial anomalies and anterior cranial fossa defects are considered the
cause. The vestibulocochlear system may be overlooked if the CT sections are not
very thin or the bone window settings need to be corrected. Unilateral hearing loss
(HL) diagnosis is also problematic in young children without otological symptoms [16].
Mondini dysplasia occurs in the rst trimester of pregnancy. It is thought to
result from a developmental loss in the seventh week of the embryonic period.
Hearing loss, vestibular anomalies, and a tendency to CNS infections may occur. In
Mondini dysplasia, CSF mostly passes into the middle ear because of the defective
oval window. Mondini dysplasia may be associated with Klippel–Feil syndrome,
Pendred syndrome, DiGeorge syndrome, CHARGE syndrome, and trisomies [17,
18]. In patients with HL and RM, Mondini dysplasia should be considered. Hearing
loss in these patients is sensorineural and occurs due to the anomalies of the organ
of Corti and contact with the subarachnoid space due to increased pressure in the
perilymphatic area. Mild -to-severe SNHL may occur. When any child presents
with RM and HL, an audiometric evaluation should be performed, and temporal
bone should be evaluated with high-resolution CT (HRCT).
Congenital perilymph stula is a stulous connection between the intracranial
subarachnoid space and the middle ear cavity via the inner ear. This connection
leads to the drainage of CSF into the middle ear as an underlying abnormality for
meningitis. While it is symptomatic in most patients in childhood, it may sometimes
present in adulthood [19]. Most patients with congenital IEMs have unilateral HL
with varying degrees of severity; however, hearing rarely may be normal. Anandi
etal. [20] reported that RM developed in a quarter of 20 patients with congenital IEMs.
B. Bursal Duramaz et al.
22.4 Clinical Manifestations
Detailed physical examination is critical in patients with RM.In most patients, the
presenting symptoms are similar to acute bacterial meningitis. However, the RM
episode can also begin insidiously and mimic aseptic meningitis. Patients usually do
not have signs and symptoms suggesting CSF leakage. The presence of a congenital
or acquired CSF leak should be questioned in case of anosmia, HL, and otitis media
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with effusion. There may be intermittent CSF rhinorrhea or otorrhea, and symptoms
may increase during meningitis. Rhinorrhea is often unilateral. Clear nasal discharge increases with the Valsalva maneuver and when the patient leans forward
[21]. Valsalva maneuver, coughing, or sneezing may increase CSF rhinorrhea. A
craniospinal examination should be performed carefully for dimples, stulas, tufts
of hair, nevus, or hemangiomas. In an adult study, symptoms were most commonly
reported as headache, nausea, neck stiffness, and fever [9].
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22.5 Recurrent Meningitis, Congenital Defects,
andHearing Loss
Without hearing rehabilitation, HL can cause detrimental effects on speech, language, developmental, educational, and cognitive outcomes in children.
Sensorineural HL results from damage, disease, or other disorders affecting the
inner ear (e.g., the cochlea) and the auditory nerve. Sensorineural HL is the most
widely reported neurological sequela of bacterial meningitis [22, 23]. Hearing loss
may result from the spreading bacterial products and inammatory mediators
through the meninges and CSF. Bacteria reach the cochlea through the cochlear
aqueduct and induce severe labyrinthitis. As a result, the blood–labyrinth barrier
breaks, leading to meningitis-associated HL [24].
A retrospective study evaluated many children with bacterial meningitis and
found an SNHL incidence during the initial hospitalization of 30.6% [25]. In this
study, the incidence of at least a unilateral severe SNHL was 21.6% among all
patients with bacterial meningitis, and permanent SNHL was seen in 5–35% of
patients. In a prospective multicenter study in the United States of America (USA),
among 151 children surviving pneumococcal meningitis, 32% had unilateral or bilateral HL at discharge [26]. Hearing loss may occur in approximately 20–30% of previously healthy children after meningitis due to S. pneumoniae and in 5–10% of
patients after meningitis caused by Hib or N. meningitidis [27]. Hearing loss is a less
common complication in patients after meningococcal meningitis in high- income
countries. In a large nationwide cohort study in the Netherlands among 578 children
who survived bacterial meningitis, HL occurred in 20 of 495 children (4%) after
meningococcal meningitis [28]. The severity of the disease, and to a lesser extent,
late admission for treatment, reected by a history of seizure(s), has been determined
to predict profound HL in a cohort of children with bacterial meningitis [29].
Furthermore, low CSF glucose levels as an indicator of bacterial density and
inammation in CSF were also shown to predict HL in childhood meningitis [25].
In a meta-analysis investigating the global and regional risk of disabling sequelae,
cognitive decit and HL were the most common combination of multiple impairments [30]. Patients should have a hearing test before or 1 month after discharge
because early rehabilitation may lessen long-term adverse outcomes. Hearing monitoring in patients with meningitis is also vital as HL may indicate brosis and subsequent ossication of the cochlear duct, and urgent cochlear implantation may be
needed before ossication makes insertion of a cochlear implant impossible [31].
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Recurrent bacterial meningitis accounts for 1–6% of meningitis cases acquired
in the community [9]. Recurrent bacterial meningitis warrants prompt investigation
and treatment of the underlying cause.
Permanent unilateral hearing impairment (UHI) affects about 1in 1000 newborns [32]. Unilateral hearing impairment is highly correlated with congenital
IEMs. It is possible to predict that patients with UHI are at risk of concomitant CSF
leakage and meningitis in their follow-up [33]. Congenital IEMs are an important
cause of RM [34].
The organisms are believed to reach the CNS through a defect caused by IEM
[35]. The percentage of IEM is up to 66.7% in UHI cases, whereas IEM is detected
in approximately 20% of patients with bilateral SNHL [33]. About 15% of RM,
especially in children, is related to IEM [1]. Among IEM, those at risk for CSF leak
account for about 18.8% of children with UHI [33]. Most IEMs are associated with
incomplete segmentation of the cochlea. Mondini dysplasia involves one-and-a-half
cochlear helices instead of the usual two-and-a-half helices. Congenital IEMs have
been recognized more recently due to advanced imaging methods [35]. Park etal.
[36] showed that the average age for identifying IEMs is 25.7months. Stein etal.
[37] reported the same result.
In conclusion, IEM should be suspected in patients with UHI or speech delay. It
should be kept in mind that HL in children with RM may be caused by this anomaly,
not by previous meningitis attacks.
B. Bursal Duramaz et al.
22.6 Diagnosis
Patients diagnosed with RM should be questioned regarding cranial injuries, family
history of recurrent infection, CSF leakage from the nose or ear, and splenectomy.
Most patients with Mondini dysplasia and other IEMs with CSF leak experience
their rst episode of meningitis in infancy or early childhood. Inner ear malformations should be investigated in children with a history of HL and meningitis or a
family history of ear anomalies.
In recurrent attacks, CSF culture may be sterile. Early diagnosis of patients is
vital to prevent episodes.
The underlying etiological cause can be estimated according to the type of bacteria detected in the patient’s CSF culture or polymerase chain reaction (PCR) test.
Repeated isolation of bacteria can guide in terms of the underlying condition. In the
presence of IEMs or Mondini dysplasia, S. pneumoniae, N. meningitidis, or H. inu-
enzae are the most commonly encountered causative agents. Streptococcus pneu-
moniae, H. inuenzae, oral streptococci, or anaerobic bacteria of the oropharyngeal
ora are common causative agents of meningitis in patients with middle ear anomalies, head trauma, or congenital CSF leakage. Neisseria meningitidis is mostly associated with complement deciencies in patients with RM.
A uid examination should be planned in case of rhinorrhea or otorrhea. The
presence of glucose and protein in the uid can be evaluated with a strip. It should
be noted that the glucose test may have false-positive and false-negative results.
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Beta (β)-2-transferrin and β-trace protein (βTP) testing can be used to distinguish
whether CSF is present or not [38].
Chronic ear or sinus infections should also be considered an underlying trigger
in a patient with RM.Also, CSF leakage should be investigated. The mainstays are
a complete and detailed record of the patient’s history and a detailed physical examination. A history of head trauma may be overlooked, and a long time could be
elapsed after head trauma [39]. When RM is associated with episodes of otitis
media, the history and physical examination should be directed toward an autogenic
source. Otoscopic and audiological evaluations should be performed to investigate
the possible otological source of RM.The probability of developing SNHL after
meningitis is between 7% and 22% [28].
A translabyrinthine stula should also be suspected in a child with RM and congenital SNHL, in which CSF leaks are often intermittent and easily overlooked.
Diagnosing congenital stulas in infants and young children can be challenging,
and good history may not be given.
Although it is difcult to make recommendations, current evidence suggests that
the initial investigation of RBM should be done with contrast-enhanced CT imaging
of the temporal bones (2mm in thin section) and anterior skull base, including the
paranasal sinuses. High-resolution CT may also be recommended. The sensitivity
and specicity for HRCT are 44–100% and 45–100%, respectively [40–44].
Magnetic resonance (MR) imaging, also helpful in diagnosis, shows the brain
parenchyma and soft tissues well. Magnetic resonance imaging detects anatomical
details and has no radiation risk. It is a sensitive and accurate non-invasive technique for detecting CSF leakage, even in patients not exposed to leakage at the
assessment time.
A cisternography technique may be needed to detect CSF leakage. Computed
tomography cisternography (CTC) is based on showing the contrast medium passing through the stula defect or detecting its presence in the paranasal sinuses. This
technique is one of the reliable approaches for accurately locating CSF leaks. The
sensitivity of CTC ranges from 33% to 100%, the specicity is 94%, and the accuracy ranges from 33% to 63% [45]. Computed tomography cisternography is a valid
option for CSF leak localization, although its ideal indications and accuracy are
only partially clear [45, 46].
Studies show that MR cisternography has a higher sensitivity to detect CSF stulas than CTC [47]. Radionuclide cisternography may also be helpful in some
cases where CT and MR imaging fails to detect CSF leaks.
When the cause has not been identied at the time of diagnosis in a pediatric
patient with RM, the following protocol is recommended:
1. Audiological evaluation: Audiogram or brainstem auditory evoked potential test.
2. Contrast-enhanced CT scan of the head with coronal images of the sinuses and
thin sections of the temporal bone.
3. Spinal ultrasound or MR imaging unless otherwise stated.
4. Immunological studies, including complete blood count, total immunoglobulin
(Ig) levels, Ig G subclasses, and total hemolytic complement levels.
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B. Bursal Duramaz et al.
22.7 Treatment
Regardless of the etiology of RM, treatment should be planned, as in acute bacterial
meningitis. Especially the choice of empirical antibiotic therapy for RBM due to
head injury, congenital anomalies, or complement deciency should be similar to
the initial meningitis episode. Antibiotics should be started immediately after the
initial meningitis work-up. Antibiotics should also target these agents in patients
with a dermal sinus or a history of previous staphylococcal or gram-negative bacterial meningitis. Rarely, in the presence of infections with multidrug-resistant organisms, intraventricular therapy can be needed when intravenous treatment is
unresponsive [48].
The duration of treatment for RM for sporadic cases should be the same as in
bacterial meningitis cases having normal conditions; the benet of extended treat-
prolonged in infections with gram-negative bacilli associated with dermoid or epidermoid cysts because squamous collections may behave like foreign bodies.
Therefore, sterility of CSF should be documented by lumbar puncture [2]. A careful
examination and diagnostic evaluation, including exploratory surgery, is essential if
a CSF stula is suspected.
Spontaneous CSF otorrhea associated with cochlear abnormalities is challenging
to correct surgically. Tympanostomy with a comprehensive middle ear examination
is recommended to determine the leak site. The oval window is the most common
leakage site in Mondini deformity. Still, it has also been reported from the round
window, hypotympanum, and other preexisting anatomical ssures [49].
Cerebrospinal uid leakage through the oval window can be treated by stapedectomy and obliterating the vestibule using fat, muscle, fascia, and cartilage [50]. In
the case of otorrhea, lling the middle ear with fat is insufcient, as it cannot permanently close the stula. Even packing with muscle or fascia alone may be insufcient, and additional vestibule grafting may be required.
A lumboperitoneal shunt procedure can be used in conjunction with primary
surgery as an adjunctive procedure to help close the defect successfully. Repeated
surgical procedures may be required in most patients before the stula is permanently closed.
Cochlear implantation may be an option for patients with Mondini deformity and
can help hear restoration [51]. Since CSF leakage (perilymph leakage) may occur
during cochlear implant insertion, the implant should only be considered in cases of
bilateral HL [52]. Surgical procedures for treating small perilymph stulas in
patients presenting with HL or vertigo usually involve simple closure of the defect
after scarring the margins and simple packing of both oval and round windows [53].
However, more precise procedures are needed to prevent recurrence in patients with
RM due to congenital perilymph stula. A review of 21 reported cases of RM and
congenital perilymph stula identied a surgical failure rate of 37.5% in patients
with simple stula closure [54]. The denitive treatment of congenital perilymph
stula is vestibular obliteration. One argument against vestibular obliteration is preserving residual hearing in the affected ear. However, HL in the affected ear is
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usually severe in most children. Rupa etal. [53] recommended vestibular obliteration in these children initially and concluded that a single operation is sufcient
with this technique in children with congenital perilymph stula to prevent subsequent meningitis episodes.
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22.8 Prevention andProphylaxis
Parents of children with IEMs should be educated about the possibility of RM due to
a middle ear infection. Contact sports, diving, and prolonged Valsalva maneuvers may
increase inner or middle ear pressure. Suspicious infections in these patients should be
treated aggressively and promptly, and patients with cavity anomalies should undergo
exploratory tympanotomy. Efforts should be made to identify and close CSF leaks, as
continued leakage increases the risk of postoperative meningitis [55].
Prophylactic antimicrobial agents are not recommended in patients with basilar
skull fractures and CSF leaks; however, pneumococcal vaccination is recommended
[56]. Repairing the leak is recommended in patients with basilar skull fractures and
a prolonged (>7days) CSF leakage. A review of 51 patients with posttraumatic CSF
leaks that did not improve within 24h showed that the meningitis risk was reduced
from 21% to 10% with prophylactic agents [57]. However, in a study conducted on
patients with traumatic pneumocephalus, ceftriaxone did not reduce the risk of bacterial meningitis [58]. In a meta-analysis examining 208 participants from four randomized studies, no signicant difference was found between the groups in terms of
meningitis frequency, all-cause and meningitis-related mortality, and the need for
surgical correction between the antimicrobial prophylaxis and control groups [59].
The main risk factor for developing posttraumatic meningitis is CSF leakage, which
is often not noticed [60]. Most leaks resolve spontaneously within 7 days, but surgery is required if they do not [56].
The most crucial prevention point is vaccinating patients with RM and congenital or acquired anatomical skull or ear defects. Vaccination of children within this
high-risk group should be routinely recommended against pneumococci, meningococci, and Hib, although meningitis can occur in patients with CSF leaks despite
being vaccinated.
Streptococcus pneumoniae is the most common cause of bacterial meningitis in
children with CSF leakage after head trauma; it is reasonable to try to prevent this
organism-associated infection with the vaccine.
In patients 2–5years old whose vaccinations have not been completed:
– If there are three doses of 13-valent pneumococcal conjugate vaccine (PCV13),
one dose of PCV13 (at least 8 weeks after any previous dose of PCV13).
– If there are less than three doses of PCV13, two doses of PCV13 (applied 8
weeks after the last dose and 8 weeks apart).
– If there is no history of 23-valent pneumococcal polysaccharide vaccine
(PPSV23), one dose of PPSV23 (at least 8 weeks after any previous dose of
PCV13) should be administered.
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