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26 Bacterial Infections inChildren andHearing Loss: AnOverview
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26.2.2 Sensorineural Hearing Loss
Sensorineural HL (SNHL) results from damage, disease, or other disorders affecting the inner ear (e.g., the cochlea) and/or the auditory (eighth cranial) nerve.
Sensorineural HL can be categorized as congenital, including hereditary and nonhereditary causes, and acquired. Congenital SNHL may occur secondary to congenital
malformations, intrauterine infections, medications, or toxins that have a teratogenic effect on the developing ear of the fetus. Congenital SNHL is mainly caused
by cytomegalovirus (CMV), rubella virus, and Zika virus infections or secondary to
congenital toxoplasmosis or syphilis. Hearing loss in these conditions frequently is
progressive.
26.2.3 Mixed Hearing Loss
Mixed HL refers to a combination of conductive HL and SNHL.
26.3 Congenital Bacterial Infections andHearing Loss
Not so many well-dened bacterial congenital infections exist. The best-dened and
well-known congenital bacterial infection is tuberculosis.
26.3.1 Congenital Tuberculosis andHearing Loss
According to the WHO, one-third of the world population has tuberculosis infection, and 20 million people suffer from the tuberculosis disease [7]. On the other
hand, congenital tuberculosis (cTB) is rarely seen, and the actual incidence is
unknown. Also, it is challenging to differentiate cTB from postnatally acquired
tuberculosis disease. The onset of cTB is heterogeneous in the age of presentation;
clinical signs and symptoms may differ with age. It may be asymptomatic at birth,
and many symptoms can occur within days to weeks.
Congenital tuberculosis occurs after Mycobacterium tuberculosis complex bacillaemia during pregnancy, leading to infection of the placenta or the maternal genital
tract. After that, the mycobacteria may pass to the fetus hematogenous from the
placenta to the umbilical vein or by the aspiration or ingestion of amniotic uid [8].
The hematogenous spread may lead to one or more primary complexes in the liver
or lungs. Also, aspiration or ingestion of infected amniotic uid results in primary
complex formation in the lungs or gastrointestinal tract. The liver and lungs are the
two most involved sites in cTB [9]. The rst diagnostic criteria for cTB were dened
by Beitzke in 1935 [10]. Cantwell etal. [11] revised the criteria for the diagnosis of
cTB in 1994, and up to 1982, less than 300 cases of cTB were reported [11].
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According to the Cantwell criteria, the infant must have proved tuberculous
lesions, plus at least one of the followings should be met for the diagnosis of cTB:
(1) detection of tuberculosis-specic lesions in the rst week of life, (2) presence of
a primary hepatic complex or caseating granulomas, (3) documented tuberculosis
infection of the endometrium or placenta, or (4) exclusion of the possibility of postnatal transmission by a thorough investigation of contacts, including the infant’s
hospital attendants, and by adherence to existing recommendations for treating
infants exposed to tuberculosis [11].
Congenital tuberculosis symptoms may present at birth but are more common in
the rst 2–4 weeks of life. Clinical manifestations of cTB may be varied, nonspecic, and difcult to differentiate from neonatal bacterial or viral sepsis. The
mortality rate of cTB is 21–100% [12]. Also, central nervous system (CNS) involvement in cTB is higher [9]. Many CNS-related complications, such as encephalomalacia, hydrocephalus, cerebral infarction, and cerebral atrophy, can be seen if the
patients survive [13]. The CNS-related complications might lead to HL, but the
incidence of HL related to cTB is unknown. Since not many reported cases exist,
data about cTB and HL could be obtained from published case reports and series.
However, a hearing evaluation was not done or mentioned in most of these reports.
Peng etal. [12] analyzed 170 cases of cTB in the literature between 1946 and
2009. Excluding one case of giving up treatment, 68 (40%) patients died of 169, and
HL was detected in 1.5% of the survivors. Li etal. [9] reviewed Chinese journals
reporting 92 cTB cases between 1976 and 2018in China. Forty (44%) patients died,
among the survivors, eight were cured, and 39 patients improved. However, the
authors did not mention long-term sequelae, including HL [9]. Du etal. [14] reported
10 cases of cTB treated in Beijing Children’s Hospital, between 2009 and 2018 that
were followed up for at least 6months. Among 10 cTB cases, hearing scanning was
not done in seven patients, but three cases passed hearing tests. Chotpitayasunondh
etal. [15] reported nine cTB cases diagnosed from 1979 to 1998; the fatality rate
was 33.3%, and no sequelae were found in the survivors.
Hearing impairment in cTB could be secondary to ear involvement. AldanAguirre etal. [16] reported a premature infant of 25weeks’ gestational age presented at 8weeks with otorrhea from the left ear, later developing facial paralysis
and cervical lymphadenitis. Cultures from ear discharge and the biopsy material
taken during a surgical procedure revealed the presence of the M. tuberculosis complex. The patient developed necrotizing otitis media, left temporal bone osteomyelitis, and cervical lymphadenitis. The infant’s mother was found to have an endometrial
biopsy positive for M. tuberculosis, suggesting a cTB diagnosis. After initiating
anti-TB treatment, the brainstem auditory-evoked response (BAER) test showed a
mild left-sided conductive HL with a normal sensory reserve for both ears [16]. Ng
etal. [17] reported a premature infant of 28weeks gestational age with congenital
tuberculous otitis that led to ipsilateral HL detected by the BAER test.
Although TB in the newborn period may present as otomastoiditis, isolated otitis
media without systemic involvement is rare, and so far, only a few cases have been
reported. Naranbhai etal. [18] reported two premature infants with isolated ear discharge
diagnosed with congenital tuberculous otitis treated successfully without sequelae.
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26.4 Acute Bacterial Meningitis andHearing Loss
26.4.1 Acute Bacterial Meningitis inNeonatal Period
Acute bacterial meningitis (ABM) is more commonly seen in the rst 28days of life
than in another period [19]. The incidence of ABM in the neonatal period ranges
from 0.25 to 0.32 per 1000 live births [20, 21]. However, the prevalence of HL may
be 10–20 times higher in high-risk infants who require treatment in neonatal intensive care units (NICUs) [22].
26.4.1.1 Etiology
In high-income countries, Streptococcus agalactiae (group B streptococcus [GBS]),
Escherichia coli, and other gram-negative bacilli are the most common causes of
neonatal meningitis [23]. Moreover, Enterococcus spp., coagulase-negative staphylococci (CONS), Staphylococcus aureus, Listeria monocytogenes, Streptococcus
pyogenes (group A streptococcus [GAS]), and alpha-hemolytic streptococci can
cause ABM, especially among preterm and very low birth weight (VLBW, <1500g)
infants [24]. Neisseria meningitidis, Streptococcus pneumoniae, and non-typeable
Haemophilus inuenzae also rarely cause meningitis in newborn infants. On the
other hand, in low- and middle-income countries, the etiology of ABM in infants
differs geographically, but GBS remains a prominent cause [25].
26.4.1.2 Hearing Loss Related toNeonatal Acute
Bacterial Meningitis
Neonatal ABM can lead to severe long-term sequelae in 12–29% and mild neurological impairment in 15–38% of survivors [26, 27]. Stevens etal. [28] investigated
the long-term outcome of neonatal meningitis between 1985 and 1987in England
and Wales. A total of 111 children who had neonatal meningitis were compared
with 113 matched controls from their birth hospital and 49 controls from general
practices. They were evaluated at nearly a mean age of 9years. The authors reported
3.6% SNHL in the neonatal meningitis group but no occurrence of HL in either
control group. Among the neonatal meningitis group, one case (0.9%) had a severe
bilateral SNHL and had been infected with E. coli. One had a severe unilateral
SNHL and had been infected with a non-E. coli gram-negative bacillus, and one had
a moderate unilateral SNHL and had been infected with L. monocytogenes; the
fourth child required a hearing aid but could not be tested because of learning difculties [28].
Libster etal. [29] investigated long-term outcomes of GBS meningitis in children between 1988 and 2006in two hospitals in the USA.They determined that 90
children with GBS meningitis and ve patients died during the acute illness. Among
85 survivors, 43 children could be evaluated at the age of 3–12years; 24 (56%) were
reported functioning normally, 11 (25%) had mild–moderate, and 8 (19%) had
severe long-term neurodevelopmental impairment. Four children (9.5%) were
detected as having SNHL.
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Doctor et al. [30] investigated the consequences of meningitis in 64 VLBW
infants who had culture-proven episodes of meningitis over 18years from 1977 to
1995. The authors investigated neurodevelopmental outcomes of 39 of 45 (87%)
meningitis survivors compared to non-meningitis survivors followed up to
20months of corrected age [30]. Causes of meningitis were CONS in 43%, other
gram-positive bacteria in 19%, gram-negative bacteria in 17%, and Candida species
in 20% of episodes. They reported HL in 2 (5%) of 39 meningitis survivors and 2%
in the control group [30].
Maqbool etal. [31] investigated the incidence of neonatal HL in high-risk neonates in a tertiary teaching hospital in India. During the one-year prospective study
period, high-risk neonates were screened for hearing impairment using the BAER
test. Two hundred neonates aged between 7 and 28days among patients with high
risk for HL, such as a family history of hereditary childhood SNHL, intrauterine
infections, craniofacial anomalies, including those with morphologic abnormalities
of the pinna and ear canal, birth weight<1500g (VLBW), hyperbilirubinemia at a
serum level requiring exchange transfusion, ototoxic medications, including but not
limited to the aminoglycosides, used for more than 5days or multiple courses or in
combination with loop diuretics, bacterial meningitis, Apgar scores of <4 at the rst
or<6 at the fth minute, needing mechanical ventilation for more than 5days, stigmata, or other ndings associated with a syndrome known to include SNHL and/or
conductive HL were randomly selected [31]. Among 200 infants, 32 had HL with
initial BAER testing. A total of 20 neonates had HL with BAER testing on follow up. The signicant risk factors for HL were ototoxic medications, hyperbilirubinemia requiring exchange transfusion, and perinatal asphyxia in 45%, 30%, and 26%
of neonates with high risk, respectively. Bacterial meningitis was present in 10% of
neonates. The presence of meningitis, stigmata, and/or syndrome associated with
HL and craniofacial anomalies was found to be independent risk factors for HL in
high-risk infant groups.
Thangavelu et al. [32] investigated HL in 4512 neonates hospitalized in the
NICU in Germany between 2009 and 2014. They found the prevalence of HL at
1.6% and permanent HL at 0.9%. They revealed that craniofacial anomalies, hyperbilirubinemia requiring exchange transfusion, oxygen supplementation to a newborn with gestation age 36weeks or older, and hydrops fetalis were associated with
permanent HL.On the other hand, commonly known risk factors such as perinatal
infections, meningitis, sepsis, and ototoxic drugs did not show signicance related
to HL in the study cohort. Coenraad etal. [33] investigated risk factors in infants
with SNHL diagnosed after failure on neonatal hearing screening (NHS) admitted
to the NICU between 2004 and 2009in Rotterdam. Each patient was matched with
two same-gender and postconceptional age controls. A total of 3316 infants were
screened with BAER testing, and SNHL was diagnosed in 58 infants. They revealed
that the presence of dysmorphic features, low APGAR score at 1min, sepsis, meningitis, cerebral bleeding, and cerebral infarction were signicantly related to
SNHL [33].
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26.4.2 Acute Bacterial Meningitis Beyond Neonatal Period
Bacterial meningitis causes 250,000 deaths worldwide yearly and severe disabilities
in survivors [34]. Permanent HL rates range from 2.5% to 18% in children with
bacterial meningitis [35–38]. Invasion of bacteria to the cochlea and labyrinth, damage to the eighth cranial nerve by bacterial toxins, disruption of microcirculation,
and toxic effects of antibiotics used in the treatment are among the mechanisms
proposed to explain HL.In a study of 124 children aged 4weeks to 16years recently
diagnosed with bacterial meningitis from 21 hospitals in England and South Wales,
92 (74%) had meningococcal, 18 (15%) pneumococcal meningitis, and one case
each of meningitis due to H. inuenzae type b, L. monocytogenes, and GBS [35]. In
the remaining 11 cases (8%), all had cerebrospinal uid (CSF) neutrophil pleocytosis, and the pathogen was unknown. All patients showed obvious HL at the initial
evaluation. Three children had permanent, 13 (10.5%) had reversible SNHL, and
nine recovered within 48h of diagnosis.
The impact on the development of the child after meningitis can be devastating.
A cochlear implant offers a serious treatment possibility for severe SNHL developing after ABM.In cases of post-meningitis HL, it is particularly important to place
a cochlear implant as early as possible due to possible intracochlear ossication,
thus avoiding the insertion of electrodes into the cochlear lumen.
26.4.2.1 Etiology
While ABM is becoming less common in high-income countries because of the
widespread use of vaccines against H. inuenzae type b (Hib), S. pneumoniae, and
N. meningitidis, and the introduction of intrapartum antibiotic prophylaxis for GBS,
ABM still occurs worldwide, with a peak incidence in young children [39–41].
After the global introduction of the Hib and pneumococcal conjugate vaccines to
the infant immunization schedule, the epidemiology of ABM has been changing,
leading to a decrement in ABM incidence [42].
The etiology of ABM in children can vary by age, geographic region, acquisition
route, and host factors. For example, GBS and E. coli are the most common pathogens in neonates and young infants; however, enteric gram-negative bacilli, S. pneu-
moniae, and N. meningitidis are less common in this age group. In older infants and
children, S. pneumoniae and N. meningitidis are the most common, accounting for
approximately 60–70% of cases [43]. Furthermore, N. meningitidis is the most
commonly observed pathogen in adolescents, accounting for nearly half of all cases
[43]. Even with a 50–60% decline in the overall incidence of pneumococcal meningitis in the USA with the widespread pneumococcal vaccination, S. pneumoniae
remains the most common cause of ABM in children [44]. The most common frequent agents vary from region to region. For example, in the meningitis belt in subSaharan Africa, N. meningitidis accounts nearly 50–60% of cases [45]. In the
European region, N. meningitidis accounts for approximately 30–50% of cases, followed by S. pneumoniae (20–40%), GBS (10–15%), and H. inuenzae (5–15%)
[46]. In North America, S. pneumoniae is the most frequent pathogen, accounting
for 35–60% of cases, followed by N. meningitidis (15–25%), H. inuenzae (15–20%,
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predominantly non-type b in the post-Hib vaccine era), GBS (10–15%), E. coli
(7%), and L. monocytogenes (2–3%) [42, 43].
Hearing loss is the most common signicant sequela in survivors of childhood
ABM [47]. Also, the most important cause of acquired HL is ABM in childhood, as
10–34% of survivors develop HL with different severity [48].
A. Soysal et al.
26.4.2.2 Hearing Loss Related toStreptococcus
pneumoniae Meningitis
Sensorineural HL after S. pneumoniae meningitis is more frequent as two- to threefold of HL resulting from meningitis with other bacterial agents in childhood [49,
50]. The rate of HL due to pneumococcal meningitis may range from 20% to 52%
[51]. Adachi etal. [51] reported 155 children with meningitis; 27 (24%) children
developed HL, and 13 of them (12%) developed profound HL in 112 children with
bacterial growth in CSF culture. Moreover, of 22 patients in whom CSF culture
yielded S pneumoniae growth, 11 (50%) developed HL, and seven (32%) showed
profound HL.
Karpinen etal. [52] reported HL in Angola in 30% of children with S. pneu-
moniae meningitis. Wooley etal. [53] reported that 59 (13.7%) developed HL in
432 children with meningitis, and the HL was bilateral in 44 (74.6%) and unilateral
in 15 (25.4%) patients. They also revealed that 15 (23.8%) of the 63 (14.6%) children with S. pneumoniae meningitis in the 432 cases had resultant HL.Wellman
etal. [54] evaluated HL in 79 children with ABM, 68 (86%) underwent hearing
testing, 11 (13.9%) of them had an SNHL, and nine (80%) of these cases with
SNHL were associated with S. pneumoniae meningitis.
Richardson etal. [35] investigated HL and long-term outcomes of pediatric meningitis between 1993 and 1995in England. Etiological agents were N. meningitidis
in 92 (74%) and S. pneumoniae in 18 (15%) of a total of 124 children with meningitis. In this study, 83 children underwent audiological tests, and three children
(2.4%) had permanent SNHL.
Most previous studies reported HL before implementing Hib and conjugated
pneumococcal vaccines. According to the largest cohort after the Hib vaccine, HL
after non-Hib meningitis developed in 7% of children [49]. The leading risk factors
of HL after bacterial non-Hib meningitis were symptoms for ≥2days before admission, absence of petechiae, CSF glucose ≤10.8mg/dL, meningitis due to S. pneu-
moniae, and presence of ataxia [49, 50].
Although the benet of dexamethasone for the prevention of HL after non-Hib
meningitis is controversial, in a recent meta-analysis, it was stated give evidence
that the adjunctive administration of dexamethasone has a signicant effect on
decreasing the possibility of HL and severe neurological sequelae in children with
bacterial meningitis but has no signicant effect on the follow-up mortality [55, 56].
26.4.2.3 Hearing Loss Related toHaemophilus influenzae Type b
Meningitis
After developing and using the Hib conjugate vaccine, invasive Hib infections and
Hib meningitis have become rare in countries implementing Hib vaccines in routine
childhood vaccination schedules [57]. The invasive Hib disease can still be seen in
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infants below 1year of age whose Hib vaccine series has not been completed or
administered, such as in several low-income countries [52]. Karppinen etal. [52]
compared HL in ABM caused by Hib, S. pneumoniae, or N. meningitidis among
children aged 2months to 13years in Angola. The HL caused by Hib meningitis
was signicantly greater at >40dB.When children with any HL were divided into
two groups, infants (n 117) and children ≥1year of age (n 103), a signicant difference was found for S. pneumoniae and Hib versus other agents. In infants, HL at a
threshold >60dB was caused more by pneumococcal meningitis, whereas Hib was
the more common causative agent among older children [52].
A meta-analysis that included patients (n 2693) from low- and middle-income
countries showed that the median risk for HL after meningitis was 11% for S. pneu-
moniae and 5% for Hib and N. meningitidis [48].
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26.5 Use ofCorticosteroids inBacterial Meningitis
forPreventing Hearing Loss
According to the analysis by Brouwer etal. [58], steroids prevented any HL in 146
(14.6%) of 1001 corticosteroid-treated patients versus 196 (20.4%) of 960in the
control group and severe HL in 57 (7.3%) of 772 corticosteroid-treated patients
versus 86 (11.2%) of 752in the control group [58].
The mechanism of dexamethasone shows that it decreases proinammatory
cytokine production such as tumor necrosis factor-alpha (TNF-α) and interleukin-1
(IL-1), increases the production of anti-inammatory cytokines, inhibits reactive
oxygen species (ROS) production by leukocytes, and decreases leukocyte adherence. Furthermore, dexamethasone decreases intracranial pressure (ICP), brain
edema, and CSF pleocytosis with pneumococcal cell wall-induced meningeal
inammation [59–64].
The use of dexamethasone in Hib meningitis has positive evidence for the prevention of post-meningitis HL and other neurological complications. Subgroup
analysis yielded no difference in mortality for corticosteroid treatment between
low- and high-income countries. For children in high-income countries, corticosteroid treatment seems protective against severe HL and other short-term neurological
sequelae [56].
26.6 Conclusion
Several bacterial infections in children can cause HL.Early recognition and treatment of these infections will stop the process leading to HL.In some selected cases,
the appropriate class, dose, and duration of prompt antibiotic therapy for the agents
causing meningitis and dexamethasone therapy will mostly prevent HL.
The surviving children from ABM should be evaluated for SNHL.If a hearing
screening or follow-up reveals abnormal results, they may be consulted for early
cochlear implantation before chronic cochlear ossication develops.
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References
1. World Health Organization. Deafness and hearing loss. 1 Apr 2021. https://www.who.int/
news- room/fact- sheets/detail/deafness- and- hearing- loss. Accessed 3 Jan 2023.
2. Kral A, O’Donoghue GM.Profound deafness in childhood. N Engl J Med. 2010;363:1438–50.
3. Centers for Disease Control and Prevention (CDC). Identifying infants with hearing loss—
United States, 1999-2007. MMWR Morb Mortal Wkly Rep. 2010;59:220–3.
4. Vohr B.Overview: infants and children with hearing loss—part I.Ment Retard Dev Disabil
Res Rev. 2003;9:62–4.
5. Mitchell RE, Karchmer MA.Chasing the mythical ten percent: parental hearing status of deaf
and hard of hearing students in the United States. Sign Lang Stud. 2004;4(2):138–63.
6. Teele DW, Klein JO, Rosner B.Epidemiology of otitis media during the rst seven years of
life in children in greater Boston: a prospective, cohort study. J Infect Dis. 1989;160:83–94.
7. World Health Organization. Tuberculosis. 27 Oct 2022. https://www.who.int/news- room/fact-
sheets/detail/tuberculosis. Accessed 3 Jan 2023.
8. Starke JR.Tuberculosis, an old disease but a new threat to the mother, fetus and neonate. Clin
Perinatol. 1997;24:107–27.
9. Li C, Liu L, Tao Y.Diagnosis and treatment of congenital tuberculosis: a systematic review of
92 cases. Orphanet J Rare Dis. 2019;14:131.
10. Beitzke H.Uber die angeborene tuberkulose Infektion. Ergeb Ges Tuberk Forsch. 1935;7:1–30.
11. Cantwell MF, Shehab ZM, Costello AM, etal. Brief report: congenital tuberculosis. N Engl J
Med. 1994;330:1051–4.
12. Peng W, Yang J, Liu E. Analysis of 170 cases of congenital TB reported in the literature
between 1946 and 2009. Pediatr Pulmonol. 2011;46:1215–24.
13. Shao Y, Hageman JR, Shulman ST. Congenital and perinatal tuberculosis. Neoreviews.
2021;22:e600–5.
14. Du J, Dong S, Jia S, Zhang Q, Hei M.Clinical characteristics and post-discharge follow-up
analyses of 10 infants with congenital tuberculosis: a retrospective observational study. Pediatr
Investig. 2021;5:86–93.
15. Chotpitayasunondh T, Sangtawesin V. Congenital tuberculosis. J Med Assoc Thail.
2003;86(Suppl 3):689–95.
16. Aldana-Aguirre JC, El-Hakim H, Phillipos E, Landry MA.Congenital tuberculosis presenting
as otorrhea in a preterm infant. BMJ Case Rep. 2018;2018:bcr2017221797.
17. Ng PC, Hiu J, Fok TF, Nelson EA, Cheung KL, Wong W.Isolated congenital tuberculosis otitis
in a preterm infant. Acta Paediatr. 1995;84:955–6.
18. Naranbhai RC, Mathiassen W, Malan AF.Congenital tuberculosis localized to the ear. Arch
Dis Child. 1989;64:738–40.
19. Thigpen MC, Whitney CG, Messonnier NE, etal. Bacterial meningitis in the United States,
1998-2007. N Engl J Med. 2011;364:2016–25.
20. Hristeva L, Booy R, Bowler I, Wilkinson AR.Prospective surveillance of neonatal meningitis.
Arch Dis Child. 1993;69(1 Spec No):14–8.
21. Okike IO, Johnson AP, Henderson KL, etal. Incidence, etiology, and outcome of bacterial
meningitis in infants aged <90 days in the United Kingdom and Republic of Ireland: prospective, enhanced, national population-based surveillance. Clin Infect Dis. 2014;59:e150–7.
22. World Health Organization. Newborn and infant hearing screening: current issues and guiding principles for action. Geneva: WHO; 2010. p.1–38. https://www.who.int/publications/i/
item/9789241599496. Accessed 3 Jan 2023.
23. Ouchenir L, Renaud C, Khan S, etal. The epidemiology, management, and outcomes of bacterial meningitis in infants. Pediatrics. 2017;140(1):e20170746.
24. Stoll BJ, Hansen N, Fanaroff AA, etal. To tap or not to tap: high likelihood of meningitis without sepsis among very low birth weight infants. Pediatrics. 2004;113:1181–6.
25. Furyk JS, Swann O, Molyneux E.Systematic review: neonatal meningitis in the developing
world. Tropical Med Int Health. 2011;16:672–9.
26 Bacterial Infections inChildren andHearing Loss: AnOverview
https://t.me/medicina_free
26. Franco SM, Cornelius VE, Andrews BF.Long-term outcome of neonatal meningitis. Am J Dis
Child. 1992;146:567–71.
27. Haffner DN, Machie M, Hone E, Said RR, Maitre NL. Predictors of neurodevelopmental
impairment after neonatal bacterial meningitis. J Child Neurol. 2021;11:968–73.
28. Stevens JP, Eames M, Kent A, Halket S, Holt D, Harvey D.Long-term outcome of neonatal
meningitis. Arch Dis Child Fetal Neonatal Ed. 2003;88:f179–84.
29. Libster R, Edwards KM, Levent F, etal. Long-term outcomes of group B streptococcal meningitis. Pediatrics. 2012;130:e8–e15.
30. Doctor BA, Newman N, Minich NM, Taylor HG, Fanaroff AA, Hack M.Clinical outcomes of
neonatal meningitis in very-low-birth-weight infants. Clin Pediatr (Phila). 2001;40:473–80.
31. Maqbool M, Najar BA, Gattoo I, Chowdhary J.Screening for hearing impairment in high-risk
neonates: a hospital-based study. J Clin Diagn Res. 2015;9:SC18–21.
32. Thangavelu K, Martakis K, Fabian S, etal. Prevalence and risk factors for hearing loss in highrisk neonates in Germany. Acta Paediatr. 2019;108:1972–7.
33. Coenraad S, Goedegebure A, van Goudoever JB, Hoeve LJ. Risk factors for sensorineural hearing loss in NICU infants compared to normal hearing NICU controls. Int J Pediatr
Otorhinolaryngol. 2010;74:999–1002.
34. World Health Organization. Meningitis. 28 Sep 2021. https://www.who.int/news- room/fact-
sheets/detail/meningitis. Accessed 3 Jan 2023.
35. Richardson MP, Reid A, Tarlow MJ, Rudd PT.Hearing loss during bacterial meningitis. Arch
Dis Child. 1997;76:134–8.
36. Zeeshan F, Bari A, Dugal MN, Saeed F.Hearing impairment after acute bacterial meningitis in
children. Pak J Med Sci. 2018;3:655–9.
37. Fortnum H, Davis A. Epidemiology of permanent childhood hearing impairment in Trent
Region, 1985-1993. Br J Audiol. 1997;31:409–46.
38. Jusot JF, Tohon Z, Yazi AA, Collard JM. Signicant sequelae after bacterial meningitis in
Niger: a cohort study. BMC Infect Dis. 2013;13:228.
39. Schlech WF 3rd, Ward JI, Band JD, Hightower A, Fraser DW, Broome CV.Bacterial meningitis in the United States, 1978 through 1981. The national bacterial meningitis surveillance
study. JAMA. 1985;253:1749–54.
40. Wenger JD, Hightower AW, Facklam RR, Gaventa S, Broome CV. The bacterial meningitis
study group. bacterial meningitis in the United States, 1986: report of a multistate surveillance
study. J Infect Dis. 1990;162:1316–23.
41. Schuchat A, Robinson K, Wenger JD, etal. Bacterial meningitis in the United States in 1995.
N Engl J Med. 1997;337:970–6.
42. Pellegrino P, Carnovale C, Perrone V, etal. Epidemiological analysis on two decades of hospitalisations for meningitis in the United States. Eur J Clin Microbiol Infect Dis. 2014;33:1519–24.
43. Nigrovic LE, Kuppermann N, Malley R, Bacterial Meningitis Study Group of the Pediatric
Emergency Medicine Collaborative Research Committee of the American Academy of
Pediatrics. Children with bacterial meningitis presenting to the emergency department during
the pneumococcal conjugate vaccine era. Acad Emerg Med. 2008;15:522–8.
44. Whitney CG, Farley MM, Hadler J, etal. Decline in invasive pneumococcal disease after the
introduction of protein-polysaccharide conjugate vaccine. N Engl J Med. 2003;348:1737–46.
45. Soeters HM, Diallo AO, Bicaba BW, etal. Bacterial meningitis epidemiology in ve countries in the meningitis belt of sub-Saharan Africa, 2015-2017. J Infect Dis. 2019;220(Suppl
4):s165–74.
46. Oordt-Speets AM, Bolijn R, van Hoorn RC, Bhavsar A, Kyaw MH.Global etiology of bacterial meningitis: a systematic review and meta-analysis. PLoS One. 2018;13(6):e0198772.
47. Alamarat Z, Hasbun R.Management of acute bacterial meningitis in children. Infect Drug
Resist. 2020;13:4077–89.
48. Edmond K, Clark A, Korczak VS, Sanderson C, Grifths UK, Rudan I.Global and regional
risk of disabling sequelae from bacterial meningitis: a systematic review and meta-analysis.
Lancet Infect Dis. 2010;10:317–28.
399
400
https://t.me/medicina_free
49. Koomen I, Grobbee DE, Roord JJ, Donders R, Jennekens-Schinkel A, van Furth AM.Hearing
loss at school age in survivors of bacterial meningitis: assessment, incidence, and prediction.
Pediatrics. 2003;112:1049–53.
50. Kaplan SL, Woods CR. Neurologic complications of bacterial meningitis in children. Curr
Clin Top Infect Dis. 1992;12:37–55.
51. Adachi N, Ito K, Sakata H.Risk factors for hearing loss after pediatric meningitis in Japan.
Ann Otol Rhinol Laryngol. 2010;119:294–6.
52. Karppinen M, Pelkonen T, Roine I, Cruzeiro ML, Peltola H, Pitkäranta A.Hearing impairment
after childhood bacterial meningitis dependent on etiology in Luanda, Angola. Int J Pediatr
Otorhinolaryngol. 2015;79:1820–6.
53. Woolley AL, Kirk KA, Neumann AM Jr, et al. Risk factors for hearing loss from meningitis in children: the Children’s Hospital experience. Arch Otolaryngol Head Neck Surg.
1999;125:509–14.
54. Wellman MB, Sommer DD, McKenna J.Sensorineural hearing loss in postmeningitic children. Otol Neurotol. 2003;24:907–12.
55. American Academy of Pediatrics. Streptococcus pneumoniae (pneumococcal) infections. In:
Kimberlin DW, Barnett ED, Lyneld R, Sawyer MH, editors. Red Book: 2021–2024 report of
the committee on infectious diseases. 32nd ed. Itasca, IL: American Academy of Pediatrics;
2021. p.717–27.
56. Wang Y, Liu X, Wang Y, Liu Q, Kong C, Xu G. Meta-analysis of adjunctive dexamethasone to improve clinical outcome of bacterial meningitis in children. Childs Nerv Syst.
2018;34:217–23.
57. Centers for Disease Control and Prevention (CDC). Progress toward elimination of Haemophilus
inuenzae type b disease among infants and children—United States, 1987-1995. MMWR
Morb Mortal Wkly Rep. 1996;45(42):901–6.
58. Brouwer MC, McIntyre P, Prasad K, van de Beek D.Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev. 2015;2015(9):CD004405.
59. Freyer D, Weih M, Weber JR, etal. Pneumococcal cell wall components induce nitric oxide
synthase and TNF-alpha in astroglial-enriched cultures. Glia. 1996;16:1–6.
60. Rowland TL, McHugh SM, Deighton J, Dearman RJ, Ewan PW, Kimber I.Differential regulation by thalidomide and dexamethasone of cytokine expression in human peripheral blood
mononuclear cells. Immunopharmacology. 1998;40:11–20.
61. Dandona P, Mohanty P, Hamouda W, Aljada A, Kumbkarni Y, Garg R.Effect of dexamethasone on reactive oxygen species generation by leukocytes and plasma interleukin-10 concentrations: a pharmacodynamic study. Clin Pharmacol Ther. 1999;66:58–65.
62. Lorenzl S, Koedel U, Dirnagl U, Ruckdeschel G, Pster HW. Imaging of leukocyteendothelium interaction using in vivo confocal laser scanning microscopy during the early
phase of experimental pneumococcal meningitis. J Infect Dis. 1993;168:927–33.
63. Koedel U, Pster HW, Tomasz A.Methylprednisolone attenuates inammation, increases brain
water content and intracranial pressure, but does not inuence cerebral blood ow changes in
experimental pneumococcal meningitis. Brain Res. 1994;644:25–31.
64. Pster HW, Frei K, Ottnad B, Koedel U, Tomasz A, Fontana A.Transforming growth factor beta 2 inhibits cerebrovascular changes and brain edema formation in the tumor necrosis
factor alpha-independent early phase of experimental pneumococcal meningitis. J Exp Med.
1992;176:265–8.
A. Soysal et al.
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