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29 Meningococcal Infections inChildren andHearing Loss
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adaptation procedures necessary to return a survivor to a quality of life as close to
normal as feasible [13, 35].
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29.10 Health-Related Quality ofLife andCost ofIMD
Complicating withHearing Loss
Invasive meningococcal disease negatively inuences patients’ health-related quality of life (HRQoL) and their family and close caregiver network in the short and
long term. After several years, even IMD survivors who had no sequelae had a negative inuence on HRQoL, hurting self-esteem and physical, mental, and psychosocial health. Health-related quality of life was worse in those with cognitive and
behavioral sequelae. A large percentage of IMD survivors experience a variety of
sequelae and a reduction in HRQoL that lasts years after infection.
Compared to adults, childhood IMD survivors experience a greater number and
more severe sequelae [22]. In a high-income country, the estimated burden of IMD
sequelae in terms of quality-adjusted life-years lost varies by type and degree of
sequelae. Hearing loss, blindness, motor decits, neurological sequelae, convulsions, scarring, mental retardation, and attention decit hyperactivity disorder
(ADHD) are all associated with signicant nancial costs [3]. Quality-adjusted lifeyears lost for most to least severe sequelae were calculated to be 0.19 for HL if 1.0
represents 1year in ideal health. The longer the interval between birth and the projected occurrences, the lower the current value of expenses will be [35].
Invasive meningococcal disease can cost the healthcare system and society a lot
of money. The high expenditures per IMD case reect the disease’s severity in each
patient, mainly due to the development of sequelae. In the study by IvanovaMarkova etal. [52], psychological impairment was the costliest outcome in most
age groups, followed by renal failure, HL, and neurological damage. Indirect
expenses and long-term repercussions, such as HL, should be considered when calculating the economic impact of IMD [52]. Davis etal. [46] compared healthcare
utilization and costs in IMD patients with and without linked sequelae to understand
better the economic impact these sequelae have. They found that predicted healthcare costs for patients with complicated IMD were three times higher than those
with uncomplicated IMD.Patients with severe IMD were more likely than those
with uncomplicated IMD to require rehospitalization after their initial IMD
admission.
Huang etal. [53] evaluated the economic impact of IMD in Germany in a sample
population of 164 IMD cases between 2009 and 2015, highlighting signicant
expenses and increased healthcare resource consumption, notably in the rst year
following diagnosis and due to IMD-related hospitalization. In the cost- effectiveness
study by Ivanova-Markova etal. [52] in Spain, sequelae costs accounted for 62.5%
of the total cost [52]. Another study looked at the expenditures incurred by all IMD
patients in France over 6years, nding that the majority of the extra costs were due
to the care of sequelae in most cases [54]. Amputation, skin scarring, mental
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retardation, and bilateral HL were the most expensive of these sequelae in the year
following the index hospitalization, all costing more than €20,000in the rst year.
As a result, policymakers and scientists may nd these ndings helpful in creating and conducting cost-effectiveness studies of vaccination programs.
E. Ç. Dinleyici et al.
29.11 Prevention
Invasive meningococcal disease must be recognized quickly and aggressively
treated as soon as possible to reduce mortality. To help improve patient outcomes,
early detection and delivery of effective antibiotic treatment, as well as proper management of IMD consequences such as circulatory shock and elevated intracranial
pressure, are crucial [50].
Vaccination is the most effective way to avoid ABM and its associated consequences. Highly effective vaccinations are available for the three most common
ABM causes. Over the last three decades, the introduction of conjugated vaccines
against H. inuenzae type b, S. pneumoniae, and N. meningitidis has resulted in a
signicant reduction in the incidence rate of ABM in countries where these vaccines
are included in routine infant and child immunization programs. Routine immunization can lead to the formation of community protection by preventing transmission
within a population in an indirect way [55]. The frequency of acquired SNHL in
children living in high-income countries has been reduced over the last three to four
decades as a result of improved newborn care and the widespread implementation
of immunization programs [29].
Vaccination is the only sensible way to prevent IMD and related morbidity and
mortality. In spite of the fact that the primary goal of the meningococcal vaccines is
to avoid severe and, in many cases, deadly complications, a secondary benet would
be a reduction in disease-related consequences such as HL, which can lead to longterm handicaps in survivors. After meningitis, the onset of SNHL might be unpredictable. Hearing loss and seizures are most common in children under the age of
1year, while skin scarring and amputation are most common in children between 1
and 4 years. These consequences are all likely to have a long-term inuence on
health and healthcare expenses, so they are crucial to consider when weighing the
benets of routine meningococcal immunization.
Immunization is provided in certain countries through national immunization
programs (NIPs), whereas in others, vaccination is only offered to high-risk populations or for outbreak control. To maximize coverage, it is best to include vaccination
using NIPs. The country- and serogroup-specic incidence of N. meningitidis by
age group is the most critical component in vaccination recommendations. It underscores the signicance of ongoing surveillance to ensure vaccines available to those
who need them most quickly. Immunizing children and high-risk patient populations with existing meningococcal vaccines may minimize disease among vaccines,
prevent outbreaks, and drastically limit N. meningitidis transmission. To reduce
IMD-related morbidity and death, global coordinated, sustained, and long-term
policies and active surveillance are urgently needed in all nations.
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29.12 Conclusion
Invasive meningococcal disease is still a signicant public health concern worldwide, not only because of its high mortality rate but also because of its severe disabling sequelae, such as HL. Vaccination of children and high-risk patient
populations may minimize N. meningitidis transmission, IMD burden, and IMDrelated complications. It is best to implement meningococcal vaccines into NIPs to
reduce the rates of IMD-related mortality and morbidity, including HL.
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Haemophilus influenzae Type b
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Meningitis inChildren andHearing Loss
TürkanAydınTeke, NazanDalgıç, andFatmaLevent
30.1 Introduction
Haemophilus inuenzae was discovered in 1889 by Richard Pfeiffer during the
inuenza pandemic and was named inuenza bacillus [1]. Since it requires blood
factors for growing, the bacterium was renamed Haemophilus, meaning “blood lov-
ing.” This gram-negative coccobacillus colonizes the nasopharynx and upper respiratory tract in humans. Depending on the presence of a polysaccharide capsule,
isolates of H. inuenzae can be encapsulated (typeable) or nonencapsulated (nontypeable) strains. Haemophilus inuenzae has six encapsulated serotypes, a–f [1, 2].
Haemophilus inuenzae capsular serotype type b (Hib) is a signicant cause of
invasive diseases in nonimmunized populations, accounting for 95% of all
strains [2, 3].
30
T. A. Teke (*)
Section of Pediatric Infectious Diseases, Dr. Sami Ulus Maternity Child Health and Diseases
Training and Research Hospital, Ankara, Türkiye
e-mail: turkanteke@gmail.com
N. Dalgıç
Section of Pediatric Infectious Diseases, İstanbul Şişli Etfal Training and Research Hospital,
University of Health Sciences, İstanbul, Türkiye
e-mail: nazandalgic@ttmail.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_30
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T. A. Teke et al.
30.2 Epidemiology
Haemophilus inuenzae type b is a human pathogen, and no known host exists other
than humans [4]. Nasopharyngeal colonization, especially by nonencapsulated
strains, is common. The transmission mode is mainly by droplet inhalation or direct
contact with secretions from the respiratory tract. During the pre-vaccine era, most
young children were colonized with Hib, the commonest cause of bacterial meningitis and other invasive diseases [3]. After the rst Hib vaccine was accredited in
1989, there has been a dramatic decrease in the incidence of Hib invasive disease in
countries with high vaccination rates [5]. The incidence of Hib invasive disease
decreased by nearly 99% in children under 5 years in the United States of America
(USA) [6]. Children below 18months have the highest risk for invasive Hib disease,
with a peak incidence between 6 and 9months; the risk decreases gradually after 2
years of age [2].
Due to maternal antibodies passed through the placenta and breastfeeding during
the rst 6 months, some infants have protection against Hib [3]. Antibodies to the
polysaccharide capsule, composed of polyribosyl-ribitol-phosphate (PRP), confer
protection against invasive Hib infections. Systemic Hib disease is rare after 6 years
of age because of naturally acquired antibodies to PRP [4]. Invasive Hib diseases
currently occur in unimmunized children. After the extensive usage of the conjugate
vaccine, invasive H. inuenzae disease in the USA is predominantly caused by nontype b serotypes and non-typeable strains [7]. Haemophilus inuenzae type b is still
one of the leading causes of invasive infections in low-income countries where vaccines are unavailable [2, 8].
30.3 Microbiology
Haemophilus inuenzae type b is a nonmotile, nonspore-forming, pleomorphic
gram-negative coccobacillus that can grow in aerobic or anaerobic conditions. The
organism requires two supplements for in vitro growth; X factor (hemin), heatstable, and V factor (nicotinamide-adenine-dinucleotide), heat-labile. Haemophilus
inuenzae type b can be cultured in most media enriched with X and V factors.
These factors are present in erythrocytes and permit the organism to grow on chocolate agar. The need for these factors differentiates Hib from other Haemophilus
species under laboratory conditions. Clinical samples should be immediately inoculated onto appropriate media because Hib is a fastidious microorganism, and its
viability is lost rapidly. Some strains benet from incubation with 5–10% carbon
dioxide [4, 8].
Haemophilus inuenzae type b has several virulence factors. The polysaccharide
capsule, the most important virulence factor, prevents phagocytosis and complementmediated lysis. Other virulence factors are noncapsular cell wall proteins, immunoglobulin A (IgA) proteases, and lipooligosaccharide (LOS) [2, 8]. Additionally, the
binding of Hib to mucus and the respiratory epithelium is mediated by pilus and
non-pilus adherence factors. Variation of bacterial antigen, entrance into host cells,
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penetration between host cells (paracytosis), LOS changes, and formation of biolm inuence persistence on mucosal surfaces [1].
Determining the capsular type expressed by Hib is essential for clinical and epidemiological purposes. Polymerase chain reaction (PCR) techniques targeting the
capsular gene locus (cap locus) have been developed to accurately identify strains
expressing the six recognized capsular types. These techniques benet patients
whose cultures are negative because of previous antibiotic use [2, 6]. Due to their
low sensitivity and specicity, antigen detection methods are not recommended.
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30.4 Pathogenesis
Haemophilus inuenzae type b infection begins with colonizing respiratory mucosal membranes with microorganisms. Otitis media, sinusitis, conjunctivitis, bronchitis, and pneumonia may develop after colonization. Anatomic factors, antecedent
viral respiratory tract infections, especially inuenza virus infection, immunodeciencies, and exposure to cigarette smoke are among predisposing factors for respiratory tract disease. Haemophilus inuenzae type b can penetrate the nasopharyngeal
epithelium from the upper respiratory tract mucosa and spread to the bloodstream.
Bacteremia precedes nearly all invasive Hib diseases, but direct extension from
adjacent sinusitis, otitis media, or conjunctivitis may occur in some situations. The
polysaccharide capsule protects Hib from phagocytosis, and the bacterium can survive and disseminate to distant sites, more commonly to the meninges [1, 2, 4].
30.5 Clinical Manifestations
Haemophilus inuenzae type b usually causes severe diseases and requires hospitalization, especially in infants. The most typical clinical presentations of Hib infection are epiglottitis, otitis media, pneumonia, bacteremia, meningitis, cellulitis,
septic arthritis, and purulent pericarditis [6].
30.5.1 Meningitis
Meningitis is the most familiar and gravest clinical presentation of invasive Hib
disease, accounting for 40–75% of invasive cases [8]. The signs and symptoms are
usually nonspecic and may include fever, vomiting, irritability, and lethargy, particularly in young infants. Classic ndings of bacterial meningitis, including headache, photophobia, and meningismus, are seen in older children. Infants often do
not have nuchal rigidity. Occasionally, fulminant Hib meningitis may occur with
seizures, coma, and respiratory arrest. Cranial nerve palsy indicates increased intracranial pressure. In addition, petechial or purpuric rash and shock may occur [1].
Between 10% and 20% of children with meningitis have cellulitis, arthritis, or pneumonia concomitantly [2, 6]. Subdural effusion is a common complication. Clinicians
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should be alert if seizures, mainly focal, hemiparesis, or neurologic deterioration,
occur [4].
T. A. Teke et al.
30.6 Diagnosis
Blood cultures are important in any febrile child at risk of Hib disease. The focal
illness may develop in 30–50% of patients with occult Hib bacteremia, so these
children should be reevaluated carefully [2, 8]. Collected body uids such as blood,
cerebrospinal uid (CSF), pleural uid, or synovial uid should be cultured on
appropriate media [3, 8]. Cerebrospinal uid analysis is necessary to identify the
causative organism and antibiotic test sensitivity. Pleocytosis with a predominance
of polymorphonuclear leukocytes is typically seen in CSF analysis. Most patients
with meningitis have hypoglycorrhachia and an elevated CSF protein concentration.
Cerebrospinal uid lactate may distinguish bacterial meningitis from aseptic meningitis, except in patients who received antimicrobial treatment before the lumbar
puncture [5]. Approximately 70–80% of patients with Hib meningitis have a positive CSF gram stain [1, 2]. Positive CSF culture is the gold standard for diagnosing
Hib meningitis [2]. All isolates of H. inuenzae are supposed to be serotyped. A
slide agglutination test may detect capsular polysaccharide antigens in CSF but has
low sensitivity and specicity [3]. Serotype-specic real-time PCR assays can
detect each serotype and be used to diagnose Hib meningitis, especially when antibiotics were previously administered [3, 9].
30.7 Treatment
30.7.1 Antibiotic Therapy
Since mortality reaches nearly 100% without treatment, Hib meningitis should be
diagnosed and treated promptly. Antimicrobial therapy should be initiated swiftly
for a good prognosis. The treatment of choice for Hib meningitis is third-generation
cephalosporins. Cefotaxime (200–225mg/kg/day, every 6h) or ceftriaxone (100mg/
kg/day, every 12h) are potential bactericidal drugs against Hib [10]. An intravenous
administration of antimicrobials should be considered to achieve high CSF levels
[1]. Treatment usually takes 7–10days for noncomplicated cases [8].
30.7.2 Corticosteroids
Administration of dexamethasone with antibiotics is recommended in children
older than 6 weeks with Hib meningitis, decreasing the rate of neurological sequelae
and sensorineural hearing loss (SNHL) [11]. Dexamethasone (0.15 mg/kg every
6h) should be started just before or concurrently with the rst dose of antibiotics in
the rst 4 days of treatment [1, 2, 8]. Dexamethasone can still be administered up to
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4h after starting the rst dose of antibiotics [12]. However, dexamethasone should
be used carefully in bacterial meningitis as it may lead to low penetration of antibiotics (e.g., vancomycin) into the CSF.Dexamethasone may cause fever recurrence
and change the clinical and bacteriological response to antimicrobial treatment [9].
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30.8 Complications
Subdural effusion or empyema, cerebritis, ventriculitis, intracerebral abscess, cortical infarction, cerebral herniation, and hydrocephalus are among the most common
complications of Hib meningitis [2]. The leading neurologic sequelae are seizures,
SNHL, vision impairment, and behavior abnormalities. Haemophilus inuenzae
type b meningitis has a mortality rate of 3–6% [8].
30.9 Haemophilus influenzae Type b Meningitis
andHearing Loss
Bacterial meningitis is the commonest cause of acquired SNHL in children [13].
Although Hib meningitis was the most common type in the pre-vaccine era, SNHL
occurred most often in children with pneumococcal meningitis. Despite adequate
treatment regimens, SNHL is a signicant neurological sequela of Hib meningitis.
In a study about acute-phase neurologic complications of Hib meningitis, 42%
(53/126) of patients had at least one acute-phase complication on neurologic examination, while 12% (15/126) had SNHL [14]. In another study, where 185 infants and
children with acute bacterial meningitis (64% with Hib meningitis) were followed
up for 15.5 years (mean duration was 8.9 years) for neurological abnormalities,
persistent SNHL was detected in 18 (10%) patients [15]. Several reports reported
SNHL in 5–10% of the patients with Hib meningitis [1, 16, 17]. In Africa, the risk
of SNHL in Hib meningitis may be up to 26% [18].
Predictors of SNHL include delayed presentation, delayed initiation of antibiotics, young age, severe illness, raised intracranial pressure at admission, reduced
CSF glucose, and elevated CSF protein [17–20]. In a prospective study involving 44
infants and children with Hib meningitis, patients were grouped according to their
pretreatment concentrations of bacteria in CSF [21]. The study revealed that patients
with greater than or equal to 107 colony-forming units (CFUs) of Hib/ml in CSF
before treatment were more likely to have neurologic sequelae, including SNHL,
than those with less than 107 CFUs of Hib/ml in CSF.The authors concluded that
the concentration of bacteria in CSF predicts SNHL in Hib meningitis. High endotoxin concentrations at the time of diagnosis in CSF correlated with permanent
neurologic complications, including SNHL, in patients with Hib meningitis was
also demonstrated [22].
The main pathogenic steps required for initiating Hib meningitis include bacterial colonizing the mucosa, spreading to the surrounding tissue, into the bloodstream, invading the meninges, replicating, and inammation of the subarachnoid
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