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A. Tekin Yılmaz et al.
Table 28.3 Drugs and dosages used to treat pneumococcal meningitis
Dose/kg/
Agent
Ceftriaxone 100mg 12–24h In combination with vancomycin in empirical therapy
Cefotaxime 225–
Vancomycin 60mg 6–8h In combination with ceftriaxone or cefotaxime in
Penicillin G 150–
Dexamethasone 0.6mg 6h for
a
Adapted and modied from Refs. [16, 65]
day
300mg
240mg
Dose
interval
OR
If the agent has been shown to be cephalosporinsusceptible, it can be used as a monotherapy.
8h In combination with vancomycin in empirical therapy
OR
If the agent has been shown to be cephalosporinsusceptible, it can be used as a monotherapy.
empirical therapy.
4–6h If the agent is shown to be penicillin-susceptible, it
can be used in the treatment.
The decision to use in treatment should be made on
2days
an individual basis. If used, it should provide the
most signicant benet in terms of preventing
hearing loss and neurological sequelae.
Either before or concurrently with antibiotic
treatment.
a
There has been no signicant change in antibiotic options for PM treatment over
the years. Even in the best-case scenario, in which effective antibiotics are used at
appropriate doses and intervals without delay, PM remains a problem due to its high
mortality and frequency of causing permanent problems.
28.7 Pneumococcal Meningitis andHearing Loss
Pneumococcal meningitis has a higher HL rate than meningitides caused by other
leading agents. Particularly since the introduction of the conjugate Hib vaccine and
the subsequent decline in Hib-induced meningitis cases, PM has become the primary cause of HL.In a study conducted before widespread Hib vaccination, the
prevalence of HL following Hib meningitis was 34% [66]. In comparison, the prevalence of HL after PM was 30%, and in this study, PM was the leading cause of HL
in children younger than 12months. Hearing loss is a common complication of PM,
occurring in up to 54% of cases [67].
The study by Worsøe etal. [67] detected some cases of HL during follow-up, in
which the initial hearing tests performed at the end of PM treatment were normal.
Ears may be affected unilaterally or bilaterally, ranging from mild HL to total deafness. The severity of clinical ndings, the CSF characteristics, the high concentration of bacteria in CSF, the delay in initiating appropriate treatment, and the presence
of concurrent otitis were determined as risk factors for developing HL [67].
However, another theory argues that effective and timely treatment cannot prevent
HL since the damage that results in HL occurs early in the process [12].
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28.7.1 The Architecture andPhysiology ofHearing
Sound is mechanically conveyed to the inner ear by increasing intensity through the
outer and middle ears. The inner ear is where sound is processed neurally. When PM
impacts tissues in the inner ear, HL develops. The cochlea, the most critical inner
ear component, is a tubular structure that rotates 2.75 times around the modiolus, a
cone-shaped bone. Two membrane structures split it into three chambers. In the
upper and lower chambers, perilymph uid lls the scala vestibuli and scala tympani. The scala media is lled with endolymph uid not connected directly to the
chambers. The densities, electrolyte levels, and electrical charges of perilymph and
endolymph uids differ. The cochlea is tonotopically structured; the basal portion is
responsive to high-frequency sounds, while the apical part is more sensitive to lowfrequency sounds.
The organ of Corti is a spiral-shaped structure that extends beyond the cochlea’s
basal membrane, which is equipped with hearing receptors. Four rows of hair cells
have hearing receptors. The rst three rows are called outer hair cells, and the
fourth-row inner hair cells. In particular, damage to the outer hair cells results in
sensorineural HL (SNHL). Hearing loss following meningitis is most noticeable in
the high-frequency ranges and is anatomically tied to the cochlea’s basal region.
Although it is unknown how bacteria, proinammatory cytokines, or bacterial
products reach the inner ear during meningitis, dissemination from the CSF, through
the bloodstream, or the eighth nerve may be possible [68]. Purulent labyrinthitis
results from infection spreading to the cochlear canal, and over time, the structure
of the membranous labyrinth becomes brous, resulting in HL.
28.7.2 Pneumococci andHearing Loss
Animal studies showed that outer hair cells are more susceptible to pneumococci;
their destruction increases in direct proportion to bacterial density and contact time
[69]. Proinammatory cytokines, whose levels increase in direct proportion to bacterial density, primarily affect outer hair cells and cause HL [68, 69]. Inner hair cells
are more resistant to pneumococci’s direct impacts. Tumor necrosis factor-alpha is
the most potent ototoxic cytokine and directly attacks hair cells [69]. In CSF, TNF-α
levels have been associated with the rate of long-term HL in patients with acute
PM [68].
Pneumolysin toxin is directly associated with HL [69]. As demonstrated in animal studies, HL is considerably reduced in meningitis caused by pneumococci that
cannot produce pneumolysin [69]. Pneumolysin has different effects on different
structures depending on the dose. While it affects inner hair cells at low concentrations, it signicantly affects outer hair cells at high concentrations. Its effect on
outer hair cells is also dose-dependent [68]. Pneumolysin has a lesser effect on outer
hair cells placed apically [68, 69]. Pneumolysin damages inner and outer hair cells;
the basal region and middle part of the hair cells are more sensitive to the toxin.
Being more susceptible of the regions responsible for high-frequency processing
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sounds to damage explains why post-meningitis HL is more pronounced in highfrequency sounds [68].
Because nitric oxide and oxygen radicals, and the cytokines secreted or released
during acute infection, are similarly ototoxic, it was postulated that the apical and
basal regions are affected differently due to their varied antioxidant production
capacities [68].
In summary, increased bacterial density, proinammatory cytokines, oxygen and
nitrogen radicals, and bacterial toxins contribute to an increased risk of HL in
PM.Concurrent otitis is identied as a risk factor [68]. Hearing loss is believed to
occur in the context of otitis due to the effect of toxins on the cochlea, not the bacteria themselves [70].
Bacteria that enter the cochlear canal via the subarachnoid space reach the perilymph uid and produce suppurative labyrinthitis histologically [71]. Histopathology
of the acute period reveals the breakdown of the labyrinth–blood barrier and the
destruction of the spiral ganglion and cochlear cells. In contrast, the long-term
period reveals brotic alterations in the perilymphatic area [72]. Hearing loss necessitating cochlear implant treatment occurs in 5% of instances following PM [73].
The implant is only helpful if sufcient healthy neurons exist in the cochlea. As a
result, therapy techniques that protect spiral ganglion cells might be benecial in the
treatment of PM [72, 73].
All children diagnosed with acute bacterial meningitis should be examined for
HL in the early stages. Hearing tests should be performed, ideally before hospital
discharge, and follow-up should be established for cases with any documented HL.
A. Tekin Yılmaz et al.
28.7.3 Unresolved Issue
Dexamethasone is used in the treatment of bacterial meningitis to reduce inammation because the severity of inammation in the subarachnoid space is linked to
mortality and long-term consequences [74]. Although steroids are commonly used
in treatment, there is still scarce scientic evidence that they improve survival or
lessen neurological damage [74, 75]. Historically, steroid usage in treating bacterial
meningitis did not diminish death, HL, or the development of other irreversible
neurological disorders, according to meta-analyses published in the late 1980s [76].
However, subgroup analyses revealed that when given before or simultaneously
with antibiotic treatment, steroid use reduces HL, particularly in children with Hib
meningitis [76, 77]. Dexamethasone treatment was not benecial in a randomized
controlled trial on the pediatric age, in which 40% of the cases were PM [46].
On the other hand, a 2015 Cochrane review concluded that dexamethasone treatment successfully reduced HL and neurological sequelae in patients with acute bacterial meningitis in high-income countries but was ineffective in others [78]. One
possible explanation for this disparity is that the chances of obtaining appropriate
therapy during the early stages of the disease vary signicantly between countries.
The effect of corticosteroids on mortality could not be established in this review.
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Dexamethasone has been shown to protect against severe HL only when given early
in the course of bacterial meningitis [78, 79].
Due to the subject’s uncertainties, although dexamethasone is still routinely used
in clinical practice, its use in compliance with recommendations is extremely low.
In addition, some discrepancies exist in the recommendations of the clinical practice guides. The American Academy of Pediatrics (AAP) recommends dexamethasone for children aged 6weeks and older after considering the benets and risks and
making a case-by-case decision, but this is not a standard recommendation [15].
Sufcient evidence does not exist to support dexamethasone use for neonatal meningitis. The Infectious Diseases Society of America (IDSA) recommends dexamethasone for adults with bacterial meningitis [80].
Regarding PM, the rise in pneumococci resistant to third-generation cephalosporins and hence the need for empiric treatment with vancomycin has given a new
dimension to the problem. Vancomycin has limited penetration into the CSF, and its
transmission into the CSF rises when meningeal permeability increases during meningitis [80]. Vancomycin may not reach an effective concentration in the subarachnoid space due to the decreased permeability of the meninges caused by
dexamethasone. However, scientic evidence could not substantiate this hypothesis
[80, 81].
Along with the unproven clinical benet, the potential side effects of dexamethasone should be considered. More caution should be taken in the assessment of hospitalized patients treated with dexamethasone, as clinical ndings may be suppressed
by dexamethasone.
In summary, dexamethasone use in treating children with PM should be determined on a case-by-case basis, with careful monitoring of clinical and laboratory
ndings in treated cases. Table28.3 shows the recommended dexamethasone dose
and duration of use [65].
435
28.7.4 New Treatment Approaches: Experimental Treatments
Early and effective treatment cannot signicantly reduce the frequency of HL and
other neurological problems in children with PM.On the other hand, the development of cell-tissue damage resulting in HL during the early stages of meningitis is
related to the host’s inammatory response rather than the bacteria itself. So, treatment research has focused on this direction. Although dexamethasone is an effective
anti-inammatory, it did not act as well as predicted, which prompted the quest for
other treatments.
As known, bacterial cell wall components produced from fast bacterial death
induced by antibiotic therapy exhibit antigenic features and bind to TLRs. The
majority of TLRs are intracellularly attached via the MyD88 protein. The activation
of NF-kB by MyD88 signals increases proinammatory cytokine levels and cell
damage [82]. New treatment approaches aim to stop or slow down this process at
any point.
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Numerous therapy combinations have been investigated in trials to control inammation by lowering the elevated antigen load. In animal trials, positive results were
observed when third-generation cephalosporins that cause bacterial lysis were combined with non-bacteriolytic antibiotics [83–85]. Daptomycin is the most extensively
investigated antibiotic in this eld, as it is efcient against cephalosporin- resistant
pneumococci. A study comparing ceftriaxone and daptomycin monotherapies determined that sterilization of CSF was faster with daptomycin, caused less inammation during the treatment phase, and caused less cortical brain damage [86]. A
comparable study demonstrated that daptomycin therapy protects against cognitive
and learning function damage [84]. In another experimental study, when daptomycin
and anti-inammatory doxycycline were added to ceftriaxone treatment, cortical
necrosis was reduced, inammatory cytokines decreased signicantly in CSF, and
HL was also reduced in the evaluation at the end of third weeks [85].
When matrix metalloproteinase inhibitors were administered in conjunction with
non-bacteriolytic antibiotics, TNF-a, IL-1, IL-6, and IL-10 levels decreased signicantly in the groups receiving adjuvant medication, while learning and cognitive
abilities improved and HL decreased [87]. Additionally, it is well established that
HL is reduced when antioxidant medication is used with conventional antibiotic
therapy to counteract the harmful action of oxygen and nitrogen radicals [88].
However, this strategy is still in its infancy and has not yet found a home in clinical
practice [88].
Animal trials have examined various anti-inammatory therapeutic alternatives,
such as antioxidant medicines [89]. Metformin was the subject of one of the most
recent investigations. In a mouse experiment, metformin administration decreased
inammatory cytokine and nitric oxide levels in CSF and astroglial cell cultures
[88]. Mice treated with metformin plus ceftriaxone had reduced cortical necrosis
and HL on a follow-up hearing test. Another property of metformin is that it is neuroprotective for inner ear ganglion cells [89].
Neurotrophins (NTs) are proteins that ensure the growth and maintenance of
neurons. Neurotrophins in the cochlea are known as NT-3 and brain-derived neurotrophic factor (BNDF). Animal experiments have shown systemic NT-3 treatment
effectively protects neurons in PM. The discovery that permanent pathological
abnormalities are signicantly more pronounced when therapy is administered after
the 24th hour reafrms that early-stage damage is related to neurological complications and HL [70].
A. Tekin Yılmaz et al.
28.8 Conclusion
Pneumococcal meningitis and associated complications continue to be a problem
despite the introduction of PCVs in childhood immunization practices over the past
25years and the expansion of treatment options. Although new treatment options
are promising, increasing vaccination rates and updating national immunization
programs in light of evolving epidemiological data appear to be the most efcient
strategies for preventing pneumococcal infections under current conditions.
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437
Monitoring all cases with a meningitis diagnosis in terms of HL will allow for
early detection and proper management of the disorder before concerns such as
HL-related learning difculties and developmental delays occur.
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