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21 Bacterial Meningitis inChildren andHearing Loss
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Other presentations may be seizure, petechiae, and purpura, particularly in meningococcal meningitis, increased intracranial pressure signs including hyper­tension, bradycardia, respiratory depression, focal neurologic decits, and other systemic ndings [1, 14].
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21.5 Diagnosis
Acute bacterial meningitis requires prompt diagnosis and optimal treatment within 1h of presentation. Antibiotics should be initiated immediately, even if a lumbar puncture (LP) cannot be performed due to sepsis symptoms, including hypotension, bradycardia, and respiratory failure [33]. However, blood cultures should be obtained before antibiotics are administered to increase the likelihood that the caus­ative pathogen will be isolated to guide subsequent antibiotic treatment and help determine the need for antibiotic prophylaxis for patient contacts. The history should include the type and duration of symptoms, presence of predisposing risk factors (immunodeciency, anatomic defect, medical devices, and trauma), travel or contact history, immunization history, and recent antibiotic use [1].
Cerebrospinal uid culture is essential in the diagnosis of bacterial meningitis and should be obtained via LP in children with suspicion of this diagnosis unless there is a contraindication to do so. Neuroimaging should be performed before LP in the presence of the focal neurologic decit, papilledema, and altered level of consciousness in the neurological examination. Lumbar puncture is contraindicated in cases with a mass lesion due to the risk of cerebral herniation and in patients with coagulopathy, severe thrombocytopenia, cardiopulmonary compromise, and local site infection where the LP would be performed [1, 14, 32, 34, 35].
Cerebrospinal uid evaluation should include macroscopic and Gram stain examination, cell count and differential, glucose and protein concentration, culture, antimicrobial susceptibility testing of isolated microorganisms, and possibly PCR [1, 34]. Cerebrospinal uid ndings in ABM include pleocytosis with a predomi­nance of neutrophils, elevated CSF protein, decreased CSF glucose, and a positive Gram stain [32, 34, 35]. Typically, CSF is clear in appearance and shows <6 white blood cells/mm3 with no neutrophils, glucose level >45 mg/dL, and protein level<45 mg/dL. In ABM, the appearance of CSF is usually cloudy. The typical CSF white blood cell count (WBC) is >1000 cells/mm3 with a predominance of neutrophils (80–95%); however, it can be lower in the early phase of ABM.The CSF glucose level is typically low, usually <60% of a concomitantly measured blood glucose level and usually <40mg/dL; protein level can be high as 100–500mg/ dL [32, 34]. A traumatic LP can impact the CSF cell count and protein measure­ments due to bloody CSF; the rst drawn tube carries the highest risk for red blood cells (RBCs) from a traumatic LP and contamination of non-CSF bacteria.
A bacterium can be determined via Gram staining in nearly 80% of the patients if an antibiotic has not already been administered. A positive Gram stain may help guide antibiotherapy. The characteristic morphologic features of the common pathogens are as follows: Gram-positive diplococci suggest S. pneumoniae,
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gram- negative diplococci suggest N. meningitidis, and small pleomorphic gram- negative coccobacilli suggest Hib, gram-positive cocci or coccobacilli indicate GBS, and gram-positive rods and coccobacilli suggest L. monocytogenes [31, 34,
35]. Acute bacterial meningitis is conrmed with the isolation of bacteria from
CSF. However, prior administration of antimicrobial agents may alter CSF bio­chemical parameters and cell count, while CSF culture may be negative [34]. The PCR test may identify the causative pathogen in pretreated children with suspected bacterial meningitis [36]. Latex agglutination and immunochromatographic antigen tests have little value in diagnosing ABM and are unavailable in many centers [32].
Neuroimaging should not be performed routinely before LP and should be reserved for patients with severely altered mental status (Glasgow Coma Scale score<10), papilledema, focal neurologic decit (excluding cranial nerve palsies), CSF shunt in place, history of hydrocephalus, recent CNS trauma or neurosurgery, severely immunocompromised status, and new-onset seizure [32]. Neuroimaging is typically recommended for the evaluation of the complications of ABM, such as hydrocephalus, subdural effusion, empyema, infarction, parenchymal abscess, and ventriculitis in patients with persistent fever (>5days), new-onset fever or seizures occurring after 48–72h despite appropriate treatment [37].
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21.6 Management
Empiric antibiotic therapy should be administered, even if LP cannot be performed in which case blood cultures should be obtained prior to antibiotic administration [32, 34, 35]. Appropriate respiratory and hemodynamic support should be based on disease severity. Patients are initially managed optimally in a pediatric intensive care unit.
The empiric antibiotic treatment differs for neonates and older children. While choosing empiric treatment, the local rate of decreased susceptibility to penicillin and third-generation cephalosporins of S. pneumoniae should be considered. Table21.1 summarizes the empiric therapy for community-acquired ABM in chil­dren [32].
Antibiotic treatment should be optimized for antibiotic susceptibility testing when the culture identies a causative pathogen. Reduced susceptibility to penicil­lin and third-generation cephalosporins of S. pneumoniae are concerns worldwide. Penicillin G or ampicillin should not be initiated empirically and should be reserved for susceptible pneumococcal or meningococcal meningitis (penicillin minimum inhibitory concentration [MIC] ≤0.06μg/mL). Cefotaxime or ceftriaxone can be used for penicillin–nonsusceptible pneumococci (penicillin MIC >0.06μg/mL). If a pneumococcal isolate is nonsusceptible to cefotaxime or ceftriaxone (MIC ≥1μg/ mL), vancomycin should be continued along with a third-generation cephalosporin. Most N. meningitidis strains are susceptible to penicillin; third-generation cephalo­sporins would be preferred in the rare instance when an isolate has reduced suscep­tibility to penicillin (MIC ≥0.06μg/mL) [38]. Table21.2 summarizes the denitive treatment and durations for bacterial pathogens causing community-acquired ABM in children.
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Table 21.1
in children
Empiric antimicrobial treatment for community-acquired acute bacterial meningitis
a
Streptococcus
Reduced Streptococcus pneumoniae antimicrobial
sensitivity to penicillin
penicillin plus cefotaxime,
Age <1month
old
pneumoniae susceptible to penicillin
– Amoxicillin/ampicillin/
or amoxicillin/ampicillin plus an aminoglycoside
1month to
Cefotaxime or ceftriaxone
18years
q6h every 6h, q8h every 8h, q12h every 12h
a
Adapted and modied from Refs. [34, 39, 40]
Table 21.2
children
Denitive therapy and duration for community-acquired acute bacterial meningitis in
a
Cefotaxime or ceftriaxone plus vancomycin ± rifampicin
Standard
Organism
treatment Alternatives Dosage
Streptococcus pneumoniae
Penicillin
susceptible (MIC
≤0.06μg/mL)
Penicillin
nonsusceptible
(MIC >0.1μg/
Penicillin or amoxicillin/ ampicillin
Ceftriaxone or cefotaxime
Ceftriaxone, cefotaxime, chloramphenicol
Cefepime, meropenem,
moxioxacin mL), third­generation cephalosporin susceptible (MIC <2mg/mL)
Cephalosporin
nonsusceptible (MIC ≥1μg/mL)
Cefotaxime/ ceftriaxone plus
Vancomycin plus
moxioxacin
vancomycin plus/minus rifampicin
Dosage Age<1week: ampicillin/
amoxicillin 50mg/kg q8h; cefotaxime 50mg/kg q8h; gentamicin 2.5mg/kg q12h Age 1–4weeks: ampicillin 50mg/ kg q6h; cefotaxime 50mg/kg q6–8h; gentamicin 2.5mg/kg q8h; tobramycin 2.5mg/kg q8h; amikacin 10mg/kg q8h
Vancomycin 10–15mg/kg q6h; rifampicin 10mg/kg q12h; cefotaxime 75mg/kg q6–8h; ceftriaxone 50mg/kg q12h
Penicillin G 300,000units/kg/ day in four to six divided doses; ampicillin 50mg/ kg q6h; cefotaxime 75mg/kg q6–8h; ceftriaxone 50mg/ kg q12h
Cefotaxime 75mg/
b
kg q6h; ceftriaxone 50mg/kg q12h
Vancomycin 15mg/kg q6h; rifampicin 10mg/ kg q12h; cefotaxime 75mg/ kg q6h; ceftriaxone 50mg/kg q12h
Duration
10– 14days
10– 14days
10– 14days
(continued)
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Z. Şahbudak Bal et al.
Table 21.2 (continued)
Standard
Organism
treatment Alternatives Dosage
Duration
Neisseria meningitidis
Penicillin
susceptible (MIC ≤0.06μg/mL)
Penicillin or amoxicillin/ ampicillin
Ceftriaxone,
cefotaxime,
chloramphenicol
Penicillin G 300,000units/kg/ day in four to six
7days
divided doses; ampicillin 50mg/ kg q6h
Penicillin
reduced susceptibility (MIC ≥0.06μg/
Ceftriaxone or cefotaxime
Cefepime,
meropenem, or
chloramphenicol
Cefotaxime 75mg/ kg q6–8h; ceftriaxone 50mg/ kg q12h
7days
mL)
Listeria monocytogenes
Amoxicillin or ampicillin, penicillin G plus gentamicin
Trimethoprim–
sulfamethoxazole
meropenem plus
gentamicin,
linezolid
Penicillin G
c
300,000units/kg/
,
day in four to six divided doses; ampicillin 50mg/
21– 28days
kg q6h
Haemophilus inuenzae
Beta-lactamase
negative
Amoxicillin or ampicillin
Ceftriaxone,
cefotaxime, or
Ampicillin 50mg/ kg q6h
7–10days
chloramphenicol
Beta-lactamase
positive
Beta-lactamase-
negative ampicillin resistant
Group B
Streptococcus
Ceftriaxone or cefotaxime
Ceftriaxone or cefotaxime, plus meropenem
Penicillin G or ampicillin
Cefepime,
ciprooxacin,
chloramphenicol
Cefotaxime 75mg/ kg q6h; ceftriaxone 50mg/kg q12h
Ciprooxacin Cefotaxime 75mg/
kg q6h; ceftriaxone 50mg/kg q12h,
d
meropenem 40mg/ kg q8h
– Penicillin G
450,000–
7–10days
7–10days
14–
21days 500,000units/kg/ day in four divided doses; ampicillin 50mg/kg q6h
MIC minimum inhibitory concentration, q6h every 6h, q8h every 8h, q12h every 12h
a
Adapted and modied from Refs. [14, 32]
b
Might consider if serious allergy to ceftriaxone/cefotaxime and would not use alone but in com­bination with vancomycin considering the paucity of data on moxioxacin treatment of pneumo­coccal meningitis
c
Alternatives are considered only if the patient cannot be desensitized to penicillin
d
Only a few case reports on the treatment of this infection, so very little information is available on which to base a recommendation of meropenem, along with ceftriaxone or cefotaxime
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21.7 Hearing Loss inChildren withAcute
Bacterial Meningitis
Acute bacterial meningitis can cause short-term complications, including seizures, focal neurological decits, brain abscesses, and long-term permanent sequelae, par­ticularly HL, cognitive impairment, hydrocephalus, and epilepsy. Sensorineural HL (SNHL) is a signicant long-term sequela, and hearing should be tested before dis­charge or within 1 month [34]. The European Society of Clinical Microbiology and Infectious Diseases (ESCMID) recommended administering dexamethasone in all suspected ABM cases [32]; the American Academy of Pediatrics (AAP) advises dexa­methasone use for children 6weeks and older in Hib meningitis [39]. However, dexa­methasone is not routinely recommended for S. pneumoniae-caused ABM; the AAP advises weighing the potential benets and risks [40]. Dexamethasone should be dis­continued if a pathogen other than these pathogens grew in the CSF culture [35]. A recent study from Denmark that evaluated all children with ABM during 1998–2016 showed that nearly every one of four children developed neurological sequelae; HL was the most common (15%) [41]. Hearing loss occurs more frequently following pneumococcal meningitis (22–30%) than meningococcal meningitis (1–8%) [35].
Once bacteria invade the meninges and disrupt the blood–brain barrier (BBB), through the hematogenous spread, direct extension from paranasal and dental infec­tions, skull base fracture causing CSF leak, or direct implementation, immune acti­vation is triggered by different pathogen-associated molecular patterns (PAMPs) [35, 42]. Toll-like receptors (TLRs) 2, 4, 5, and 9 rst recognize bacteria and Nod­like receptors (NLRs), which lead to the activation of intracellular signaling path­way factors such as nuclear factor-kappa B (NF-κB) [35, 42]. Nuclear factor- kappa B is a transcriptional activator of the genes that encode the pro-inammatory cyto­kines and adhesion molecules such as TNF-α, IL-1, IL-8, and the intercellular adhe­sion molecule 1 (ICAM-1). Tumor necrosis factor-alpha and IL-1β are released as inactive precursors, transforming into active forms by proteases (caspase 1 [Casp]). They are signicant inducers of NF-κB and the key molecules resulting in menin­geal inammation [42]. Tumor necrosis factor-alpha and IL-1β activate proteolytic enzymes (matrix metalloproteinase [MMP]-8, MMP-9) and oxidants (peroxyni­trite); chemokines and adhesion molecules subsequently trigger leukocyte accumu­lation and activation of proteolytic enzymes and oxidants [35, 43]. Matrix metalloproteinase-8 and MMP-9 cause extracellular matrix degradation and tissue destruction; nitric oxide, superoxide, and peroxynitrite cause oxidant-induced deoxyribonucleic acid (DNA) strand breakage and energy depletion lipid peroxida­tion that leads to loss of membrane integrity [43]. These host inammatory responses result in vasculitis, focal ischemia, increased intracranial pressure, transmigrating leukocytes, glial cells and astrocyte stimulation, cortical necrosis, and hippocampal neuronal loss stemming [35, 42].
The chemokines and adhesion molecules trigger massive leukocyte accumula­tion into the subarachnoid space. Tumor necrosis factor-alpha and IL-1β, together with activated leukocytes, contribute to the release of oxidants, leading to the blood labyrinth barrier breakage and cochlea cytotoxicity. Another contributing
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mechanism is the occlusion of the inner ear’s blood vessels due to septic emboli and thrombus, leading to cochlear hypoxia, ischemia, and neural damage [35].
Hearing loss may develop early after infection, whereas late-onset HL can also occur. Early detection is crucial because patients can develop cochlea ossication, and a cochlea implant should be placed before obliteration. Furthermore, early diag­nosis is essential to minimize the development of speech and language delay, bal­ance disturbances, and behavioral disorders. Audiology assessment is recommended for children diagnosed with conrmed ABM before discharge or within 1 month [35, 39, 40, 44].
Unilateral or bilateral SNHL occurs in around 10% of children with ABM.Bilateral severe or profound HL has been mainly observed in children after
S. pneumoniae meningitis (14–32%), followed by N. meningitidis (4–23%) and H. inuenzae (20%) [33]. A 20-year invasive pneumococcal disease (IPD) surveil-
lance, which included 83 children with meningitis, reported that 14% developed HL of the 51 patients who underwent auditory assessment [45]. At the time of dis­charge, 31% of 161 pediatric survivors of pneumococcal meningitis had SNHL among patients seen at eight USA children’s hospitals between 2007 and 2013 [46]. A 1-year follow-up analysis of IMD conducted in Israel determined that 7% of the children developed HL, while half of the cases were severe [47].
In a study from Bangladesh, short-term follow-up (30–40days) determined that 33% of the children had HL, while long-term follow-up (6–24months) showed that only 18% were permanent, which demonstrated that HL developed after pneumo­coccal meningitis could be reversible [48]. Roine etal. [49] also showed that HL could be reversible and frequently improves in children with initially severe HL.The decrease in HL in a long-term period was attributed to recovered patients and revers­ible HL. In contrast, some patients with normal ears or moderate impairment became severely impaired.
The risk factors for HL after ABM were reported as underlying comorbidity, late (illness >24h before intervention) admission, the severity of meningitis (mechani­cal ventilation requirement, presence of septic shock signs), raised intracranial pres­sure at admission, low glucose, and high protein in CSF [50].
Z. Şahbudak Bal et al.
21.7.1 Adjunctive Therapy toPrevent Hearing Loss inChildren
withAcute Bacterial Meningitis
Adjunctive therapies are recommended for reducing short- and long-term neurologi­cal sequelae of ABM.These therapies targeted ve main areas: (1) non- bacteriolytic antibiotic use such as rifampin and daptomycin to modulate bacterial killing and the release of bacterial products, (2) initiation of the inammatory response via host recognition of bacteria or its products, (3) adjuvant dexamethasone to modulate the uncontrolled inammatory response, (4) host inammatory and neurotoxic media­tors inhibition, and (5) modulation of the apoptotic pathways [35].
Experimental animal models of bacterial meningitis were conducted to evaluate TNF-α, matrix metalloproteinases, nitric oxide and antioxidants, neuroprotective factors (melatonin and brain-derived neurotrophic factor), and other
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anti- inammatory therapies (triptans) because of the signicant role of host uncon­trolled inammatory response in neuronal damage; however, not yet proved and not in clinical use [35]. In combination with cipemastat (Trocade®), a metalloproteinase inhibitor, daptomycin, reduced neuroinammation and brain damage in the pneu­mococcal meningitis rat model [51]. G-protein cannabinoid receptor type 2 (CB2) agonists are another potential candidate that downregulates pro-inammatory pro­cesses but did not alter brain damage in experimental pneumococcal meningitis [52].
Bacterial meningitis causes apoptotic damage to the hippocampus. Vitamin B12 lessened hippocampal damage by deactivating pro-inammatory genes in an exper­imental model of S. pneumoniae meningitis in infant rats [53].
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21.7.1.1 Adjuvant Dexamethasone Therapy
In experimental models, corticosteroids reduced inammatory response and improved outcomes. However, dexamethasone use in children is still controversial. A meta-analysis evaluated dexamethasone adjuvant therapy in ABM included 2029 patients from ve trials of all ages and showed that dexamethasone use in ABM did not alter mortality, severe neurological sequelae, or severe bilateral deafness; mean­while, a nearly 5% decrease was observed in HL in survivors [54].
A recent meta-analysis of adjunctive dexamethasone use in ABM reported that dexamethasone signicantly reduces HL compared to standard antibiotics and severe neurological sequelae; in contrast, the mortality did not decrease [55].
The most recent Cochrane meta-analysis demonstrated that HL was reduced by corticosteroid treatment in children with H. inuenzae meningitis [56]. In contrast, corticosteroids did not signicantly reduce HL in ABM cases caused by pathogens other than H. inuenzae. Corticosteroids were shown to decrease severe HL, any HL, and short-term neurological sequelae, mainly in high-income countries but not in low-income countries.
Meningeal inammation in the initial phase of the disease affects neuronal dam­age; the late presentation may lead to missing the opportunity for corticosteroids. A recent large study from Taiwan enrolled 8083 ABM episodes and found that steroid­administered children signicantly had a more extended hospital stay, higher hospi­tal costs, and mortality [57]. However, the study did not evaluate the subgroups according to pathogens. A recent study showed an association between delayed cerebral injury and steroid use in adults, and this association was attributed to effects on cerebral blood vessels leading to vasospasm [58].
Dexamethasone should be used before or simultaneously as the rst dose of the antibiotic(s). However, another concern is the reduced penetration of vancomycin into the CSF by reducing meningeal inammation with dexamethasone, leading to treatment failures [54, 55].
21.7.1.2 Adjuvant Glycerol Therapy
Meningeal inammation leads to increased vasogenic and cytotoxic brain edema, decreasing cerebral perfusion. From this point, hyperosmotic agents have been studied to reduce neurological damage by reducing intracranial pressure. Glycerol is a cheap and widely available hyperosmotic agent [35].
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Z. Şahbudak Bal et al.
A prospective, randomized, double-blind study comparing adjuvant dexametha­sone or glycerol with placebo under 16years in Latin America demonstrated that severe neurological sequelae were less frequently observed in glycerol and dexa­methasone plus glycerol received patients than in the placebo group; however, a signicant difference was not observed for HL [59]. The same author group evalu­ated hearing impairment degrees in dexamethasone and dexamethasone plus glyc­erol administered patients and found no signicant difference from placebo at any threshold levels (40, 60, and 80 decibels [dB]) [60]. A smaller study evaluated glyc­erol and acetaminophen as adjunctive therapies in ABM contrasty and found no effects on neurological sequelae and deafness; however, the study group primarily consisted of pneumococcal meningitis [61]. A double-blind, randomized controlled trial in Malawian adult patients demonstrated an increased risk of death with glyc­erol in adults with bacterial meningitis in Malawi’s high HIV seroprevalence setting [62]. The most recent Cochrane meta-analysis evaluating ve studies with 922 par­ticipants on glycerol use in ABM showed a signicant decrease in HL [63]. The comparison of glycerol and placebo showed no signicant impact on death, while decreased neurological disability was determined.
21.8 Conclusion
Acute bacterial meningitis still causes signicant morbidity and mortality in chil­dren, particularly in low-income and sub-Saharan African meningitis belt countries. Hearing loss may develop early after infection, but late-onset HL can also occur. Reversible SNHL has been determined in the follow-up of children with pneumo­coccal meningitis. Early detection is crucial because patients can develop cochlea ossication, and a cochlear implant should be placed before obliteration. Children with ABM should be evaluated for HL in the hospital or within 1 month of dis­charge. Dexamethasone may be used in ABM caused by Hib but is not routinely recommended for pneumococcal meningitis and should be discontinued if another microorganism is detected in the CSF. Glycerol is cheap and widely available; how­ever, the studies on glycerol used to prevent neurological sequela in patients with ABM are limited and controversial.
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